Facts: The New Brain
Given the velocity of change and the potential future impacts on ourselves and society, we must quickly discard brain myths and outdated research conclusions from the past and replace them with verifiable understanding from new research studies that allow us to “see” and even change or enhance the brain’s responses to stimuli.
The remarkable advances of our age will challenge us to govern or manage their impacts on ourselves, our children, our businesses and institutions, and our society.
The NEW brain – is here and its future is evolving rapidly.
The Corpus Callosum comprises the bundle of fibers that bridges the right and left hemispheres of the cerebrum, allowing the two hemispheres to communicate with one another.
The Cerebral Cortex is a gray sheet of tissue, often referred to as gray matter, which covers the outermost layer of the cerebrum. More than two-thirds of this layer is folded into grooves, which increase the brain’s surface area, allowing for inclusion of many more neurons.
The frontal lobe is responsible for initiating and coordinating motor movements; for higher cognitive skills, such as problem solving, thinking, planning, and organizing; and for many aspects of personality and emotional makeup.
The parietal lobe is involved with sensory processes, attention, and language. Damage to the right side of the parietal lobe can result in difficulty navigating spaces, even familiar ones. If the left side is injured, the ability to understand spoken and/or written language may be impaired.
The occipital lobe helps process visual information, including recognition of shapes and colors.
The temporal lobe helps process auditory information and integrate information from the other senses.
The hippocampal formation in the temporal lobe plays a role in short-term memory.
The amygdala has a role in learned emotional responses.
The basal ganglia are cerebral nuclei deep in the cerebral cortex. They assist in coordinating muscle movements and rewarding useful behaviors.
The thalamus prioritizes most sensory information before passing it on to the cerebral cortex.
The hypothalamus is the control center for appetites, defensive and reproductive behaviors, and sleep-wakefulness.
The Midbrain consists of two pairs of small hills called colliculi. These collections of neurons play a critical role in visual and auditory reflexes and in relaying this type of information to the thalamus. The midbrain also has clusters of neurons that regulate activity in widespread parts of the central nervous system and are thought to be important for reward mechanisms and mood.
The Hindbrain includes the pons, the medulla oblongata, and the cerebellum.
The pons and the medulla oblongata control respiration, heart rhythms, and blood glucose levels.
The cerebellum has two hemispheres which help control movement and cognitive processes that require precise timing, and which also play an important role in Pavlovian learning.
The Central Nervous System (CNS) comprises the forebrain, midbrain, hindbrain, and spinal cord. The brain is protected by the skull, while the spinal cord, which is about 17 inches (43 cm) long, is protected by the vertebral column.
The Peripheral Nervous System (PNS) consists of nerves and small concentrations of gray matter called ganglia.
The Somatic Nervous System is made up of neurons connecting the CNS with the parts of the body that interact with the outside world. Somatic nerves in the cervical region are related to the neck and arms; those in the thoracic region serve the chest; and those in the lumbar and sacral regions interact with the legs.
The Autonomic Nervous System is made of neurons connecting the CNS with internal organs. It is divided into two parts.
The Sympathetic Nervous System mobilizes energy and resources during times of stress and arousal.
The Parasympathetic Nervous System conserves energy and resources during relaxed states, including sleep.
The Cell Body of a neuron contains the nucleus and cytoplasm.
Dendrites extend from the neuron cell body and receive messages from other neurons.
Synapses are the contact points where one neuron communicates with another. The dendrites are covered with synapses formed by the ends of axons from other neurons.
Axons extend and branch out from the neuron cell body and end at Nerve Terminals. Neurons transmit or receive electrical impulses along their axons, which can range in length from a tiny fraction of an inch (or centimeter) to three feet (about one meter) or more. On many axons, a Myelin Sheath covering accelerates the transmission of electrical signals along the axon. The myelin sheath is made of specialized cells called glia.
Glia in the brain outnumber neurons by more than 10 to one and perform many jobs, including transporting nutrients to neurons, cleaning up brain debris, digesting parts of dead neurons, and helping to hold neurons in place.
How Does the Neuron Send a Message?
An Ion is an electrically charged atom. An Ion Channel is a sometimes-permeable, water-filled molecular tunnel that passes through a cell membrane to allow ions or small molecules to leave the cell. Nerve impulses involve the opening and closing of ion channels. The flow of ions creates an electrical current that produces tiny voltage changes across the neuron’s cell membrane. When a nerve impulse begins, a dramatic reversal in the electrical potential occurs on the cell’s membrane, as the neuron switches from an internal negative charge to a positive charge state.
The charge, called an Action Potential, passes along the axon’s membrane at speeds up to several hundred miles per hour, allowing the neuron to fire impulses multiple times a second.
At the moment when the voltage change reaches the end of an axon, the Nerve Terminals located there release Neurotransmitters – the brain’s chemical messengers – converting the message from an electrical to a chemical form.
The chemical message diffuses across the synapse, and binds to Receptors on the surface of the target cell, which may be another neuron, a muscle or a gland cell.
Each Receptor has a distinctly shaped region that selectively recognizes a particular chemical messenger and acts as on-off switch. This interaction alters the target cell’s membrane potential and triggers a response from the target cell, such as the generation of an action potential, the contraction of a muscle, the stimulation of enzyme activity, or the inhibition of neurotransmitter release.
ACh is synthesized in axon terminals. When an action potential arrives at the nerve terminal, electrically charged calcium ions rush in, and ACh is released into the synapse, where it attaches to ACh receptors on the target cells. On voluntary muscles, this action opens sodium channels and causes muscles to contract. Much less is known about ACh in the brain. Recent discoveries suggest that it may be critical for normal attention, memory, and sleep. Because ACh-releasing neurons die in Alzheimer’s patients, finding ways to restore this neurotransmitter is a goal of current research. Drugs that inhibit acetylcholinesterase — and increase ACh in the brain — are presently the main drugs used to treat Alzheimer’s disease.
Amino Acids generally serve as the building blocks of proteins. They are widely distributed throughout the body and the brain. Certain amino acids can also serve as neurotransmitters in the brain.
Glycine and Gamma-Aminobutyric Acid (GABA) inhibit the firing of neurons.
Glutamate and aspartate act as excitatory signals, activating, among others, N-methyl-d aspartate (NMDA) receptors which, in developing animals, have been implicated in activities ranging from learning and memory to development and specification of nerve contacts. The stimulation of NMDA receptors may promote beneficial changes in the brain, whereas overstimulation can cause nerve cell damage or cell death.
Catecholamines include the neurotransmitters dopamine and norepinephrine, which are widely present in the brain and peripheral nervous system.
Dopamine is present in three principal circuits in the brain: the dopamine circuit that regulates movement; the circuit thought to be important for cognition and emotion; and the circuit that regulates the endocrine system, where dopamine directs the hypothalamus to manufacture hormones and hold them in the pituitary gland either for release into the bloodstream, or to trigger the release of hormones held within cells in the pituitary.
Norepinephrine is secreted by the sympathetic nervous system throughout the body to regulate heart rate and blood pressure. Acute stress increases the release of norepinephrine from sympathetic nerves and the adrenal medulla, the innermost part of the adrenal gland. Like dopamine, deficiencies in norepinephrine occur in patients with conditions that lead to memory loss and a decline in cognitive functioning. Thus, researchers believe that norepinephrine may play a role in both learning and memory.
Serotonin is present in the brain and other tissues, particularly blood platelets and the lining of the digestive tract. In the brain, serotonin has been identified as an important factor in sleep quality, mood, depression, and anxiety.
Peptides are short chains of amino acids that are linked together. They are synthesized in the cell.
Enkephalin, literally meaning “in the head,” is an opiate peptide produced by the brain that closely resembles the opium derivative morphine that is used medically to kill pain. It is one of a group of opioid peptides named Endorphins, meaning “endogenous morphine.” These peptides are released by brain neurons in times of stress to minimize pain and enhance adaptive behavior.
Some sensory nerves contain a peptide called substance P, which causes the sensation of burning pain. The active component of chili peppers, capsaicin, causes the release of substance P.
Trophic Factors are small protein substances that are necessary for the development, function, and survival of specific groups of neurons. Researchers have identified genes that code for receptors and are involved in the signaling mechanisms of trophic factors.
The Pituitary Gland secretes factors into the blood that act on the endocrine glands to either increase or decrease hormone production. A feedback loop of communication travels from the brain to the pituitary to an endocrine gland and back to the brain. The communications activate and control basic behavioral activities, eating, drinking, and the regulation of body functions.
The brain contains receptors for thyroid hormones (those produced by the thyroid) and the six classes of steroid hormones, which are synthesized from cholesterol — androgens, estrogens, progestins, glucocorticoids, mineralocorticoids, and vitamin D. Thyroid and steroid hormones bind to receptor proteins that in turn bind to DNA and regulate the action of genes, altering the production of gene products that participate in synaptic neurotransmission as well as affecting the structure of brain cells.
The metabolic hormones insulin, insulin-like growth factor, ghrelin, and leptin are taken up from the blood and act to affect neuronal activity and certain aspects of neuronal structure.
Stress and stress hormones, such as the glucocorticoid cortisol, also alter brain function, including the brain’s capacity to learn. Severe and prolonged stress can impair the ability of the brain to function.
Certain Gases and Lipids can act as neurotransmitters. Because gases cannot be easily stored, they are made by enzymes when needed and simply diffuse into adjacent neurons and act upon chemical targets such as enzymes.
Nitric oxide neurotransmission governs erection in the penis and the relaxation that contributes to the normal movements of digestion. In the brain, it is the major regulator of the intracellular messenger molecule cyclic GMP. Neuronal damage following a stroke may be attributable in part to nitric oxide.
Prostaglandins are a class of compounds made from lipids by an enzyme called cyclooxygenase. These very small and short-lived molecules have powerful effects, including the induction of a fever and the generation of pain in response to inflammation. Aspirin reduces a fever and lowers pain by inhibiting the cyclooxygenase enzyme.
Endocannabinoids are in essence cannabis (marijuana) made by the brain. They increase in the brain under stressful conditions and control behaviors by controlling the release of neurotransmitters, usually by inhibiting them.
Following the action of neurotransmitters at their receptors, Second Messengers may further convey the chemical message of a neurotransmitter (the first messenger) from the cell membrane to the cell’s internal biochemical machinery.
For example, adenosine triphosphate (ATP) is the chemical source of energy in cells and is present throughout the cytoplasm of all cells. When norepinephrine binds to its receptors on the surface of the neuron, the activated receptor binds a G protein on the inside of the membrane. The activated G protein causes the enzyme adenylyl cyclase to convert ATP to cyclic adenosine monophosphate (cAMP), the Second Messenger, which then exerts a variety of influences within the cell, ranging from changes in the function of ion channels in the membrane to changes in the expression of genes in the nucleus.
Second Messenger effects may endure for a few milliseconds to as long as many minutes. They also may be responsible for long-term changes in the nervous system.
During the early stages of embryonic development, three layers emerge — the endoderm, the ectoderm, and the mesoderm. These layers undergo many interactions to grow into organ, bone, muscle, skin, or nerve tissue.
Differentiation. The process of differentiation is accomplished by signaling molecules released by the mesoderm. These molecules turn on certain genes and turn off others, triggering some ectoderm cells to become nerve tissue in a process called neural induction. The remaining cells of the ectoderm, which have not received the signaling molecules diffusing from the mesoderm, become skin.
The type of cell created by the signaling molecules depends upon how close and how concentrated the signaling molecules are in proximity to the particular cell.
For example, the signaling molecule called sonic hedgehog is secreted from mesodermal tissue lying beneath the developing spinal cord. The nearest adjacent nerve cells are converted into a specialized class of glia. Cells that are slightly farther away and exposed to slightly lower concentrations of sonic hedgehog become the motor neurons that control muscles. Greater distance and even lower concentrations promote the formation of interneurons, which relay messages to other neurons, not muscles.
Migration. The next step for new neurons is a journey to the proper position in the brain.
Three to four weeks after a human baby is conceived, the ectoderm begins to thicken and build up along the middle.
As the cells continue to divide, a flat neural plate grows, followed by the formation of parallel ridges, similar to the creases in a paper airplane, that rise across its surface.
Within a few days, the ridges fold in toward each other and fuse to form a hollow neural tube. The top of the tube thickens into three bulges that form the hindbrain, the midbrain, and the forebrain.
Later in the process, at week seven, the first signs of the eyes and the brain’s hemispheres appear.
As neurons are produced, they move from the neural tube’s ventricular zone, or inner surface, to near the border of the marginal zone, or outer surface.
After neurons stop dividing, they form an intermediate zone, where they gradually accumulate as the brain develops. The neurons then migrate to their final destination.
Glia provide a temporary scaffolding for ushering neurons to their destination projecting radially from the intermediate zone to the cortex. The result of this process is that the cells that arrived the earliest (the oldest ones) form the deepest layer of the cortex, whereas the later-arriving (the youngest) neurons form the outermost layer. Glia guide about 90 percent of migration in humans.
Inhibitory interneurons, small neurons with short pathways usually found in the central nervous system, migrate tangentially across the brain.
Migration is a delicate process and can be affected by different factors.
External forces, such as alcohol, cocaine, or radiation, can prevent proper migration, resulting in misplacement of cells, which may lead to mental retardation or epilepsy.
Mutations in genes that regulate migration have been shown to cause some rare genetic forms of retardation and epilepsy in humans.
Making Connections. Once the neurons reach their final location, they must make the proper connections so that a particular function, such as vision or hearing, can emerge.
Neurons become interconnected through (1) the growth of dendrites — extensions of the cell body that receive signals from other neurons and (2) the growth of axons — extensions from the neuron that can carry signals to other neurons.
Growth cones, enlargements on the axon’s tip, actively explore the environment as they seek out their precise destination.
Growth cones bear molecules that serve as receptors for environmental cues.
The binding of particular signals with receptors tells the growth cone whether to move forward, stop, recoil, or change direction. Families of signaling molecules include proteins such as netrin, semaphorin, and ephrin.
Once axons reach their targets, they form connections with other cells at synapses. The regulated inputs from the thousands of synapses each neuron receives are responsible for the astounding information-processing capacity of the brain.
Dendrites also are actively involved in the process of initiating contact with axons and recruiting proteins to the “postsynaptic” side of the synapse.
Still other molecules coordinate the maturation of the synapse after it has formed so that it can accommodate the changes that occur as our bodies mature and our behavior changes. Defects in some of these molecules may be the cause of disorders such as autism, while the loss of other molecules may degrade synapses and result in aging.
Just as genes turn on and off signals to regulate the development of specialized cells, a similar process leads to the production of specific neurotransmitters.
For some cells, such as motor neurons, the type of neurotransmitter is fixed, but for other neurons, it is not.
For example, when certain immature neurons are maintained in a dish with no other cell types, they produce the neurotransmitter norepinephrine. If the same neurons are maintained with specific cells, such as heart tissue, they produce the neurotransmitter acetylcholine.
Many researchers believe that location of the synapse itself may influence the signal to engage the gene and thereby determine the chemical messengers that a neuron will produce.
Myelination, the wrapping of axons by extensions of glia, increases the speed at which signals may be sent from one neuron to another by a factor of up to 100x.
In between the myelin are gaps, called nodes of Ranvier, that are not covered in myelin. Saltatory conduction (saltatory means “to jump”), in which the electrical signal moves faster over the insulated portion, jumping from one node to another, accounts for this rapid transmission of electrical signals.
The process of myelination occurs throughout the human lifespan.
Apoptosis is activated if a neuron loses its battle with other neurons to receive life-sustaining chemical signals called trophic factors.
Each type of trophic factor supports the survival of a distinct group of neurons.
Researchers have found that injuries and some neurodegenerative diseases kill neurons not by inflicting damage but by activating the cells’ own death programs.
Brain cells also form excess connections at first.
Communication between neurons with chemical and electrical signals is necessary to weed out the connections.
The connections that are active and generating electrical currents survive, whereas those with little or no activity are lost.
Thus, the circuits of the adult brain are formed, at least in part, by sculpting away incorrect connections to leave only the correct ones.
It is important to note that there are multiple critical periods, organized sequentially, as individual brain functions are established.
The developing nervous system must obtain certain critical experiences, such as sensory, movement, or emotional input, to mature properly. Such periods are characterized by high learning rates and enduring consequences for neuronal “connectivity.
After a critical period, connections diminish in number and are less subject to change, but the ones that remain are stronger, more reliable, and more precise.
These turn into a unique variety of sensory, motor, or cognitive “maps.”
The last step in the creation of an adult human brain, the frontal lobes, whose function includes judgment, insight, and impulse control, continues into the early 20s.
Injury or deprivation of environmental input occurring at specific stages of postnatal life can dramatically reshape the underlying circuit development, making it more difficult to correct later in life.
In one experiment, a monkey raised from birth to 6 months of age with one eyelid closed permanently lost useful vision in that eye because of diminished use. This gives cellular meaning to the saying “use it or lose it.”
Similarly, cochlear implants introduced in infancy are most effective in restoring hearing to the congenitally deaf.
Cognitive recovery from social deprivation, brain damage, or stroke is also greatest early in life.
Likewise, enriched environments or stimulation may bolster brain development, as revealed by animals raised in toy-filled surroundings. They have more branches on their neurons and more connections than isolated animals. Similarly, children can learn languages or develop musical ability (absolute pitch) with greater proficiency than adults.
Heightened activity in a critical period may increase the incidence of certain disorders in childhood, such as epilepsy. Fortunately, as brain activity subsides, many types of epilepsy fade away by adulthood.
Plasticity is the ability of the brain to modify itself and adapt to challenges of the environment. The degree to which our brains are able to adapt is the defining attribute of our species.
Experience-Expectant Plasticity refers to the integration of environmental stimuli into the normal patterns of development.
Certain Environmental Exposures during limited critical, or sensitive, periods of development are essential for healthy maturation.
For example, finches need to hear adult songs before sexual maturation in order for them to learn to sing at a species-appropriate level of intricacy.
It all begins with light.
Light passes through the cornea, which does about three-quarters of the focusing, and then the lens, which adjusts the focus.
Both combine to produce a clear image of the visual world on a sheet of photoreceptors called the retina, which is part of the central nervous system but located at the back of the eye.
As in a camera, the image on the retina is reversed so that objects to the right of center project images to the left part of the retina and vice versa.
Likewise, objects above the center project to the lower part and vice versa.
Photoreceptors gather visual information by absorbing light and sending electrical signals to other retinal neurons for initial processing and integration.
The optic nerve sends the signals to other parts of brain to process the image and allow us to see.
The size of the pupil, which regulates how much light enters the eye, is controlled by the iris.
The shape of the lens is altered by the muscles just behind the iris so that near or far objects can be brought into focus on the retina.
Primates, including humans, have well-developed vision using two eyes, called binocular vision.
Visual signals pass from each eye along the million or so fibers of the optic nerve to the optic chiasm, where some nerve fibers cross over. This crossover allows both sides of the brain to receive signals from both eyes.
When you look at a scene with both eyes, the objects to your left register on the right side of the retina. The visual information then maps to the right side of the cortex. The result is that the left half of the scene you are watching registers in the cerebrum’s right hemisphere. Conversely, the right half of the scene registers in the cerebrum’s left hemisphere.
A similar arrangement applies to movement and touch: Each half of the cerebrum is responsible for processing information received from the opposite half of the body.
Photoreceptors, are neurons specialized to turn light into electrical signals. Two major types of photoreceptors are rods and cones.
Rods are extremely sensitive to light and allow us to see in dim light, but they do not convey color. Rods constitute 95 percent of all photoreceptors in humans.
Cones work under most light conditions, are responsible for acute detail and color vision, and are the source of most of our vision. The human eye contains three types of cones (red, green and blue), each sensitive to a different range of colors. Cones work in combination to convey information about all visible colors. Using only three types of cones, we can see thousands of colors.
Light is focused on the fovea (containing red and green cones) in the central part of the retina. The area around the fovea, called the macula, is critical for reading and driving. Death of photoreceptors in the macula, called macular degeneration, is a leading cause of blindness among the elderly.
Visual processing mechanisms are not yet completely understood. Recent findings from anatomical and physiological studies in monkeys suggest that visual signals are fed into at least three separate processing systems. One system appears to process information mainly about shape; a second, mainly about color; and a third, movement, location, and spatial organization.
Human psychological studies support the findings obtained through animal research.
These studies show that light intensity illuminating contrasts and textures informs the perception of movement, depth, perspective, the relative size of objects, the relative movement of objects, shading, and gradations in texture.
Perception also requires various elements to be organized so that related ones are grouped together. This stems from the brain’s ability to group the parts of an image together and also to separate images from one another and from their individual backgrounds.
To further inform perception, he brain extracts biologically relevant information at each stage and associates firing patterns of neuronal populations with past experience.
Sound waves are collected by the external ear — the pinna and the external auditory canal — and funneled to the tympanic membrane (eardrum) to make it vibrate.
Attached to the tympanic membrane, the malleus (hammer) transmits the vibration to the incus (anvil), which passes the vibration on to the stapes (stirrup). The stapes pushes on the oval window, which separates the air-filled middle ear from the fluid-filled inner ear to produce pressure waves in the inner ear’s snail-shaped cochlea.
The separation of frequencies occurs in the cochlea, which is tuned along its length to different frequencies, so that a high note causes one region of the cochlea’s basilar membrane to vibrate, while a lower note has the same effect on a different region of the basilar membrane.
Riding on the vibrating basilar membrane are hair cells topped with microscopic bundles of hairlike stereocilia, which are deflected by the overlying tectorial membrane.
Hair cells convert the mechanical vibration to electrical signals, which in turn excite the 30,000 fibers of the auditory nerve.
The auditory nerve then carries the signals to the brainstem.
Because each hair cell rides on a different part of the basilar membrane, each responds to a different frequency. As a result, each nerve fiber carries information about a different frequency to the brain.
Auditory information is analyzed by multiple brain centers as it flows to the superior temporal gyrus, or auditory cortex, the part of the brain involved in perceiving sound.
In the auditory cortex, adjacent neurons tend to respond to tones of similar frequency. However, they specialize in different combinations of tones.
Some respond to pure tones, such as those produced by a flute, and some to complex sounds like those made by a violin.
Some respond to long sounds and some to short, and some to sounds that rise or fall in frequency.
Other neurons might combine information from these specialist neurons to recognize a word or an instrument.
Sound is processed in different regions of the auditory cortex on both sides of the brain.
For most people, the left side is specialized for perceiving and producing speech. Damage to the left auditory cortex, such as from a stroke, can leave someone able to hear but unable to understand language.
Taste itself is focused on distinguishing chemicals that have a sweet, salty, sour, bitter, or umami taste (umami is Japanese for “savory”).
Tastants, chemicals in foods, are detected by taste buds, special structures embedded within small protuberances on the tongue called papillae.
Other taste buds are found in the back of the mouth and on the palate.
Interactions between the senses of taste and smell enhance our perceptions of the foods we eat.
Each of us has between 5,000 and 10,000 taste buds. Each taste bud consists of 50 to 100 specialized sensory cells, which are stimulated by tastants such as sugars, salts, or acids.
When the sensory cells are stimulated, they cause signals to be transferred to the ends of nerve fibers, which send impulses along cranial nerves to taste regions in the brainstem.
From here, the impulses are relayed to the thalamus and on to a specific area of the cerebral cortex, which makes us conscious of the perception of taste.
Airborne odor molecules, called odorants, are detected by specialized sensory neurons located in a small patch of mucus membrane lining the roof of the nose.
Axons of these sensory cells pass through perforations in the overlying bone and enter two elongated olfactory bulbs lying against the underside of the frontal lobe of the brain.
Odorants stimulate receptor proteins found on hairlike cilia at the tips of the sensory cells, a process that initiates a neural response. Each odorant has its own pattern of activity, which is set up in the sensory neurons.
This pattern of activity is then sent to the olfactory bulb, where other neurons are activated to form a spatial map of the odor.
Neural activity created by this stimulation passes to the primary olfactory cortex at the back of the underside, or orbital, part of the frontal lobe. Olfactory information then passes to adjacent parts of the orbital cortex, where the combination of odor and taste information helps create the perception of flavor.
In hairy skin areas, receptors may consist of webs of sensory nerve cell endings wrapped around the base of hairs. The nerve endings are remarkably sensitive.
Signals from touch receptors pass via sensory nerves to the spinal cord, where they synapse, or make contact with, other nerve cells, which in turn send the information to the thalamus and sensory cortex.
Larger areas of the cortex are devoted to sensations from the hands and lips.
Much smaller cortical regions represent less sensitive parts of the body.
Different parts of the body vary in their sensitivity to tactile and painful stimuli due to variation in the number and distribution of receptors. For example, the cornea is several hundred times more sensitive to painful stimuli than are the soles of the feet. The fingertips are good at touch discrimination, but the torso is not.
The sensory fibers that respond to stimuli that damage tissue and can cause pain are called nociceptors.
Different nociceptor subsets produce molecules that are responsible for the response to noxious (i.e., painful) thermal, mechanical, or chemical stimulation. These same molecules respond to plant-derived chemicals, such as capsaicin, garlic, and wasabi, that can produce pain.
Some nociceptors in the skin respond to chemical stimuli that cause itch. Histamine is an example of such a nociceptor, and it can be released in response to certain bug bites or allergies.
Tissue injury also causes the release of numerous chemicals at the site of damage and inflammation.
Prostaglandins enhance the sensitivity of receptors to tissue damage and ultimately can induce more intense pain sensations. Prostaglandins also contribute to the clinical condition of allodynia, in which innocuous stimuli can produce pain, as when sunburned skin is touched.
Persistent injury can lead to changes in the nervous system that amplify and prolong the “pain” signal.
Pain messages are picked up by receptors and transmitted to the spinal cord via small myelinated fibers and very small unmyelinated fibers.
From the spinal cord, the impulses are carried to the brainstem, thalamus, and cerebral cortex and ultimately perceived as pain.
These messages can be suppressed by a system of neurons that originates in the midbrain. This descending pathway sends messages to the spinal cord where it suppresses the transmission of tissue damage signals to the higher brain centers.
The cerebellum is specifically involved in motor tasks that involve coordinated timing.
The amygdala appears to play an important role in the emotional aspects of memory, attaching emotional significance to otherwise neutral stimuli and events. The expression of emotional memories also involves the hypothalamus and the sympathetic nervous system, both of which support emotional reactions and feelings.
How are memories created and stored?
Much evidence supports the idea that creating and storing a memory involves a persistent change in synapses, the connections between neurons.
Turning on certain genes could lead to modifications within neurons that change the strength and number of synapses, stabilizing new memories.
The phenomenon of long-term potentiation (LTP) occurs when stimulation results in a long-lasting increase in the strength of a synaptic response. LTP occurs prominently in the hippocampus, as well as in the cerebral cortex and other brain areas involved in various forms of memory.
LTP takes place as a result of changes in the strength of synapses at contacts involving N-methyl-d-aspartate (NMDA) receptors. Subsequently, a series of molecular reactions plays a vital role in stabilizing the changes in synaptic function that occur in LTP.
These molecular events begin with the release of calcium ions into the synapse, activating the cyclic adenosine monophosphate (cAMP) molecule in the postsynaptic neuron.
This molecule then activates several kinds of enzymes, some of which increase the number of synaptic receptors, making the synapse more sensitive to neurotransmitters. In addition, cAMP activates another molecule, called cAMP-response element binding protein (CREB).
CREB operates within the nucleus of the neuron to activate a series of genes, many of which direct protein synthesis. Among the proteins produced are neurotrophins, which result in growth of the synapse and an increase in the neuron’s responsiveness to stimulation. This cascade is essential for long-term memory.
In addition, studies using genetically modified mice have shown that alterations in specific genes for NMDA receptors or CREB can dramatically affect the capacity for LTP in particular brain areas. The same studies have shown that these molecules are critical to memory.
Over the course of the first hour or so of sleep, the brain progresses through a series of stages during which brain waves slow down.
The muscles and the eyes relax. Heart rate, blood pressure, and body temperature all fall.
If awakened during this time, most people recall only fragmented thoughts, not active dreams.
Over the next half hour or so, brain activity alters drastically, from deep slow wave sleep to rapid eye movement (REM) sleep.
REM sleep is accompanied by atonia, or paralysis of the body’s muscles. Only the muscles that allow breathing and control eye movements remain active.
During REM sleep, active dreaming takes place. Heart rate, blood pressure, and body temperature become much more variable.
The alternating Sleep Cycles of slow wave and REM sleep alternate during the night with the cycles of slow wave sleep becoming progressively less deep and the REM periods becoming progressively longer until waking occurs. The pattern of sleep cycles changes as humans mature.
Infants sleep up to 18 hours per day, and they spend much more time in deep slow wave sleep.
As children mature, they spend less time asleep and less time in deep slow wave sleep.
Older adults may sleep only six to seven hours per night. Some may experience early waking that they cannot avoid and spend very little time in slow wave sleep.
The brain systems governing Wakefulness include the upper brainstem, hippothalamus, and thalamus.
Nerve cells in the upper brainstem use the neurotransmitters acetylcholine, norepinephrine, serotonin, and glutamate to connect with the forebrain.
In the hypothalamus, nerve cells containing orexin and histimine play key roles. During non-REM sleep, a group of nerve cells called the ventrolateral preoptic (VLPO) nucleus actively suppress arousal symptoms. Damage to the VLPO nucleus produces irreversible insomnia.
Activation of the thalamus and the basal forebrain by acetylcholine is important in maintaining consciousness and activity in the cerebral cortex.
The Sleep-Wakefulness Cycle is influenced by (1) the circadian system (time of day or night) and (2) by how long we have been awake.
The circadian timing system is regulated by the suprachiasmatic nucleus, a small group of nerve cells in the hypothalamus that acts as a master clock.
These cells express clock proteins, which go through a biochemical cycle of about 24 hours.
The suprachiasmatic nucleus also receives input directly from the retina, and the clock can be reset by light so that it remains linked to the outside world’s day-night cycle.
In addition, the suprachiasmatic nucleus provides signals to an adjacent brain area, called the subparaventricular nucleus, which in turn contacts the dorsomedial nucleus of the hypothalamus.
The dorsomedial nucleus then contacts the ventrolateral preoptic nucleus and the orexin neurons in the lateral hypothalamus.
It is the orexin neurons that directly regulate sleep and arousal.
With prolonged wakefulness, increasing levels of adenosine are evident in the brain, initially in the basal forebrain and then throughout the cortex.
The increased levels of adenosine serve the purpose of slowing down cellular activity and diminishing arousal.
Adenosine levels then decrease during sleep.
Lack or loss of control is a particularly important feature of severe psychological stress, which can have physiological consequences.
Stress also can help the body. When confronted with a physical challenge, controlled stress responses can provide the extra strength and energy needed to cope. A physiological response to stress protects the body and brain and helps re-establish or maintain homeostasis.
The chronic aspects of stress are the most harmful.
Prolonged stress may repeatedly elevate physiological stress responses or fail to shut them off when they are not needed. Instead of being helpful, these mechanisms can upset the body’s biochemical balance and accelerate disease.
Scientists now believe that an individual’s perception of external events ultimately shapes their internal physiological response. Controlling that perception may be helpful in avoiding harmful consequences.
A stressful situation activates three major communication systems in the brain, all of which regulate bodily functions
The voluntary nervous system sends messages to muscles in response to sensory information.
The autonomic nervous system includes the sympathetic and the parasympathetic branches. Each of these systems has a specific task in responding to stress.
The sympathetic branch causes arteries supplying blood to the muscles to relax in order to deliver more blood, allowing greater capacity to act. At the same time, blood flow to the skin, kidneys, and digestive tract is reduced. The stress hormone epinephrine, also known as adrenaline, is quickly released into the bloodstream to put the body into a general state of arousal and enable it to cope with the challenge.
The parasympathetic branch helps regulate bodily functions and soothe the body once the stressor has passed, preventing the body from remaining in a state of mobilization too long.
Over the short run, epinephrine mobilizes energy and delivers it to muscles for the body’s response. The glucocorticoid cortisol, by contrast, promotes energy replenishment and efficient cardiovascular function.
The neuroendocrine system releases various stress hormones into the blood and stimulates the release of other hormones, which affect bodily processes such as metabolic rate and sexual function.
The release of glucocorticoids and epinephrine over long periods of time to improve memory, boost immune function, enhance muscular activity, and restore physiological balance can instead have negative consequences.
Memory is impaired, immune function is suppressed, and energy is stored as fat. Hypertension (high blood pressure), atherosclerosis (hardening of the arteries), and abdominal obesity can result.
Epinephrine also increases the release and activity of body chemicals that cause inflammation. This continual chemical activity can lead to arthritis and accelerated aging of the brain. Overexposure to glucocorticoids also increases the number of neurons damaged by stroke.
Prolonged glucocorticoid exposure before or immediately after birth causes a decrease in the normal number of brain neurons and smaller brain size. Scientists have identified a variety of stress-related disorders, including high blood pressure, clogged arteries, impotency and loss of sex drive in males, irregular menstrual cycles in females, colitis, and adult-onset diabetes.
Stress also can contribute to sleep loss when people get caught in a vicious cycle: elevated glucocorticoids delaying the onset of sleep, and sleep deprivation raising glucocorticoid levels.
We now know that the brain reaches its maximum weight near age 20, and subtle changes in the brain’s chemistry and structure begin at midlife for most people.
During a lifetime, the brain is at risk for losing some of its neurons, but normal aging does not result in widespread neuron loss. This fact distinguishes normal aging from the neurodegenerative changes that occurs as part of the disease process in Alzheimer’s or Parkinson’s disease or after a stroke.
Brain tissue can respond to damage or loss of neurons in several ways. The remaining healthy neurons are able to expand their dendrites and fine-tune their connections with other neurons. If the cell body of the neuron remains intact, a damaged brain neuron can readjust by inducing changes in its axon and dendrites. However, a damaged brain cannot respond with a robust generation of new neurons.
Studies show that many areas of the brain, especially in the cortex, maintain most of their neurons throughout life. The connectivity between neurons changes with aging, indicating that the brain is capable of being modified or improved.
Your brain can’t make new cells.
Your brain constantly generates new cells and remains adaptable — or “plastic” — as you age.
You only use 10 percent of your brain.
The dense population of neurons in your brain are continually evolving to carry as much information as possible while expending the least energy. The engagement of the whole brain is required to meet this challenge and can sometimes affect our ability to pay attention or multitask.
The bigger your brain the smarter you are.
The unique capabilities of the human brain are attributable to the complexity of its cerebral cortex with its 16 billion neurons – more than any other creature in the animal kingdom– and to specialilzed cells called glia. Sizewise, however, our human brain comprises only about 2 percent of our body mass – far less than the tree shrew’s brain at 10 percent of its body mass.
Listening to classical music makes you smarter.
A small study conducted more than 20 years ago, showed that college students who listened to a Mozart sonata and then took an IQ test got higher spatial scores than those who didn’t. The effect wore off in less than 15 minutes and researchers dispute the mechanics of the study. By contrast, researchers have found that young children who watch classical music-based television learn fewer words, as do those who watch regular television. But learning how to play a musical instrument has been shown to enhance cognitive skills in the long term.
Drinking alcoholic drinks always kills brain cells.
Moderate amounts of alcohol do not kill brain cells. Some studies find moderate amounts of alcohol may be healthful and even protect the brain by reducing the risk of stroke. Only years of chronic or binge drinking will kill neurons.
Drug use makes holes in your brain.
Key brain regions in drug addicted people are reduced in size, but no actual holes are formed as a result of drug use. Only physical trauma can create a hole in your brain.
Vaccines cause autism.
This link has been thoroughly reviewed, studied, and rejected by scientific consensus, and some of the original research purporting this link has been repudiated. Scientists are seeking genetic factors that may cause autism.
Playing games keeps your brain young.
A healthy diet and regular exercise can help maintain memory and general cognition. Have fun working crosswords and playing other games to help you maintain vocabulary and other skills, but doing so won’t enhance overall brain function.