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How do we know brain Is not involved in knee reflex?

How do we know brain Is not involved in knee reflex?

How do we know that compressing the knee generates a feedback signal that makes the leg extend even before the signal reach the brain?


Q: How do we know brain Is not involved in knee reflex?

A: The brain is involved in the knee reflex in the control of how fast/slow and strong/weak the reflex occurs, but it's not essential in the occurrence of the knee reflex. The knee reflex is still present even when the spinal cord is cut or destroyed at any level above L2 [1], which is above the reflex arc pathway (L2-4) and which cuts off the connection between the brain and the reflex arc. This is usually evident clinically. The only exception that the knee reflex may be absent after the incident is that the condition called “spinal shock” occurs [3]. However, this condition is temporary, and the knee reflex will return, usually even brisker than before the incident (due to the absence of inhibitory control from the brain). This confirms that the brain is not essential in the knee reflex and only has regulatory roles.

Q: How do we know that compressing the knee generates a feedback signal that makes the leg extend even before the signal reach the brain?

A: Electrophysiologic studies show that the latency of the knee reflex is normally about 46 msec [1] while the evoked potential (P37) recorded at the scalp over the leg area after electrical stimulation of the posterior tibial nerve is about 37 msec.[4] So, comparing data from these comparable but not identical experiments, it can be estimated that the knee reflex occurs, indeed, after the signal reaches the brain, as you asked. But don't forget that the former latency is the time of the complete loop while the latter latency is of only halfway. It will take longer than 37 msec for the signal to complete the loop of leg-brain-leg and move the knee.

References

  1. Xu D, Guo X, Yang CY, Zhang LQ. Assessment of Hyperactive Reflexes in Patients with Spinal Cord Injury. BioMed Research International. Vol 2015, Article ID 149875. http://dx.doi.org/10.1155/2015/149875

  2. Wikipedia. Patella reflex.

  3. Atkinson PP, Atkinson JLD. Spinal Shock. Mayo Clinic Proceedings. 1996 Apr; 71(4): 384-389.

  4. Walsh P, Kane N, Butler S. The clinical role of evoked potentials. Journal of Neurology, Neurosurgery & Psychiatry 2005;76:ii16-ii22. http://dx.doi.org/10.1136/jnnp.2005.068130


Knee Jerk Reflex (Patellar Reflex)

The knee jerk reflex (seen in the figure to the right) is called a monosynaptic reflex because there is only one synapse in the circuit needed to complete the reflex. It only takes about 50 milliseconds between the tap and the start of the leg kick. That is fast! The tap below the knee causes the thigh muscle to stretch. Information is then sent to the spinal cord. After one synapse in the ventral horn of the spinal cord, the information is sent back out to the thigh muscle that then contracts.


Background

Reflexes require no thought. They are automatic, fast, and of huge importance to a human's ability to successfully respond to their environment. Despite the magnificent information-processing power of the billions of neurons in our brain, we need a lot of stuff to be done automatically. Without reflexes, our brains would be overloaded with worrying about constantly updating the position of our unstable bodies to keep us upright. Without reflexes, our ability to engage in complex thought (black holes, neuroscience, what to do this weekend, how do I make an instrumented reflex hammer?) would be limited. Without reflexes, your reactions to painful stimuli would require thought, and. don't take it personally.. but you think very slowly. Don't feel bad, all humans are slow thinkers, and we need more speed to respond to dangerous painful stimuli. So we let our spinal cord do that fast work for us.

One example of a reflex is the patellar stretch reflex. Our spinal cord partners with sensors in our muscles, called muscle spindles, to keep track of where our bodies are in space and how stretched or contracted our muscles are. The way that these sensors interact with our spinal cord is through a reflex pathway. Stretching the muscle activates the muscle spindle at the end of the sensory neuron (embedded in your muscle) and starts the reflex. The reflex is to prevent overstretching of the muscle and compensates with a contraction.

As you can see, there is only one connection (a synapse) needed for the information from the sensory neuron to get to the motor neuron and cause a muscle contraction. Because of this single synapse, this can happen very fast. In a young, healthy person, it takes 15-30 milliseconds for the stretch stimulus to produce a muscle contraction, by comparison, it takes 5-10 times that long to blink your eye in response to a stimulus, or 150-300 milliseconds. This is super useful for correcting your muscle length in response to rapid changes such as a slip or trip. These situations require very fast corrections to prevent falling and injury. If you had to consciously flex your leg in response to the leg stretch (a reaction) it would be much slower than the 15-30 seconds of reflex.

Now let's try to measure this reflex! And perhaps let's measure a reaction too!

Before you begin, make sure you have the Backyard Brains Spike Recorder installed on your computer/smartphone/tablet. The Backyard Brains Spike Recorder program allows you to visualize and save the data on your computer when doing experiments. We have also built a simple lab handout to help you tabulate your data.

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What is a Patellar Reflex? (with pictures)

The patellar reflex is a type of deep tendon reflex that occurs when an area just below the patella, also known as the kneecap, is struck. In healthy individuals, when the right spot is tapped, this causes the lower leg to kick out almost instantaneously. Medical professionals may check this reflex during a routine neurological exam, looking for responses that are exaggerated, delayed, or not present.

This reflex is what is known as a monosynaptic reflex, because only one synapse needs to be crossed to complete the circuit that triggers it. When the area below the kneecap is hit with a reflex hammer, it hits the patellar tendon, which causes the quadriceps muscle in the thigh to contract, leading the leg to kick out. This involuntary response does not involve the brain, only the spinal cord, and while it feels instantaneous to the observer, around 50 milliseconds are actually involved in the response time, as people would see if they saw a radically slowed film of the event.

If someone does not have a patellar reflex, he or she is said to be exhibiting Westphal's sign. This indicates that there is a problem in the patient's spinal cord or peripheral nerves. The healthcare professional usually assesses the reflex on both legs to see the extent of the problem. It is also possible for a patient to experience an exaggerated reflex, in which the leg kicks out more radically than would be expected.

A number of reflexes can be used to assess physical and neurological health. Patellar reflexes provide information about specific nerves in the leg involved, along with the spinal cord, and they may be used in routine physicals to check on a patient's health, as well as in specific neurological exams to explore possible causes for neurological symptoms. If the reflex is abnormal, a medical professional may recommend additional testing to learn more about the cause of the abnormality, and to start developing a diagnosis, along with treatment options.

This particular reflex is so well-known that the common name for it, “kneejerk reflex,” is sometimes used to describe a situation in which someone responds to something without really thinking. In a metaphorical kneejerk response, someone can lash out verbally instead of kicking physically, sometimes causing social tension. This reflex can also be observed in animals, and it is used in routine neurological screening by veterinarians as well.

Ever since she began contributing to the site several years ago, Mary has embraced the exciting challenge of being a InfoBloom researcher and writer. Mary has a liberal arts degree from Goddard College and spends her free time reading, cooking, and exploring the great outdoors.

Ever since she began contributing to the site several years ago, Mary has embraced the exciting challenge of being a InfoBloom researcher and writer. Mary has a liberal arts degree from Goddard College and spends her free time reading, cooking, and exploring the great outdoors.


Beware your doctor’s knee-jerk reflex: 3 questions to ask

We are, I trust, all but universally familiar with the knee-jerk, or patellar, reflex. A doctor taps the patellar tendon with a rubber mallet, and our leg kicks forward in response.

The reaction is famously unthinking. In fact, it is literally so. What makes a reflex a reflex is that the brain is substantially uninvolved. The stretch of a tendon by the mallet is transmitted to the spinal cord, and the compensatory command to move against the stretch is sent right back out from the spinal cord to the muscles. The brain only gets involved as chaperone, pointing out to the nerves and muscles in question that the tap of a mallet is far from a dire threat to life and limb, and the response need not be unduly vigorous. In the aftermath of a stroke that damages the brain’s involvement in this network, and removes the calming influence of a rational assessment, reflexes become hyper-intense.

Since reflexes are reflexive, unthinking, and even a bit silly — we use them as a metonym for other actions of that sort. When we act without thinking, we admonish one another against such “knee-jerk” behavior.

Bringing this full circle, then, from reflex hammers in medical context to metonyms in the context of popular understanding, I write to offer a precaution: Beware your doctor’s knee-jerk reflex.

There are three particular prompts for this warning at this time.

First, I recently saw and began treating a patient for the fluoroquinolone syndrome. Within just a couple of weeks, I heard from a friend who had classic symptoms of it as well, following treatment with Levaquin. In both cases, there was a valid indication for antibiotic use. But there was also good reason to doubt the need for such a high-powered, broad-spectrum antibiotic in both cases. Often, the easiest way for a busy clinician to be sure to “cover the bases” with an antibiotic is to go after a fly with an elephant gun. The collateral damage can, predictably, be considerable a consequence of knee-jerk prescribing.

Second, a paper published in JAMA indicates that cancer screening tests are routinely ordered in both men and women with life expectancies less than 5 years (due either to advanced age or serious illness, or both). The tests in question are all good tests, recommended by the United States Preventive Services Task Force. But the whole point of screening is to look for trouble early, so it does not progress over time. If there isn’t much time left, looking for potential future trouble not currently causing any is very unlikely to do any good, and can — as the authors note — do harm. Why order the test then? Reflex.

Third, and finally, a study was just published in Critical Care Medicine indicating that demonstrably futile care in the intensive care unit is not merely futile, but potentially as bad as fatal. As the rate-limiting resources of intensive care are allocated to cases where they cannot do any meaningful good, those more likely to benefit are denied access. The misallocation of resources in this case is again the product of inertia, going with the prevailing flow, or — reflex.

And so it is that while we might all submit on occasion to the knee-jerk test, we should not submit to the knee-jerk tendencies that all too readily drive behavior — even in clinics and hospitals. Self-defense is simple, and accessible to us all.

1. Always ask “why?” This seems obvious, but even in this modern era, many patients take it as an article of faith that a doctor’s recommendation is thoughtful and well informed. It may well be but on any given occasion, it could also be a knee-jerk — born of prevailing tendencies, distractions, and want of time. The question “why” is easily addressed by those who have already thought it over and is a necessary reality check for those of us who have not.

2. Always ask “what else?” In the case of the fluoroquinolone syndrome, it’s bad enough when a fluoroquinolone was a genuinely thoughtful, warranted choice. It’s downright tragic when a much-less-potentially-toxic, narrow spectrum antibiotic would have served at least as well. “What else?” is a reminder that there is generally more than one way to test or treat, and the one we want is the BEST of them: most likely to help, least likely to hurt. It prods our providers to do the extra work of getting us there when we remind them we want to know the options, and comparison shop them.

3. Always ask “then what?” This would certainly defend against a screening colonoscopy in an 85 year old with congestive heart failure. If I have this test, then what? The answer would have to be: We can find potential cancer early, and fix it now so it doesn’t cause you trouble in ten years. That would invite all concerned to revisit the relevance of that “help” ten years in the future of someone exceedingly unlikely to live that long.

Clinical assessment that includes a test of the knee-jerk reflex is fine. Clinical decisions driven by it are not, but they too, are out there. Forewarned, I hope, will prove to be forearmed.


How do we know brain Is not involved in knee reflex? - Psychology

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The analysis of the anatomical and physical bases of learning and memory is one of the great successes of modern neuroscience. Thirty years ago little was known about how memory works, but now we know a great deal. This Chapter will discuss four issues that are central to learning and memory. First, what are the different types of memory? Second, where in the brain is memory located? One possibility is that human memory is similar to the memory chip in a personal computer (PC), which stores all the memory in one location. A second possibility is that our memories are distributed and stored in different regions of the brain. Third, how does memory work? What types of changes occur in the nervous system when a memory is formed and stored, are there particular genes and proteins that are involved in memory, and how can a memory last for a lifetime? Fourth, is the issue of importance to many people, especially as we age: How can memory be maintained and improved, and how can it be fixed when it is broken?

Psychologists and neuroscientists have divided memory systems into two broad categories, declarative and nondeclarative (Figure 7.1). The declarative memory system is the system of memory that is perhaps the most familiar. It is the memory system that has a conscious component and it includes the memories of facts and events. A fact like 'Paris is the capital of France', or an event like a prior vacation to Paris. Nondeclarative memory, also called implicit memory, includes the types of memory systems that do not have a conscious component but are nevertheless extremely important. They include the memories for skills and habits (e.g., riding a bicycle, driving a car, playing golf or tennis or a piano), a phenomenon called priming, simple forms of associative learning [e.g., classical conditioning (Pavlovian conditioning)], and finally simple forms of nonassociative learning such as habituation and sensitization. Sensitization will be discussed in detail later in the Chapter. Declarative memory is "knowing what" and nondeclarative memory is "knowing how" .

Figure 7.1
Memory systems in the brain. (Modified from Squire and Knowlton, 1994)

Figure 7.2
Word recognition memory test.

Figure 7.3
Object recognition memory test .

Everyone is interested in knowing how well they remember so let us take a simple memory test. The test (Figure 7.2) will present a list of 15 words, then there will be a pause and you will be asked whether you remember some of those words. Sorry, you have to put your pen down for this test and do not read further in the Chapter until you complete the test.

This memory test called the DRM test after its creators James Deese, Henry Roediger and Kathleen McDermott. It was not meant to be a trick, but to illustrate a very interesting and important feature about memory. We like to think that memory is similar to taking a photograph and placing that photograph into a filing cabinet drawer to be withdrawn later (recalled) as the “memory” exactly the way it was placed there originally (stored). But memory is more like taking a picture and tearing it up into small pieces and putting the pieces in different drawers. The memory is then recalled by reconstructing the memory from the individual fragments of the memory. The reason so many individuals incorrectly believe that “sweet” was on the list is because there were so many other words on the list that had a sweet connotation. “Failing” this test is actually not a bad outcome. Individuals with Alzheimer’s disease generally do not say that “sweet” was on the list. They cannot make the normal associations involved in the recall of a memory.

The word list gives insights into memory processing and retrieval, but it is not a really good test of “raw” memory ability because it can be affected by distortions and biases. To avoid these problems, psychologists have developed other memory tests. One is the object recognition test (Figure 7.3) to test declarative memory. This test is also good because, as we will see later, it can even be used on animals. The test involves presenting a subject with two different objects and they are asked to remember those objects. There is a pause and then two objects are shown again, one of which is new and the other having been shown previously. Subjects are asked to identify the novel object, and to do so, they need to remember which one was shown previously. A somewhat related test is the object location test in which subjects are asked to remember the location of an object on a two-dimensional surface.

Examples of nondeclarative memory, such as associative learning, can be tested by pairing one stimulus with another and later testing whether a subject has learned to make the association between the two stimuli. The classical example is the paradigm developed by the Russian physiologist Ivan Pavlov, which is now called classical or Pavlovian conditioning. In classical conditioning (Figure 7.4), a novel or weak stimulus (conditioned stimulus, CS) like a sound is paired with a stimulus like food that generally elicits a reflexive response (unconditioned response, UR unconditioned stimulus, US) such as salivation. After sufficient training with contingent CS-US presentations (which may be a single trial), the CS is capable of eliciting a response (conditioned response, CR), which often resembles the UR (or some aspect of it).

Figure 7.4
Classical (Pavlovian) conditioning.

7.3 Localization of Memory

Now let us turn to this issue about where is memory located. There are three basic approaches.

  1. Imaging. Modern imaging techniques like fMRI (functional magnetic resonance imaging) or PET (positron emission tomography) allows one to “see” areas of the brain that are active during specific brain tasks. If a subject is placed in an fMRI scanner and given a memory test, one can determine what areas of the brain are active, and that activity presumably is related to where in the brain the memory is processed and/or stored.

Figure 7.5
PET brain scan during an object location test. (from A. M. Owen, et al., J. Cog. Neurosci. 8:6, 588-602, 1996.)

  1. Brain lesions. In this experimental procedure, small parts of the brains of mice or rats are surgically removed or chemically inactivated and the animals are systematically examined to determine whether the lesion affected any memory system.

  2. Brain disease and injury. Here scientists take advantage of individuals who have had unfortunate brain injuries, for example, through stroke or through a brain tumor in a specific area of the brain. If one finds a memory deficit in the patient, it is likely that the region of the brain that was injured is involved in that memory.

A classic study on localization of memory was the result of surgery performed on Henry Molaison, a patient who was only known to the scientific community as “H.M.” until his death in 2008. H. M. is famous in neuroscience literature because his brain provided major insights into the localization of memory function. In the 1950’s, H.M. was diagnosed with intractable epilepsy, and while there are pharmacologic treatments, in some cases the only treatment is to remove the portion of the brain that is causing the seizures. Consequently, H.M.'s hippocampus was removed bilaterally. Figure 7.6 (right) is an MRI of a normal individual showing the hippocampal region, whereas Figure 7.6 (left) shows a MRI of patient H.M. after the removal of the hippocampus.

Figure 7.6
Bran scans of H.M. (left), and a normal individual (right). ( Copyright © 1997 by Suzanne Corkin, used with permission of The Wylie Agency LLC. )

Before the operation, H.M. had a fine memory, but after the operation, H.M. had a very severe memory deficit. Specifically, after the operation H.M.'s ability to form any new memories for facts and events was severely impaired he had great difficulty learning any new vocabulary words he could not remember what happened the day before. So if H.M. had an interview the day following a previous interview, he would have little or no memory about the interview or events during it. This study clearly indicated that the hippocampus was critical for memory formation. But whereas H.M. had great difficulty forming new memories for facts and events, he still had all of his old memories for facts and events. Specifically, he had all his childhood memories, and all of his memories prior to the operation. This type of memory deficit is called anterograde amnesia. (In contrast, retrograde amnesia refers to loss of old memories.) The studies on H.M. clearly indicated that whereas the hippocampus is critical for the formation of new memories, it is not where the old memories are stored. It is now known that those old memories are stored in other parts of the brain, such as in the frontal cortex. The process by which an initially labile memory is transformed into a more enduring form is called consolidation. This process involves the memory being stored in a different part of the brain than the initial site of its encoding.

H.M. was also interesting in that while his ability to form new memories for facts and events was severely impaired, he could form new memories for skills and habits. While he could form new memories for skills and habits, he did not know that he had the skills! He had no awareness of the memory he couldn’t declare that he had it. This finding clearly indicated that the memory for skills and habits are not formed in the hippocampus. Collectively, we learned from these studies on H.M. and other patients that memory is distributed throughout the nervous system, and different brain regions are involved in mediating different types of memory.

Figure 7.7 summarizes many decades of research on the anatomical locus of memory systems. The medial temporal lobe and structures like the hippocampus are involved with memories for facts and events the striatum is involved with memories for skills and habits the neocortex is involved with priming the amygdala is involved with emotional memories and the cerebellum with simple forms of associative learning. Lower brain regions and the spinal cord contain even simpler forms of learning. In summary, memory is not stored in a single place in the brain. It is distributed in different parts of the brain.

Figure 7.7
Memory systems and their anatomical loci. (Modified from Squire and Knowlton, 1994)

Model systems to study memory mechanisms

Figure 7.8
Aplysia californica and its nerve cells.

Much of what has been learned about the neural and molecular mechanisms of learning and memory have come from the use of so called “model systems” that are amenable to cellular analyses. One of those model systems is illustrated in Figure 7.8A . Aplysia californica is found in the tidal pools along the coast of Southern California. It is about six inches long and weighs about 150 grams. At first glance it is an unpromising looking creature, but neuroscientists have exploited the technical advantages of this animal to gain fundamental insights into the molecular mechanisms of memory. Indeed, the pioneering discoveries of Eric Kandel using this animal were recognized by his receipt of the Nobel Prize in Physiology or Medicine in 2000. Aplysia have three technical advantages.

First, it exhibits simple forms of nondeclarative (implicit) learning like classical (Pavlovian) conditioning, operant conditioning and sensitization.

Second, Aplysia have a very simple nervous system. Compared to the 100’s of billions of nerve cells in the human brain, the entire nervous system of this animal only has about 10,000 cells. Those cells are distributed in different ganglia like the one illustrated in Figure 7.8B . Each ganglia like this one has only about 2,000 cells, yet it is capable of mediating or controlling a number of different behaviors. This means that any one behavior can be controlled by 100 neurons or even less. One has the potential of working out the complete neural circuit underlying a behavior, and then, after training the animal, the neural circuit can be examined to identify what has changed in the circuit that underlies the memory.

Third, the ganglia contain neurons that are very large. Figure 7.8B shows a ganglion under a dissecting microscope. It is about 2mm in diameter. The spherical structures throughout the ganglia are the cell bodies of individual neurons. Each neuron is identifiable and has a unique localization and function. A related advantage is that individual neurons can be removed and placed in culture medium where they can survive for many days. Indeed, multiple neurons can be removed from the ganglia and they reestablish their normal synaptic connections, thereby providing a very powerful experimental system to study the physiology of nerve cells and the properties of the connections between them. Figure 7.8C shows an example of a sensory neuron (small cell to the right) and a motor neuron (large cell to the left) in culture. In the micrograph it is possible to see the shadow of a microelectrode that has impaled the sensory neuron, and the shadow of a microelectrode that has impaled a motor neuron for performing intracellular recordings.

Sensitization, a simple form of nondeclarative learning amenable to detailed cellular analyses

Figure 7.9
Drawing of Aplysia (A) and data graph (B) of sensitization.

Figure 7.10
Reflex responses of a control animal (A), an animal that received sensitization training (B), and a sensitized animal (C).

Figures 7.9 and 7.10 illustrate a simple behavior exhibited by the animal and a simple form of learning called sensitization. The animal is tested by stimulating its tail with a weak electric shock (7.9) or a weak mechanical tap (7.10) . These stimuli elicit defensive reflex withdrawals of the body, which includes the tail and nearby sites such as the gill and a fleshy spout called the siphon. In response to test stimuli delivered every five minutes, the withdrawals are fairly reliable. They are about the same duration each time (Figures 7.9B, C, 7.10A) . But if a strong noxious stimulus (e.g., an electric shock) is delivered to another part of the animal such as its body wall, subsequent test stimuli to the tail give enhanced responses (Figure 7.9B and 7.10B) . This is an example of a simple form of learning called sensitization. It is defined as the enhancement of the response to a test stimulus as a result of delivering a strong generally noxious stimulus to the animal. In a sense, the animal is learning that it is in a “fearful” environment. Sensitization is a ubiquitous form of learning that is exhibited by all animals including humans.

Neural circuit and mechanisms of sensitization

    Neural circuit. We can take advantage of the large nerve cells of Aplysia, and the ability to make intracellular recordings from them, to work out the underlying neural circuit. Figure 7.11 illustrates a simplified view of the key components of the underlying neural circuit. Stimulation of the skin activates sensory neurons (SN) (only one of which is illustrated here) which make glutamatergic excitatory synaptic connections (triangles) with motor neurons (MN). If the summated synaptic input to the motor neurons is sufficiently large, the motor neurons will be activated and action potentials will propagate out of the ganglion to cause an eventual contraction of the muscle. So stimulation of the skin excites sensory neurons, the sensory neurons activate motor neurons, and motor neurons contract the muscles. Also, it should be evident that the greater the activation of the motor neurons, the greater will be the subsequent reflex response. This reflex in Aplysia is similar to the knee jerk or stretch reflex mediated by similar circuitry in the vertebrate spinal cord.

Figure 7.11
Neural circuit for the defensive withdrawal reflex.

Figure 7.12 A
Before sensitization. Slide the blue ball to control the animation.

Figure 7.12 B
During sensitization. Slide the blue ball to control the animation.

Figure 7.12 C
After sensitization. Control the animation by sliding the blue ball.

  1. Mechanisms of short-term sensitization. The mechanisms for the short-term memory for sensitization are illustrated in Figure 7.12B . The sensitizing stimulus leads to release of the neurotransmitter 5-HT. 5-HT binds the two types of receptors on the sensory neuron one is coupled to the DAG/PKC system, and the other is coupled to the cyclic AMP/PKA system. These are the same general cascades that you learned in biochemistry. Learning mechanisms have evolved to co-opt some of the biochemical machinery that are already present in all cells used them specifically for a memory mechanism in nerve cells. The protein kinases exert two types of actions. First, they regulate the properties of different membrane channels (the small gates on the illustration (Figure 7.12) represent membrane channels that underlie the initiation and the repolarization of the action potential). Consequently after a sensitizing stimulus, the amount of calcium that enters the synaptic terminal during an action potential and causes the release of transmitter will be enhanced. In addition, the modulation of the membrane channels leads to an increase in the excitability of the sensory neuron and as a result a greater number of action potentials will be elicited by a test stimulus to the skin. Second, the kinases regulate other cellular processes involved in transmitter release, such as the size of the pool of synaptic vesicles available for release in response to the influx of Ca 2+ with each action potential. Finally, 5-HT leads to changes in the properties of the postsynaptic motor neuron. Specifically, 5-HT leads to an increase in the number of glutamate receptors. The consequences of these processes can be seen by comparing the strength of the synaptic connection produced by a single action potential before (Figure 7.12A) and after (Figure 7.12C) sensitization. The specific details of all the currents and processes are not critical. However, it is important to know the general principles. One principle is that learning involves the engagement of second messenger systems. Here both the protein kinase C (PKC) and the protein kinase A (PKA) systems are involved. This is a fairly general principle. In every example of learning that has ever been examined, whether vertebrate or invertebrate, second messenger systems are engaged. A second principle is that memory involves the modulation of neuronal membrane channels. These can include channels that directly regulate transmitter release (i.e., Ca 2+ channels in the presynaptic neuron), channels that regulate neuronal excitability, and channels that mediate synaptic responses in the postsynaptic neuron. A third principle is that cyclic AMP is one of the critical second messengers that is involved in memory. Given this information, you can begin to think about how memory could be improved based on your knowledge of the underlying biochemistry.

Figure 7.13
Structural changes in sensory neurons associated with long-term sensitization. (Modified from M. Wainwright et al., J. Neurosci. 22:4132-4141, 2002.)

  1. Mechanisms of long-term sensitization. There are two major differences between short-term and long-term memories. Long-term memories involve changes in protein synthesis and gene regulation, whereas short-term memories do not. And, long-term memories in many cases involve structural modifications. Figure 7.13 illustrates examples of the processes of two sensory neurons that have been filled with a dye, one from an untrained animal and one from a trained animal. Shown are the thick axonal process of the neuron and many fine branches. Along the branches are seen small dot-like swellings or varicosities. These varicosities are the presynaptic terminals of the sensory neurons that make contact with other neurons like the motor neurons. (The motor neurons cannot be seen because only the sensory neurons were filled with the dye.) Part B of Figure 7.13 shows an example of a sensory neuron that has been injected with a dye in an untrained animal, and Part A shows one that has been filled with a dye 24 h after sensitization training. There is a major difference between these two neurons. The neuron from the trained animal has a greater number of branches and a greater number of synaptic varicosities than the neuron from the untrained animal. Therefore, long-term memory involves changes in the structure of neurons including growth of new processes and synapses. So, to the extent that you remember anything about this material on memory tomorrow, or next week, or next year, it will be because structural changes in synapses are beginning in your brains!

Figure 7.14
Genes implicated in long-term sensitization.

Long-term potentiation (LTP): A likely synaptic mechanism for declarative memory

An enduring form of synaptic plasticity called long-term potentiation (LTP) is believed to be involved in many examples of declarative memory. It is present in the hippocampus, which is known to be involved in declarative memories. LTP can be studied in brain slice preparations where an electric shock (test stimulus) can be delivered to afferent fibers and the resultant summated EPSP can be recorded in the postsynaptic neuron (Figure 7.15A). If the pathway is repeatedly stimulated (e.g., every minute), the amplitude of EPSP is constant (Figure 7.15B).

Delivering a brief 1-sec duration train of high frequency (100 Hz) stimuli (i.e., the tetanus) to the afferent nerve produces two types of enhancement in the postsynaptic neuron. First, there is a transient facilitation called post-tetanic potentiation (PTP) that dies away after several minutes. Second, following the PTP is a very enduring enhancement of the EPSP called LTP. LTP is the kind of mechanism necessary to store a long-term memory (Figure 7.15B).

Figure 7.16
Animation of the induction and expression of LTP.

The NMDA-type glutamate receptor is critical for some forms of LTP, in particular LTP at the CA3-CA1 synapse in the hippocampus. The postsynaptic spines of CA1 neurons have two types of glutamate receptors NMDA-type glutamate receptors and AMPA-type glutamate receptors (Figures 7.16A). Both receptors are permeable to Na + and K + , but the NMDA-type has two additional features. First, in addition to being permeable to Na + , it also has a significant permeability to Ca 2+ . Second, this channel is normally blocked by Mg 2+ .

Even if glutamate binds to the NMDA receptor and produces a conformational change, there is no efflux of K + or influx of Na + and Ca 2+ because the channel is "plugged up" or blocked by the Mg 2+ . Thus, a weak test stimulus will not open this channel because it is blocked by Mg 2+ . A weak test stimulus will produce an EPSP, but that EPSP will be mediated by the AMPA receptor. It is as if the NMDA receptor were not even there.

Now consider the consequences of delivering a tetanus (Figure 7.16B). During the tetanus, there will be spatial and temporal summation of the EPSPs produced by the multiple afferent synapses on the common postsynaptic cell (Figure 7.15A). Consequently, the membrane potential of the postsynaptic neuron will be depolarized significantly, much more so than the depolarization produced by a single afferent test stimulus. Because the inside of the cell becomes positive with the large synaptic input, the positively charged Mg 2+ is repelled by the inside positivity and is "thrust" out of the channel. Now the channel is unplugged and Ca 2+ can enter the spine through the unblocked NMDA receptor. The Ca 2+ that enters the cell activates various protein kinases, which then trigger long-term changes. One component of the long-term change is the insertion of new AMPA receptors into the postsynaptic membrane (Figure 7.16C) . Therefore, after the tetanus, the transmitter released from the presynaptic neuron by a test stimulus will bind to a greater number of receptors on the postsynaptic neuron. If more receptors are bound and hence opened, a larger (potentiated) EPSP (i.e., LTP) will be produced (Figure 7.16C). In addition to an increase in the number of postsynaptic AMPA receptors, there is evidence that a greater amount of transmitter is released from the presynaptic neurons. The combination of the presynaptic and postsynaptic effects would act synergistically to increase the size of the synaptic potential in the postsynaptic neuron. Note that this example of a synaptic mechanism for declarative memory bears some similarity to the synaptic mechanism for the example of nondeclarative memory (sensitization) discussed previously. Although the specific details differ, both involve activation of second messenger systems and regulation of membrane channels. Therefore, at a fundamental mechanistic level, there does not appear to be significant differences between the two major classes of memory systems. The major difference appears to be the brain region and the neural circuit and into which the learning mechanism is embedded.

Figure 7.17
A data plot of enhanced memory in transgenic mice.

With a knowledge of some of the genes and proteins involved in memory, we can use this information to try to both test the role of specific proteins in memory and also to improve memory. One experimental way of approaching the issue is to use transgenic technology in which a gene of interest can be over expressed in an animal by introducing it into an egg cell. When the offspring develop into adults, their performance on memory tests can be examined. An example of this approach is illustrated in Figure 7.17 . Here the role of the NMDA receptor was examined by Joe Tsien and his colleagues, who were then at Princeton University. If NMDA receptors are important for the induction of LTP, and LTP is important for declarative memory, one would expect that animals that had a greater number of NMDA receptors would learn more readily. NMDA receptors were over expressed in mice and the mice were tested on the object discrimination test that was discussed earlier in the Chapter.

To assess the performance of a mouse on the object recognition task, the experimenter measures the amount of time for some predefined period the mouse spends exploring the one object, versus the amount of time the mouse spends exploring the other object. If the mouse remembers that it had seen one of the objects previously, it will spend more time exploring the novel one. As illustrated in Figure 7.17 , one hour after the initial presentation of the objects, the mice do very well on the test. Indeed, they are correct about 100% of the time. They know the novel object. However, one day later the memory performance is rather poor, and after three days it is even worse. By one week, mice show no recognition memory.

What about the mice that received the extra NMDA receptors? Now one day after training they have perfect memory! So the extra receptors have led to an improved memory performance. That’s the good news – but the bad news is that the memory is no better one week later. This somewhat disappointing finding should not be surprising. Although NMDA receptors are important in memory, they are not the whole story. As indicated earlier in the Chapter, memory involves the synergistic engagement of multiple genes and proteins. So to improve memory further, it will be necessary to manipulate multiple genes. At the present time it is difficult to do so, but, it probably will become possible in the near future. It will also be possible to over express genes of interest in targeted areas of the human brain. The future for treating individuals with memory disabilities looks very promising.

This animation by Graduate students Julia Hill and Natalia Rozas De O'Laughlin of the Neuroscience Graduate Program at McGovern Medical School at UTHealth explains the concept of synaptic plasticity. It placed third in the 2011 Inaugural Society for Neuroscience Brain Awareness Video Contest.

A 50-year old patient with recent damage to the hippocampus from a stroke would likely have all of the following deficits EXCEPT:

A. Difficulty learning new facts

B. Difficulty describing a recent event

C. Difficulty learning a new vocabulary word

D. Difficulty recalling a childhood memory

E. Difficulty remembering a face

A 50-year old patient with recent damage to the hippocampus from a stroke would likely have all of the following deficits EXCEPT:

A. Difficulty learning new facts This answer is INCORRECT.

The hippocampus is involved in declarative memory including the memory for facts.

B. Difficulty describing a recent event

C. Difficulty learning a new vocabulary word

D. Difficulty recalling a childhood memory

E. Difficulty remembering a face

A 50-year old patient with recent damage to the hippocampus from a stroke would likely have all of the following deficits EXCEPT:

A. Difficulty learning new facts

B. Difficulty describing a recent event This answer is INCORRECT.

The hippocampus is involved in declarative memory including the memory for recent events.

C. Difficulty learning a new vocabulary word

D. Difficulty recalling a childhood memory

E. Difficulty remembering a face

A 50-year old patient with recent damage to the hippocampus from a stroke would likely have all of the following deficits EXCEPT:

A. Difficulty learning new facts

B. Difficulty describing a recent event

C. Difficulty learning a new vocabulary word This answer is INCORRECT.

The hippocampus is involved in declarative memory including the memory for vocabulary words (semantic memory).

D. Difficulty recalling a childhood memory

E. Difficulty remembering a face

A 50-year old patient with recent damage to the hippocampus from a stroke would likely have all of the following deficits EXCEPT:

A. Difficulty learning new facts

B. Difficulty describing a recent event

C. Difficulty learning a new vocabulary word

D. Difficulty recalling a childhood memory This answer is CORRECT!

The hippocampus is involved in the formation of new memories, but not in the storage of old memories after they have been consolidated.

E. Difficulty remembering a face

A 50-year old patient with recent damage to the hippocampus from a stroke would likely have all of the following deficits EXCEPT:

A. Difficulty learning new facts

B. Difficulty describing a recent event

C. Difficulty learning a new vocabulary word

D. Difficulty recalling a childhood memory

E. Difficulty remembering a face This answer is INCORRECT.

The hippocampus is involved in object recognition.

Short term memories can involve all of the following processes EXCEPT:

A. Regulation of gene expression

B. Activation of second-messenger systems

C. Modulation of membrane channels

D. Modulation of transmitter release

Short term memories can involve all of the following processes EXCEPT:

A. Regulation of gene expression This answer is CORRECT!

Regulation of gene expression is associated with long-term memories and not short-term memories.

B. Activation of second-messenger systems

C. Modulation of membrane channels

D. Modulation of transmitter release

Short term memories can involve all of the following processes EXCEPT:

A. Regulation of gene expression

B. Activation of second-messenger systems This answer is INCORRECT.

Activation of second-messenger systems such as cAMP is associated with short-term memory.

C. Modulation of membrane channels

D. Modulation of transmitter release

Short term memories can involve all of the following processes EXCEPT:

A. Regulation of gene expression

B. Activation of second-messenger systems

C. Modulation of membrane channels This answer is INCORRECT.

Both voltage-gated and transmitter-gated channels are associated with short-term memory.

D. Modulation of transmitter release

Short term memories can involve all of the following processes EXCEPT:

A. Regulation of gene expression

B. Activation of second-messenger systems

C. Modulation of membrane channels

D. Modulation of transmitter release This answer is INCORRECT.

Changes in synaptic strength are associated with short-term memory.

Classical conditioning is an example of:

A. Semantic memory

B. Episodic memory

C. Implicit memory

D. Declarative memory

E. Nonassociative memory

Classical conditioning is an example of:

A. Semantic memory This answer is INCORRECT.

Semantic memory is a type of declarative memory, whereas classical conditioning is a type of nondeclarative (implicit) memory.

Classical conditioning is an example of:

A. Semantic memory

B. Episodic memory This answer is INCORRECT.

Episodic memory is a type of declarative memory, whereas classical conditioning is a type of nondeclarative (implicit) memory.

Classical conditioning is an example of:

A. Semantic memory

B. Episodic memory

C. Implicit memory This answer is CORRECT!

D. Declarative memory

E. Nonassociative memory

Classical conditioning is an example of:

A. Semantic memory

B. Episodic memory

C. Implicit memory

D. Declarative memory This answer is INCORRECT.

Classical conditioning is an example of nondeclarative memory.

Classical conditioning is an example of:

A. Semantic memory

B. Episodic memory

C. Implicit memory

D. Declarative memory

E. Nonassociative memory This answer is INCORRECT.

Classical conditioning is a form of associative learning, which is in contrast to examples of nonassociative memory like sensitization.


Segawa Dopa Responsive Dystonia

Neurological Examinations

Muscle stretch reflexes demonstrate a rigid hypertonus, but there is no plastic rigidity, and repeated testing will produce fluctuations in the tonus. The tremor is a high-frequency postural tremor (8–10 Hz), but a parkinsonian, resting tremor is not observed. However, adult onset patients may show resting tremor of lower frequency. These clinical signs show asymmetry, but the pattern of involvement of the sternocleidomustoideus (SCM) differs between rigidity and tremor. That is, the side predominantly affected in the SCM is contralational to that of extremities in rigidity, while it is ipsilateral in tremor. However, in adult onset cases, the side of predominance of the rigid hypertonus is ipsilateral between the SCM and the muscles of extremities. Bradykinesia or postural instability appears with advancing symptoms of dystonia. However, freezing phenomena or the marche a petit pas of Parkinson’s disease (PD) are not seen, and locomotion is preserved throughout the course of illness. The tendon reflexes are brisk and ankle clonus may be observed, but the plantar reflexes are flexor. Although some patients exhibit sustained dorsiflexion of the toe, this is ‘striatal toe sign’, not elicited by plantar stimulation, and is associated with basal ganglia involvement. There are neither cerebellar signs nor sensory disturbances. Psychomental activities are preserved normally.


The Human Sexual Response

Richard E. Jones PhD , Kristin H. Lopez PhD , in Human Reproductive Biology (Fourth Edition) , 2014

Why Did Orgasm Evolve?

To humans, orgasm is an intensely pleasurable experience, but is it directly necessary for reproduction? The answer is no. As discussed in Chapter 9 , female orgasm is not necessary for fertilization to occur, and some men can ejaculate without having an orgasm.

One theory about the evolution and adaptive value of orgasm is as follows. Most men experience orgasm when they ejaculate, whereas fewer than half of American women experience orgasm each time they have sex. A vast majority of women do not have orgasm unless they receive effective clitoral stimulation, and one idea is that only a man who is caring, knowledgeable, and sensitive can assist his partner in orgasm. The orgasmic response in the woman would then be a reward to the man i.e. it would make sex more pleasurable for him. Thus, a pair bond based on caring, sensitivity, and pleasure is mediated at least partially by female orgasm. Female orgasm then may have evolved as a mechanism of mate choice, ensuring that a woman’s long-term partner is sensitive to her needs (sexual and otherwise) and thus more likely to be a good provider for their offspring. Other theories of female orgasm include the idea that muscular contractions during orgasm may help draw sperm into the uterus. Finally, the sense of relaxation and sleepiness often produced by orgasm may promote sperm retention by the female reproductive tract.


Where can I get more information?

The National Institute of Neurological Disorders and Stroke conducts and support a wide range of research on neurological disorders, including myoclonus. For information on other neurological disorders or research programs funded by the NINDS , contact in the Institute&rsquos Brain Resources and Information Network ( BRAIN ) at:

Interested individuals may wish to contact the following organizations for additional information:

National Organization for Rare Disorders (NORD)
55 Kenosia Avenue
Danbury, CT 06813-1968
203-744-0100
800-999-6673

MedlinePlus
U.S. National Library of Medicine, NIH

Publication date: March 2021

Publicaciones en Español:

Prepared by:
Office of Communications and Public Liaison
National Institute of Neurological Disorders and Stroke
National Institutes of Health
Bethesda, MD 20892

NINDS health-related material is provided for information purposes only and does not necessarily represent endorsement by or an official position of the National Institute of Neurological Disorders and Stroke or any other Federal agency. Advice on the treatment or care of an individual patient should be obtained through consultation with a physician who has examined that patient or is familiar with that patient's medical history.

All NINDS-prepared information is in the public domain and may be freely copied. Credit to the NINDS or the NIH is appreciated.


Understanding the Stretch Reflex (or Myotatic Reflex)

By Brad Walker | First Published April 24, 2009 | Updated May 13, 2019

The nervous system of mammals is very complex. For most major actions in the body the brain must decide what movement or action must be taken, the nerve impulses must be transmitted out of the brain, down the spinal cord and out to the intended receiver. Then when the action is carried out the impulse must return back via the reverse pathway to tell the brain it was completed and start the next process. This is the path for any brain-controlled, conscious, impulses. Although it takes a lot of words to explain, it is really a very rapid process.

However, there are many processes in the body that do NOT require direct thought to complete. The heart functions, breathing, metabolic processes, disease fighting and many other autonomic processes happen automatically in the body. The body uses signals to increase, decrease, or maintain many of these actions. If the carbon dioxide levels in the body begin to rise, for example, the autonomic nervous system calls for an increase in respiratory rate.

Another automatic response by the nervous system is the reflex. The body reacts in a predetermined way based on specific stimulus. This may be a practiced response or a pre-programmed one. The stretch reflex (or myotatic reflex) is one of those responses.

What is the Stretch Reflex?

The stretch reflex (also called the myotatic reflex, the muscle stretch reflex and sometimes the knee-jerk reflex), is a pre-programmed response by the body to a stretch stimulus in the muscle. When a muscle spindle is stretched an impulse is immediately sent to the spinal cord and a response to contract the muscle is received. Since the impulse only has to go to the spinal cord and back, not all the way to the brain, it is a very quick impulse. It generally occurs within 1-2 milliseconds.

The synergistic muscles, those that produce the same movement, are also innervated when the stretch reflex is activated. This further strengthens the contraction and prevents injury. At the same time, the stretch reflex has an inhibitory aspect to the antagonist muscles. When the stretch reflex is activated the impulse is sent from the stretched muscle spindle and the motor neuron is split so that the signal to contract can be sent to the stretched muscle, while a signal to relax can be sent to the antagonist muscles. Without this inhibitory action, as soon as the stretched muscle began to contract the antagonist muscle would be stretched causing a stretch reflex in that one. Both muscles would end up contracting simultaneously.

Side note: The deep tendon reflex (sometimes referred to as the golgi tendon reflex) helps prevent injury by enabling a muscle to respond to increases in tension. If a muscle is put under excessive tension (contraction) the golgi tendon organs (GTO’s) are excited and the deep tendon reflex is activated, which causes the muscles to relax, thereby protecting the muscle from being over stretched or torn. Note that in day-to-day movement, tension in the muscles is not sufficient to activate the GTO’s deep tendon reflex. By contrast, the threshold of the muscle spindle stretch reflex is set much lower.

Examples of the Stretch Reflex in action

The stretch reflex is very important in posture. It helps maintain proper posturing because a slight lean to either side causes a stretch in the spinal, hip and leg muscles to the other side, which is quickly countered by the stretch reflex. This is a constant process of adjusting and maintaining. The body is constantly under push and pull forces from the outside, one of which is the force of gravity.

Another example of the stretch reflex is the knee-jerk test performed by physicians. When the patellar tendon is tapped with a small hammer, or other device, it causes a slight stretch in the tendon, and consequently the quadriceps muscles. The result is a quick, although mild, contraction of the quadriceps muscles, resulting in a small kicking motion.

Anatomy of the Stretch Reflex

Located within the belly of the muscle, between and parallel to the main muscle fibers, are muscle spindles. These muscle spindles are made up of spiral threads called intrafusal fibers, and nerve endings, both encased within a connective tissue sheath. These spindles monitor the speed at which a muscle is lengthened and are very sensitive to stretch.

If a muscle is stretched (lengthened) too far or too quickly the muscle spindles are excited and the stretch reflex is activated, which causes the muscles to contract, thereby protecting the muscle from being over stretched or torn.

These impulses travel from the spinal cord to the muscle and back again in a continuous loop. Conscious movement comes from impulses in the brain travelling down the spinal cord, over this loop, and then back to the brain for processing. The stretch reflex skips the brain portion of the trip and follows the simple loop from muscle to spinal cord and back, making it a very rapid sequence.

The diagram to the right shows how nerve impulses triggered by the stretch reflex travel between the spinal column and the muscles.

The gamma efferent cells in the loop work to keep the muscles ready for the stretch reflex, even when inhibited or contracted. This is important because if the muscle is working against a load and shortening during contraction and an additional load is added, the muscle recognizes the stretch immediately and can compensate with a stronger contraction. This also protects the inhibited antagonist muscles from being injured from excessive stretching.