Neuroscience Articles

Cheat Sheet / Updated 02-22-2022

Why is Neuroscience important? The most complex structure in the universe is the three pound mass of cells within your skull called the brain. The brain consists of about 100 billion neurons, which is about the same number as all the stars in our Milky Way galaxy and the number of galaxies in the known universe. It also contains about a trillion glial cells, which contribute to the proper function of neurons. Like any complex machine, the brain contains a lot of parts, each of which has subparts, which themselves have subparts, all the way down to the “nuts and bolts” — the neurons and glia. In this Cheat Sheet, you find information on the key parts of the brain and the role and function of the cells that make up the nervous system.

Article / Updated 08-30-2021

Mental illness can clearly occur in a genetically normal brain which has suffered organic damage during development or later. It can also arise from trauma or stress that leads to indirect changes in the brain from factors like chronic stress or sleep deprivation. Well-known environmentally generated brain dysfunctions include the following: Fetal alcohol syndrome: Fetal alcohol syndrome develops when the mother drinks excessive alcohol during pregnancy. Alcohol crosses the placental barrier and can damage neurons and brain structures leading to cognitive and functional disabilities such as attention and memory deficits, impulsive behavior, and stunted overall growth. Fetal alcohol exposure is a significant cause of intellectual disability, estimated to occur in about 1 per 1,000 live births. It is associated with distinctive facial features, including a short nose, thin upper lip, and skin folds at the corner of the eyes. Maternal stress: If a mother is highly or chronically stressed while pregnant, her child is more likely to have emotional or cognitive problems, such as attention deficits, hyperactivity, anxiety, and language delay. The fetal environment can be altered when maternal stress changes the mother's hormone profile. It is thought that this occurs through the hypothalamic-pituitary-adrenal axis via the secretion of cortisol, a stress hormone that has deleterious effects on the developing nervous system. More recently, it has been shown that epigenetic changes in DNA expression can affect germ cells and, therefore, be inherited. Post-traumatic stress syndrome (PTSD): PTSD is a severe anxiety disorder that develops after psychological trauma, such as the threat of death, as in war, or a significant threat to one's physical, sexual, or psychological integrity that overwhelms the ability to cope, as in sexual assault. Traumatic events cause an overactive adrenaline response, which persists after the event, making an individual hyper-responsive to future fearful situations. PTSD is characterized by cortisol dysregulation and high catecholamine secretion characteristic of the classical fight-or-flight response. These hormones divert resources from homeostatic mechanisms, such as digestion and immune responses, toward those needed for immediate, intense muscular exertion. Extreme or chronic stress can eventually damage the brain as well as the body. Some evidence shows that desensitization therapies, in which the PTSD sufferer re-experiences aspects of the stressor in a controlled environment, can mitigate some of its effects. Such therapy, if successful, may be superior to generic anti-anxiety medication that may deal only with the symptoms, rather than the cause of the disorder.

Article / Updated 09-11-2016

Although pain is a necessary function for preventing damage to the body, in some cases, pain itself becomes disabling. Chronic pain can occur in disease conditions such as cancer, in which case the normal function of pain that forces you to rest, protect, or not use some injured part of the body until it heals is simply inappropriate in a disease state in which destruction is occurring from the cancer all over the body that cannot be healed from rest. Pain can also arise from psychological factors or from factors that cannot be medically identified and are assumed to be psychological. Examples include some types of chronic pain and depression. Pain from both medically identified sources and that which is psychological (or cognitive) appears to activate a brain area called the anterior cingulate cortex. The anterior cingulate cortex is the anterior portion of an area of the mesocortex, just above the corpus callosum. The anterior cingulate appears to be a high-level cortical monitoring center. It tends to be activated by pain, anticipation of pain, and failure in goal-seeking activity. Its function seems to be to arbitrate between taking different strategies in response to experience. At a low level, after placing your hand on a hot stove burner, it may make you cautious when you're around the stove. At a higher level, getting reprimanded for sending a flaming email at work may make you wary of doing so again. Considerable individual differences with respect to pain tolerance exist, just as there can be differences in tolerance in different situations for a particular person. Men are reported to be less tolerant of chronic pain than women, though they are more tolerant of acute pain. Pain tolerance generally increases with age, based on tests for pain tolerance such as the total time one can stand to have one's arm immersed in ice water. It is not clear whether the increase in tolerance with age is based on psychological or physical factors. Athletic training and strong motivation to obtain some goal can significantly reduce the disabling effects of pain. Suggestions that different cultures or ethnic groups have intrinsically different pain thresholds — in other words, there's a physiological difference among cultures about pain tolerance — have almost always been shown to be the effect of at what point the perceived stimulus is reported as painful or unbearably painful, not whether the pain itself is perceived. Cultures that encourage expression of emotions in general tend to be associated with lower pain-reporting tolerance.

Article / Updated 09-11-2016

The sense of pain can be reduced in several ways, including the body's own production of endorphins. Feeling pain is, well, painful. Wouldn't you be better off if you could just eliminate pain? The answer to the question of whether you would be better off without a sense of pain is a resounding no. This situation actually occurs in some people. One of these is a condition called peripheral neuropathy, in which many neurons such as pain receptors in the peripheral nervous system die or become inactive due, for example, to vascular problems associated with diabetes. Loss of pain sense in parts of the body can also be the result of certain strokes and types of brain damage. People with peripheral neuropathy tend to injure themselves without knowing: They burn themselves while cooking, break bones during routine physical activity, and develop asymptomatic skin lesions that are ignored until they become serious infections. The sense of pain is necessary to prevent harm to the body. The loss of feeling in a limb is so disabling that people with sensory peripheral neuropathy are effectively paralyzed in that limb, refusing to use it, even if the motor neuron circuitry is actually intact.

Article / Updated 09-11-2016

Most psychoactive drugs mimic the action of known neurotransmitters, but until a few decades ago, there was no known neurotransmitter that mediated the general effects of pain. Here's a mystery that puzzled researchers for a long time: Why does a substance produced by a poppy plant (morphine) relieve pain? This all changed with the discovery of endogenous opioids (that is, opioids that are developed naturally within the body). Of these morphinelike substances, the most common are the endorphins (a term which is an abbreviation of endogenous morphines). Common situations in which endorphins are produced include childbirth and running the last few miles of a marathon. Opiates like morphine and heroin reduce the feeling of pain because they mimic the action of substances the body produces on its own to control pain. These drugs bind these same receptors and, at low doses, produce similar effects. However, when injected in large doses, these drugs produce the opposite of pain — a "high" — and are addictive. The drug naloxone antagonizes the effects of these opioids and is often given to addicts to reverse the effects of heroin they have injected. The existence of endorphins also explains another mystery of pain management, the placebo effect. The placebo effect occurs when patients are given a substance that itself has no pain-blocking potential but, because the patients believe they have been given a real drug that will alleviate the pain, find that the pain is actually alleviated. Although the placebo effect is robust and common, those in the medical community tend to dismiss it as being "psychological," that is, not based on any physiologically demonstrable or quantifiable basis. However, it turns out that the drug naloxone not only reduces the effects of opioids, such as heroin, but it also reduces the placebo effect. What this means is that the placebo effect isn't just psychological; it actually has a physiological component, involving the cognitive stimulation, from belief, of the body's internal endorphin production that objectively and measurably reduces pain by binding the endorphin receptors.

Article / Updated 09-11-2016

The mapping of skin receptors to a specific area of neocortex illustrates one of the most fundamental principles of brain organization, cortical maps. The projection from the thalamus is orderly in the sense that receptors on nearby parts of the skin project to nearby cortical neurons. The figure shows a representation of the skin map on the somatosensory cortex. The fundamental idea about a given area of cortex being devoted to receptors in a given skin area is that activity in this area of cortex is necessary for the perception of the skin sense (along with other parts of the brain). You perceive activity in that bit of cortex area as a skin sensation not because that area has some special skin perceiving neurons, but because it receives inputs from the skin and has outputs that connect to memories of previous skin sensation and other associated sensations. In other words, the perception produced by activity in this and other areas of cortex is a function of what neural input goes to it and where the outputs of that area of cortex go. This skin map on the cortex is called a homunculus, which means "little man." However, the surface area of the somatosensory cortex onto which the skin receptors project is not really a miniature picture of the body; it is more like a band or strip, as established in the studies by Canadian neurosurgeon Wilder Penfield. Because of the difficulty in mapping a three-dimensional surface onto a two-dimensional sheet (think of how two-dimensional maps of the earth compare to the three-dimensional globes), the image is distorted, depending on choices that the "map-maker" makes about what is relatively more important to represent accurately versus what is less. Also note that some areas of the body, such as the hands and fingers, are located in the cortex map close to areas such as the face that are actually quite distant, body-wise. Some researchers suggest that the phantom limb feelings (including pain) that sometime occur after an amputation may occur because some neural projections from the face invade the part of the cortex that was being stimulated by the limb and cause sensations to be perceived as being located there, even when the limb is gone.

Article / Updated 09-11-2016

Skin receptors allow you to respond to things that contact your skin and to be aware of what those things are. The output of most somatosensory receptors participates in at least three different kinds of neural circuits: Local reflexes are those that primarily involve contraction of a single muscle, such as a flexor like the biceps that contracts when, for example, you touch something hot. The circuit for this action consists of the neurons in your fingertip that contain the temperature sensor for heat. These contact spinal cord interneurons in the dorsal root area of the spinal cord. These interneurons activate motor neurons in the same spinal segments, which cause contraction of muscles that withdraw your finger. Coordinated movement involves receptor connections through interneurons to other spinal cord segments. When you throw a ball, mechanoreceptors in the skin of the hand work with proprioceptive and kinesthesis receptors associated with muscles in your fingers, hand, arm, and shoulder. Even your leg muscles are involved. Locomotor activities like walking also require coordination between spinal segments so that you do not, for example, try to move one foot before the other has hit the ground. Receptor output from any one segment in the spinal cord can project up or down to other spinal cord segments for coordinated activity of multiple muscles. Messages from skin receptors are also passed to the brain where you become conscious of them. There are two major pathways, the lemniscal pathway and the spinothalamic pathway. Both of these pathways lead to the ventral posterior nucleus of the thalamus on the opposite side of the body from the skin receptors, following the nearly universal principle that the right side of the brain deals mostly with the left side of the body, and vice versa.

Article / Updated 09-11-2016

Although not located in the skin, receptors mediating proprioception (position sense) and kinesthesis (movement sense), are either free nerve endings or structures similar to mechanoreceptors like Ruffini corpuscles (refer to the first figure below) and have similar layouts as the cell bodies in the dorsal root ganglia (refer to the second figure). These receptors are embedded in muscles, tendons, and ligaments around joints. The receptors in muscles and tendons that have relatively sustained responses called proprioreceptors signal muscle force and joint position. Similar receptors with more short-lived, or transient, responses signal when the joint is moving, allowing us to have the movement sense of kinesthesis. For example, proprioreceptors allow you to touch your nose with your eyes closed. Transient, kinesthetic receptors allow you to reach out quickly and then stop your hand in the right place to grab a thrown ball. Different types of senses are sometimes referred to as sensory modalities, whether on a large scale (such as vision versus touch) or within touch (for mechanical versus temperature sensation).

Article / Updated 09-11-2016

You can detect more than just various kinds of pressure on your skin. Two other skin senses are temperature and pain. These receptors have similar structures, or, really, lack of structure. All the mechanoreceptors consist of an axon terminal with ion channel receptors embedded in some sort of structure, such as a corpuscle, disk, or myelin wrapping, that gives the receptor its particular responsiveness to different mechanical stimulation frequencies. Receptors for temperature and pain look like the axon terminals without any other structure around them. They are typically called free nerve endings. Free nerve endings for temperature have ion channels that respond to particular temperatures, while other free nerve endings generate action potentials in response to extreme force on the skin or other potentially damaging stimuli that is felt as pain. Some receptors — those having what are called transient receptor potential (TRP) channels — respond to both. Different temperature receptors respond best to particular temperatures. Warmth receptors respond best to particular temperatures above body temperature (98.6 degrees Fahrenheit), while cold receptors respond best to particular temperatures below body temperature. You judge a wide range of temperatures (cool, damp, chilly, cold, warm, humid, hot, and so on) by sensing the unique ratio of activation of the different receptors activated at any particular temperature. Extreme heat, cold or skin pressure, however, activates receptors that are interpreted as pain. Although different types of pain receptors work by different mechanisms, what they have in common is that the sense of pain signals impending damage to the skin. Pain receptors also exist that respond to chemical damage from acids or bases, and other types of damage such as that caused by a cut. Pain and temperature sensations tend to be carried by small caliber axons in a spinal cord tract called the lateral spinothalamic tract. A more medial pathway called the lemnical tract carries fine touch information via larger caliber axons with faster conduction velocities.

Article / Updated 09-11-2016

Somatosensory neurons, the tips of which form the mechanoreceptors, have an unusual morphology, or structure. This morphology is crucial to their function. Their morphological classification is called pseudounipolar. Although this rather unwieldy name isn't particularly illuminating about their function, understanding their structure explains some aspects about how these receptors work. The figure shows a diagram of a typical mechanoreceptor neuron. The cell bodies of somatosensory receptor neurons for most of our skin (below the head and neck) are located in a series of what are called ganglia (concentrations of neural cell bodies) just outside the dorsal root of the spinal cord. They are thus called dorsal root ganglia. These ganglia and the neurons they contain are part of the peripheral nervous system. The cell bodies of the somatosensory neurons have no dendrites. Instead, a single axon leaves the cell body and then bifurcates, or separates into two paths, a short distance away. One end of the axon enters the spinal cord at the dorsal root and makes conventional synapses on spinal interneurons, enabling the stretch reflex and the relaying somatosensory information to other spinal cord segments and up the spinal cord to the brain. Here's the interesting part: The other end of the axon goes away from the dorsal root ganglion in a bundle with other axons and ends up in the skin, where it forms one of the receptor types: Merkel disk, Meissner corpuscle, Ruffini corpuscle, or Pacinian corpuscle. The mechanoreceptors are activated directly when a mechanical force stimulates an axonal ending of one of these neurons. This activation occurs through a special ion channel that responds to the stretching of the membrane (in a typical neurotransmitter receptor, the activation is triggered by voltage or ligand binding). Here's what happens: The stretching causes action potentials to originate in the axonal ending and then proceed toward the cell body in the dorsal root ganglion (most axons conduct action potentials away from the cell body). The action potential continues past the axonal bifurcation point near the cell body into the spinal cord, where it reaches axon terminals and makes conventional synapses onto spinal interneurons. The interneurons connect the receptor neuron to motor neurons for reflexes and also send messages about the receptor activation to other spinal cord segments and up to the brain.