More than half of the estimated 100,000 genes in human DNA seem to be dedicated to building and maintaining the nervous system.

Within the brain, the autonomic nervous system regulates and adjusts baseline body function and responds to external stimuli. It consists of two mutually inhibitory subsystems: those nerves which activate tissues-- the sympathetic or arousal system, and those which slow structures down for rest and repair--the parasympathetic or quiescent system. The sympathetic is ergotropic that is releases energy, and the parasympathetic is trophotropic, that is conserving energy. The two sides of our autonomic system reflect the two main processes in life "growth" or "protection." These two mechanisms cannot operate optimally at the same time. Consider that our nervous system is either wired for eating (parasympathetic) or running away from being eaten ourselves (sympathetic). So the two systems generally act in opposition to each other; yet where dual control of an organ exists, both systems operate simultaneously although one may be operating at a higher level of activity than the other.

Energy expended in fueling defense takes it way from the process of growth. The consequent inhibition of growth reduces energy generation. The Hypothalamus-Pituitary-Adrenal Axis mobilizes defense against threat and when it is not activated growth flourishes. Hence chronic stress is enervating and debilitating. Thus we can see that children who grow up in stressful homes are deprived in cellular nutrition and growth, in cellular energy generation itself and consequently in mental-emotional-social development. Adrenal hormones constrict blood flow to the forebrain and stress hormones repress the prefrontal cortex activity, thus diverting energy and consciousness to the hind-brain survival faculties. The hyperactivity of the HPA axis and sympathetic nervous system is perhaps one of the reasons why high kundalini activity can make us dumb, that and the excessive production of opiates of course.

SYMPATHETIC

The arousal system is the source of our fight or flight response, and is connected to the adrenal glands, the amygdala. The dominant (analytical) mind is connected to the arousal system and reaches into our left cerebral hemisphere. It is sometimes called the "ergotropic" system because it releases energy in the body to react to the environment.

The sympathetic system comprises of paravertebral sympathetic trunks which run up the front side of the spine from the cranial base to the coccyx. Sympathetic nerves run mostly from the thoracic and lumbar region and are longer and less direct than the parasympathetic nerves thus their effect is more diffuse. Instead of separate ganglion for each vertebrae certain segments collect together to form a single large ganglion eg: the cervical ganglion in the neck and the stellate ganglion in the upper thoracic region. Connected to the ganglion are plexus that pass to the organs. The cardiac plexus via the stellate ganglion supplies the heart and lungs. The solar plexus is connected with the lower thoracic spinal nerves and supplies sympathetic fibers to the stomach, intestines, adrenals and other viscera. The heart is supplied by sympathetic nerves arising mainly in the neck, because the heart develops initially in the cervical region and later migrates into the thorax taking its nerves down with it.

The neurotransmitter of the preganglionic sympathetic neurons is acetylcholine (ACh). It stimulates action potentials in the postganglionic neurons, affecting their targets through adrenergic receptors. The neurotransmitter released by the postganglionic neurons is noradrenaline (also called norepinephrine). The action of noradrenaline on a particular gland or muscle is excitatory is some cases, inhibitory in others. (At excitatory terminals, ATP may be released along with noradrenaline.)

The release of noradrenaline stimulates heartbeat, raises blood pressure, dilates the pupils, dilates the trachea and bronchi, stimulates the conversion of liver glycogen into glucose, shunts blood away from the skin and viscera to the skeletal muscles, brain, and heart, inhibits peristalsis in the gastrointestinal tract, inhibits contraction of the bladder and rectum and inhibits the immune system to save energy.

Stimulation of the sympathetic branch of the autonomic nervous system prepares the body for fight or flight. This emergency response is controlled by the hypothalamus and amygdala through the HPA axis. Activation of the sympathetic system is quite general because a single preganglionic neuron usually synapses with many postganglionic neurons; the release of adrenaline from the adrenal medulla into the blood ensures that all the cells of the body will be exposed to sympathetic stimulation even if no postganglionic neurons reach them directly.

One important exception to the activating response of the sympathetic system is that the alimentary adrenergic nerves "inhibit" the activity of the gastrointestinal tract while activity in the cholinergic (parasympathetic) supply results in "activation" of the gastric and intestinal systems. This is because during the adrenaline induced fight or flight response or during demanding activity, the blood and energy is needed by the brain and muscles, leaving digestive and eliminative functions until times of rest and relaxation.

Hormones produced by the outer region of the adrenal cortex regulate the body's metabolism, blood composition, and even body shape. The inner region produces hormones that are the body's first line of defense against stress, whether it be physical or emotional. This inner region of the adrenals is called the adrenal medulla and is considered to be part of the sympathetic nervous system. Adrenaline and norepinephrine act as neurotransmitters when they are released by neurons, and as hormones when they are produced by suprarenal glands.

PARASYMPATHETIC

The parasympathetic or reposing side of the autonomic nervous system promotes relaxation, sleep, growth and repair. It is sometimes called the "trophotropic" system because it conserves energy. It includes the endocrine glands, parts of the hypothalamus and the thalamus, and reaches into the right cerebral hemisphere. Thus the non-dominant, holistic mind is connected with the quiescent system and involves the hypothalamus and hippocampus. After the activity of sympathetic stimulation the parasympathetic system reverses the changes when the danger is over and returns the body functions to normal.

The main nerves of the parasympathetic system are the tenth cranial nerves, the vagus nerves. They originate in the medulla oblongata with separate branches going to the heart and respiratory system, and there are branches throughout the abodomen after passing through the oesophageal opening of the diaphragm. Other preganglionic parasympathetic neurons also extend from the brain as well as from the sacral end of the spinal cord. The ganglia of this system are located near the structures to be innervated or actually in the walls of the organ, therefore the postganglionic fibers are much shorter than those of the sympathetic system. This is one of the reasons why sympathetic effects are usually more diffuse than parasympathetic effects. The sacral parasympathetic fibers supply the rectum, bladder and reproductive organs; and nerves from the two lowest ganglia enter the kundalini gland. Cranial fibers run with the vagus nerve supplying enervation to the heart, stomach and small intestines. True parasympathetic nerves are all motor. Sensory nerves within the parasympathetic system are general visceral sensory nerves that simply run with the parasympathetic fibers and are not strictly part of the system. There is not parasympathetic supply to the limbs or gonads.

Acetylcholine (ACh) is the neurotransmitter at all the pre- and many of the postganglionic neurons of the parasympathetic system. However, some of the postganglionic neurons release nitric oxide (NO) as their neurotransmitter. In the parasympathetic nervous system, the postganglionic neurons' ACh is received by muscarinic ACh receptors. Acetylcholine (ACh) opens cation channels for Na+ and Ca+ to flow into and K+ to flow out of a cell. ACh is an example of a direct messenger.

Parasympathetic stimulation causes the heartbeat to slow, lowers blood pressure constricts pupils and changes the lens for near vision, increases blood flow to the skin and viscera, stimulates glands to secrete saliva and mucus, stimulates gut peristalsis. Contracts the bladder and uterus, causes erection of penis and *censored*oris,

Plexus are complex webs of nerves and ganglia that affect the internal organs, particularly by controlling arterial blood flow, hence oxygen and nutrient supply. The location of the plexus are associated with the chakra system. The cervical plexus contains nerves mainly connected to the skin and muscles of the head and neck, but it also contains the phrenic nerve which runs to the diaphragm. The cardiac plexus directly affects the heart and lungs. The solar plexus is the largest in the body. It is involved in the flight or flight activation of the redirection of blood from the digestive organs to the brain and muscles. The solar plexus stimulates the production of adrenaline and activates the kidneys. The pelvic plexus has lumbar and sacral spinal connections and is concerned with elimination and sexuality. Kundalini can be felt as bliss, tingle and heat moving through these plexus at various times.

The Medulla oblongata is part of the brainstem at the top of the spinal cord. The central canal of the spinal cord continues into the forth ventricle of the medulla. It is in the medulla that the nerves from the two hemispheres cross over and head down the spine to control the opposite sides of the body. The parasympathetic nerves that feed all the visceral organs down to the intestines leave the spinal cord from this cranial area. However the colon, urinary organs and the sex organs are parasympathetically fed by nerves leaving the sacrum area at the bottom of the spine.

The Substantia gelatinosa is the H shaped gray matter in the spinal cord which surrounds the central canal. This is where the nerve fibers carrying information from the peripheral to the central nervous system terminate. The Substantia gelatinosa is made up of unmylenated neurons, some of which inhibit pain signals by producing opioids. Since kundalini invariably involves the sensation of bliss part of the endorphin releases could be from the gray matter in the spinal cord itself. Avram Goldstein, one of the first discoverers of endorphins proposed that endorphins in the amygdala create the tingling down the spine, and the shuddering discharge of emotion that we experience as a thrill. In the brain a thin outer shell of cellular gray matter, (the cortex) covers the cerebral hemispheres and clusters of cellular gray matter in the center of the brain form the deep nuclei. A nucleus is a mass of nerve cell bodies and dendrites inside the CNS. Clusters of nerve cells outside the CNS are referred to as ganglion.

The Locus cerculeus in the floor of the forth brain ventricle is an alarm center which helps attentiveness, and governs arousal, fear, anxiety and terror. It has extensions of its noradrenergic neurons reaching into nearly every part of the cortex, and is thought to be instrumental in directing the attention of the cortex. Researchers have found both the Locus cerculeus and the amygdala and other regions of limbic system to be practically saturated with shorted lived opioid peptides (chained amino acids) called enkephalins.

Opiates--In response to physical injury, terror, and severe emotional stress, the amygdala, hypothalamus, brainstem, striatum and related limbic system nuclei secrete enkephalins. Like corticosteroids, enkephalins are released as part of the fight or flight response, and insure that an animal or human can continue to do battle, or to successfully run away, although severely injured. Enkephalins are a five amino acid protein chain, the smallest opioid to be used by the body. Although the enkephalin combination of aminos is found within endorphins they actually come from different precursors and have dissimilar distribution patterns. When stained endorphin regions show up as definite streaks, pathways or fibers while enkephalins tend to show up as discrete dots. The strongest of the opioids is the 17 chained amino acid dynorphin. Dynorphin in the spinal cord helps in processing sensory information. As well as the spinal cord it is also found in parts of the pituitary gland, the hypothalamus, medulla, pons and the mid brain.

The three genera of opioid peptides endorphins, dynorphins and enkephalins are used as hormones in the body and something more like neurotransmitters in the brain. They are inhibitory neurotransmitters, making it more difficult for the neuron membrane to become depolarized and fire off an electrical signal. In this way the endorphin system of nerves acts to inhibit other neuronal systems in the brain. The effect of opiates is to inhibit the reaction of tissue to electrical stimulation. Without this inhibitory action to slow down neuron firing, the racing electric activity would result in convulsions and death. Endorphins slow breathing, reduce blood pressure and decrease sensitivity to pain. Endorphins reduce smooth muscle contraction, thus causing the smooth muscles in the arteries to dilate increasing blood flow. Hypoxia or low oxygen creates acidosis stress which increases beta-endorphins as part of the parasympathetic response to achieve balance.

Long-term potentiation (LTP) is the long-lasting strengthening of the connection between two nerve cells. Like corticosteroids, enkephalins abolish LTP and theta activity, disrupt learning and memory, and induce hippocampal seizure activity without convulsions, which is accompanied by abnormal, high voltage EEG paroxysmal waves which can last from 15 to 30 minutes. Enkephalins can also trigger hyperactivation of hippocampal pyramidal cells--neurons which normally display synaptic growth and dendritic proliferation in response to new learning. Enkephalins can also alter the pre- and post-synaptic substrates, thereby injuring hippocampal neurons and producing a hippocampal amnesia as well as a state dependent memory loss.

Myelination of the nerves proceeds from the bottom to the top, back to front and from left to right. Kundalini generally also follows this path of flow and development over the period of an awakening. We tend to get right body and right-brain kundalini effects occurring in December and towards the end of ones awakening. Myelin is a fatty substance that includes acetylcholine. When we overwork the other neurotransmitters we burn out our acetylcholine as well. Since the myelin sheath is what facilitates Ôspeed' in the transmission of a nerve impulse, the impairment of our myelin slows down our brain...this is obviously a major contributor to the spiritual burn-out effect from excessive nerve activity during an awakening.

Kundalini awakening is a method that the body uses to promote new growth, because after myelination finishes it's harder to change or evolve the nervous system. Kundalini is so outrageously pervasive that I am sure that not only is there a lot of neurons dying off, there is also demyelination and remyelination that occurs. Research will probably prove that there are major changes in the pattern of myelination resulting from a kundalini awakening, and the function we are left with in the end is a result of these changes. This serves as a good case for AQAL developmental practices and experiences during an awakening because if we "fail to use it, we lose it." In other words "substantiation" equals agency, praxis or use.

GLIAL CELLS

Glial cells perform a variety of functions in the central nervous system and make up 50% of CNS by volume, and 95-98% by numbers. Neurons are the "active" or functional cells of the nervous system and carry electrical signals. Glial cells are small supporting cells that do not carry electrical signals. In support of neurons glial cells offer:

Nourishment--Glia attach neurons to blood vessels and supply nutrients and oxygen to neurons, maintain ionic balance and help control the chemical composition of fluid surrounding neurons. The L-arginine for NO production is mainly supplied mainly from glial cells. They produce cerebrospinal fluid!

Insulation--Glia produce the fatty insulating myelin sheath around axons to insulate one neuron from another, to form a matrix surrounding neurons and hold them in place, this matrix serves to isolate synapses limiting the dispersion of transmitter substances released.

Phagocyctosis--Glia act as scavengers, removing debris after injury or neuronal death and to destroy and remove the carcasses of dead neurons. Phagocytosis occurs when an astrocyte contacts a piece of neural debris with its processes (arm of the astrocyte) and then pushes itself against the debris eventually engulfing and digesting it.

Glycoysis--Aerobic glycolysis in the CNS involves interactions between neurons and astrocytes. The entrance of glucose into the central nervous system from the capillaries occurs primarily through astrocytes. Astrocytes are strategically placed between capillaries and neurons and play an essential role in neuronal energy metabolism and brain glycogen is localized in astrocytes in brain tissue. Astrocytes provide nourishment to neurons by receiving glucose from capillaries, Astrocytes first metabolize glucose to its metabolic intermediate lactate and secrete lactate, releasing it into the extra cellular fluid surrounding the neurons. The neurons receive the lactate from the extra cellular fluid and transport it to their mitochondria to use as a primary substrate for oxidative metabolism to create energy. In this process astrocytes store a small amount of glycogen, which stays on reserve for times when the metabolic rate of neurons in the area is especially high.

Neuronal activity regulates the rate of aerobic glycolysis by a mechanism involving glutamate release from neurons and glutamate uptake into astrocytes. Glutamate is the primary neurotransmitter released by excitatory synapses in the CNS. Glutamate is taken up by astrocytes by a Na+ cotransporter. Na+ influx into astrocytes stimulates the astrocytic sodium pump which produces ADP. Increased levels of astrocytic ADP will stimulate glycolysis and lactate transport into neurons. Lactate uptake by neurons will stimulate neuronal oxidative ATP production. Glucose can be incorporated into lipids, proteins, and glycogen, and it is also the precursor of certain neurotransmitters such as g-aminobutyric acid (GABA), glutamate, and acetylcholine.

Schwann cells support the peripheral nervous system, while the central nervous system is supported by glial cells. As the peripheral nerves form, the Schwann cells migrate peripherally from the spinal ganglia, parallel to the axons, and encase them with their cytoplasm. The myelin sheath is created by a synthesis and wrapping of Schwann cell plasma membrane around the axon. During the breakdown of damaged axons Schwann cells participate in myelin phagocytosis prior to the recruitment of macrophages. They produce heat shock protein, only when they have transformed into these myelin-"eating" cells from myelinating cells. I am convinced that during the die-off some axons do die and Schwann cells would change to their phagocytic mode in order to absorb the dead axons. Research might find that whole neurons die-off at this time, rather than just certain dendrite connections.

The Enteric Brain--The stomach or enteric brain comprises of 100 million nerves surrounding the esophagus, stomach and intestines and many of its structures and chemicals parallel those of the main brain. It has sensory and motor neurons, information processing circuits, and the glial cells (defined). It uses the major neurotransmitters: dopamine, serotonin, acetylcholine, nitric oxide and norepinephrine. Both the brain in the skull and the enteric brain originate from a structure called the neural crest, which appears and divides during fetal development.

GLUTAMATE

Glutamate is a major excitatory amino acid neurotransmitter accounting for an estimated 40% of all nerve signals in the human brain, and involved in phenomena such as neural development, learning, and memory formation. Glutamate is ordinarily released under close cellular biochemical control and re-uptake, for in excess amounts it is an intense excitant of nerve cells and potentially toxic. The neurotransmitters glutamate and aspartate act as excitatory signals, while glycine and GABA inhibit the firing of neurons. The activity of GABA is increased by Valium and by anticonvulsant drugs. Glutamate or aspartate activates N-methyl-d-aspartate (NMDA) receptors, one of three major classes of glutamate receptors, which have been implicated in activities ranging from learning and memory to the specification and development of nerve contacts in a developing animal. Nitric Oxide (NO) can diffuse across the synaptic cleft back into the synapse that originally released the glutamate. This retrograde transport of NO is thought to reinforce long term potentiation and thus is considered to be a possible molecular mechanism promoting long term memory and learning.

Glutamate may play the central role in kundalini awakening. The prolonged firing of kindling releases glutamate which activates the N-methyl-D-aspartate (NMDA) receptors in the spinal cord, which may sensitize the spinal cord neurons to become more responsive to all inputs, resulting in perpetual hyperexcitability.

When glutamate is produced and released by a synapse it activates the NMDA receptor leading to an influx of calcium ions; which in turn bind to calmodulin (CaM), activating the enzyme that synthesizes Nitric Oxide (NOS). Calmodulin is a calcium-binding protein that is considered a major transducer of calcium signals.

Glutamate receptors are selective for calcium ions. Prolonged activation of glutamate receptors stimulates eNOS via Ca/CaM complex binding to the synthetase. NO can only be synthesized, however, if the amino acid arginine is available. Thus neuronal NOS critically depends on arginine, which is mainly synthesized in adjacent glial cells and is transported into neurons. Arginine uptake into neurons is controlled by non-NMDA glutamate receptors. This became evident when these receptors were blocked by arginine-uptake inhibitors such as L-lysine which functions as antagonist to glutamate receptors.

The N-methyl-D-Aspartate (NMDA) receptor is a subtype of glutamate-activated ionotropic channels, that is implicated in synaptic mechanisms underlying learning, memory and the perception of pain. It is also believed to be a target of the intravenous general anesthetic agent ketamine and possibly nitrous oxide. Because it is affected by anesthetic agents, the NMDA receptor is probably key to the "conscious" aspect of consciousness.

Presumably, glutamate acts at NMDA receptors on NOS terminals to stimulate the formation of NO, which diffuses to adjacent terminals to enhance neurotransmitter release. In the cerebellum NOS occurs in the glutamate-containing granule cells as well as in the GABA containing basket cells. Many of the cerebral cortical NOS neurons also contain GABA. Release of both acetylcholine and dopamine from the nerve cells is blocked by NOS inhibitors and enhanced by plentiful L-arginine.

One possible reason why where is such a hemispheric difference in the flow of kundalini could be the different placement of glutamate receptors between the left and right side of the brain. According to Isao Ito and his team they found more NMDA receptors on dendrites at the tip of neurons in the right hemisphere and in the left-brain they were found at the base of neurons. This may explain why the left is more kundi-excitable, active, analytic, logic, language, focus, decision oriented. The right represents a more parasympathetic nature, involved in emotion and memory.

The overall excited condition of kundalini arousal is probably mainly carried both on norephinephrine nerves and via glutamate receptors. Nitric Oxide and Ca2+ levels being the rate mediating factors in the maintenance of the charge through the glutamate system. After the body recycling periods of the die-offs are finished, the slow depletion of arginine will reduce NO and Growth Hormone production...thus reducing both hyperneural activity and regeneration of tissue and the awakening will very gradually come to a close. For reduced concentrations of NO will down regulate the NMDA receptors reducing the excitation of the neurons. Also since calcium resources of the body would be used to buffer the acidic products from the increased metabolic rate, calcium availability might eventually become a limiting factor bringing the hyper-excitation of neurons to an end.

Since glutamate can be made from any sugar, carbohydrates or even from proteins or fats, it is always somewhat readily available as an excitatory neurotransmitter. However since a low-glycemic diet does reduce kundalini and seizures, it is apparent that glutamate levels are also a mediating factor in the firing rate of neurons.

GLUTAMATE TOXICITY

Glutamate neurotoxicity can cause neuronal cell death. Reactive oxygen species are mediators of delayed neuronal degeneration caused by activation of ionotropic glutamate receptors. Oxidative stress was also shown to precipitate programmed cell death or apoptosis. The lineage between these two phenomena relate to the facts that the mitochondria are the source of 80% or more of the oxyradicals generated in the neuron and that Ca2+ dysregulation causes excessive activation of glutamate ionotropic receptors, disrupting the mitochondrial electron transport system.

The immediate effect of glutamate on neurons is its role in activating glutamate receptors, (NMDA is a methylated derivative of aspartate). The stimulation of NMDA receptors may promote beneficial changes in the brain, whereas overstimulation can cause nerve cell damage or cell death during seizure, trauma and stroke. When neurons are damaged, glutamate pours out, builds up in the synapses, and kills them by overexciting them, enlarging the area of brain damage. Both oxygen deprivation and overexcitation of neurons can create an abnormal buildup of glutamate that kills neurons by overstimulating them.

Glutamate works by attaching to N-methyl-D-asparate (NMDA) receptors, proteins on the cell surface. The action of NMDA receptors appears particularly important because they have the special ability to let large amounts of calcium into neurons. When the brain suffers an injury such as a stroke, neurons release glutamate onto nearby neurons which become excited, causing excess calcium release to activate enzymes which eventually leads to destruction of the cell. Because of their "gatekeeper" role, NMDA receptors are important targets for developing therapies to reduce glutamate action. Drugs that block these proteins, called NMDA receptor blockers, can prevent glutamate from harming neurons and stop the enhanced glutamate excitatory activity typically seen in epilepsy.

NO is associated with the main excitatory neurotransmitter Glutamate and the generation of action potentials in the nerves. Small amounts of it open up the calcium ion channels of the nerves (along with glutamate, an excitatory neurotransmitter) sending a strong excitatory impulse. Larger amounts of NO can force the calcium channels to fire more rapidly which can lead to apoptosis or programmed cell death. Thus NO mediates the neurotoxicity of glutamate through the formation of cGMP by activation of glutamate receptors. As stated in the section on Nitric Oxide, cGMP participates in signal transduction within the nervous system.

In the brain a stimulus (such as glutamate) acting at NMDA receptors triggers Ca2+ influx which binds to calmodulin, thereby activating NOS. This mode of activation explains how glutamate neurotransmission stimulates NO formation in a matter of seconds. In blood vessels, acetylcholine acting at muscarinic receptors on endothelial cells activates the phosphoinositide cycle to generate Ca2+, which stimulates NOS to produce NO for blood vessel dilatation.

The influx of Ca2+ into the neuron activates an enzyme called calcium-calmodulin-dependent kinase II (CaMKII). Kinases attach phosphate groups to proteins and altering their functioning. In this case, CaMKII phosphorylates a second type of Glutamine receptor called AMPA receptors, which makes them more permeable to sodium ions (Na+) thus lowering the resting potential of the cell and making it more sensitive to incoming impulses. In addition, there is evidence that the activity of CaMKII increases the number of AMPA receptors at the synapse.

PROTECTING GLUTAMATE RECEPTORS

Studies found that alpha-lipoic acid improves memory in aged mice, probably by a partial compensation of NMDA receptor deficits. It is though that its free radical scavenger properties preserve cell membrane and so protect loss of NMDA receptors. It also protects membranes and receptors through improved sugar and insulin metabolism. Alpha lipoic acid is a unique antioxidant because it prevents and may even reverse the attachment of sugar to protein, a process known as glycation or crosslinking. Alpha lipoic protects cells from AGEs by allowing better metabolism of sugar in the cell, this prevents its buildup and also by allowing the body's natural repair mechanisms to work better.

A team of researchers led by Bruce N. Ames, professor of molecular and cell biology at UC Berkeley, fed older rats acetyl-L-carnitine and alpha-lipoic acid. They found that the combination of the two supplements effectively reduce aging by tuning up the mitochondria, rejuvenating and energizing cells and both spatial and temporal memory, and reduced the amount of oxidative damage to RNA in the brain's hippocampus, an area important in memory. It is advisable therefore for those undergoing kundalini to take L-carnitine and alpha-lipoic supplements as well as adopt a low glycemic diet.

Apparently the glutamate receptors in the brains of drug addicts retreat into the cell membrane perhaps to try and prevent the cell from becoming over stimulated by all the chemical stimulants. I was thinking that during the peak when the sympathetic NS is fired up and endorphins are blasting full bore the brain would exhibit conditions "similar" to a drug addicts brain. Perhaps in kundalini initiates the glutamate receptors also retreat into the cell, thus adding to the burn out and lengthy recovery period after the peak. "One of the problems in addiction is that neurons in some parts of the brain lose glutamate receptors from the cell surface, and those receptors are important for communication between neurons. The researchers have sidestepped this problem by crafting a peptide that mimics a portion of the tail of the glutamate receptor and, once inside a neuron, serves as a decoy to prevent the loss of glutamate receptors." eurekalert.org/pub_releases/2005-11/hhmi-gab112305.php

STRESS RESPONSE CYCLE

Wilhelm Reich observed that life has a four beat bioenergetic formula: tension--charge--discharge--relaxation.

Kundalini occurs in nested cycles that follow the basic stress response pattern that Hans Selye outlined in the 1950's. First there is "adaptation" a person intermittently secretes slightly higher levels of the fight or flight hormones in response to a slightly higher level of stress. Secondly "alarm," begins when the stress is constant enough, or great enough, to cause sustained excessive levels of certain adrenal hormones. Lastly "exhaustion," sets in as the body's ability to cope with the stress becomes depleted. But we now know that rather than the stress-response hormones and transmitters “running out” during the exhaustion phase. It is the stress response itself that is damaging, because the body spends so many resources on stress adaptation that it causes the allostatic economy of the body to become bankrupt.

During an awakening all the neurotransmitters and hormones move through the phases of:

1.Adaptation: HEATING--homeostatic balance, strengthening and preparation. Building of hormonal and neurological resources.

2.Alarm: PEAK--similar to immediate threat response; heightened use of both on/off facilitating an expanded state of being. Adrenalin and histamine production.

3.Exhaustion: BURNOUT—depletion of resources for dealing with metabolites and free radical damage and production of hormones and neurotransmitters. As adrenal levels plummet this adrenal exhaustion sometimes accompanies, or is mistaken for low thyroid. Prolonged release of high cortisol leads to adrenal exhaustion. Decline in the immune system.

4.Recovery: SUBSTANTIATION--repair and building up resources again once the hypertonality has died down. Growth on a new level reflecting the psychosomatic "space" that has been created from the die-off and self-digestion.

Adrenal hormones constrict blood flow to the forebrain and stress hormones repress the prefrontal cortex activity diverting energy and consciousness to the hindbrain and survival faculties. Besides stress being enervating, prolonged hypothalamic-pituitary-adrenocortical activation also makes us dumber. "The longer you stay in protection, the more you compromise your growth." 147, Bruce Lipton, The Biology of Belief.

NEUROTRANSMITTERS

In the body there are at least 50 known neurotransmitters which convey a rich selection of possible messages between neurons, and many of these neurotransmitters have over a dozen different types of receptors.

Neurotransmitters, the brains messenger molecules come in two forms, monoamines and neuropeptides.

1. Small-molecule neurotransmitters--The key monoamines are:

Serotonin is made from the amino acid Tryptophan. It calms, elevates pain threshold, promotes sleep and feeling of well being, reduces aggression and compulsive behavior.

Dopamine is made from the amino acids Phenylalanine and Tyrosine. It increases feelings of well-being, alertness, sexual excitement and aggression; and reduces compulsive behavior.

Norepinephrine is made from Dopamine it also increases well being and reduces compulsivity

GABA is made from the amino acid Glutamic acid (Glutamine or Glucose). It reduces anxiety, elevates the pain threshold reduces the blood pressure and heart rate and reduces compulsive behavior.

As well as glutamate, aspartate, glycine, biogenic amines, ATP & NO, histamine and prostaglandins.

2. Neuropeptides:

Amino Acids made in cell body and transported to synaptic terminals. They share opiate receptors and regulate pain (analgesics) and pleasure. Neuropeptides are manufactured in the endoplasmic reticulum and are called opioid peptides because they behave in the brain like opiates such as morphine. Their functions include regulating immune response, raising pain threshold stimulating feeling of well being, regulating sexual activity, promoting emotional balance and enhancing learning. As well as reducing compulsive behavior. There are three groups of neuropeptides--Endorphins, Enkephalins and Dynorphins and substance P (pain)

The thing to keep in mind is that excessive use of the on-switch neurotransmitters burns out the off-switch neurotransmitters. While peaking we are so neuro-hormonally pumped up that we do not actually feel the true consequences of the free radical damage until after the hormones and neurotransmitters run out. When one is pumped up on Spirit you simply can't imagine that burnout and damage will occur. It is apparent that kundalini cycles through the various nerve/receptor systems at different times reflecting both lunar and seasonal rhythms.

During the peak it is probably focused more on the norephinephrine nerves, moving first through the limbic system and then through the norephinephrine net that traces through the cortex. Epinephrine (adrenaline) and the closely related norephinephrine are the chief neurotransmitters at the post ganglion terminations of the sympathetic nerves. Norepinephrine is made from dopamine which in turn is derived from the amino acids Phenylalanine and Tyrosine. It increases feelings of well-being, alertness, sexual excitement and aggression; and reduces compulsive behavior.

When it moves through the digestive system it is probably focused on the serotonin system. When in a collapse phase such as a die-off or exhaustion then GABA, acetylcholine and serotonin would be more prominent during this parasympathetic dominant phase. GABA is most common inhibitory transmitter in a third of all synapses. ACh (acetylcholine) inhibits the heart via the vagus. Opiate and endocannaboid receptors and nerve centers are highly active during all kundalini activity even in the exhaustion phase. Acetylcholine is generally associated with the parasympathetic effects, however it is thought that acetylcholine is probably the chief neurotransmitter for the preganglionic fibers of both systems.

Contenders for the neuro-excitatory substances involved in kundalini include the primary excitatory neurotransmitter glutamate in combo with Nitric Oxide and histamine, prostaglandins even the body's fuel molecule ATP. When ATP is split apart a great deal of energy is released to power the cell. This involves the conversion of ATP into its stepped down product cAMP. Then cAMP activates a protein called Kinase which makes the neuron membrane more excitable. Thus the whole neuron becomes less inhibited and more easily "turned on" by neurotransmitters fitting into the receptor sites.

Each person is different of course and will exhibit either dopamine, serotonin, GABA or acetycholine dominance, and so the ability to withstand a kundalini awakening differs as does their experience of the awakening itself. There are infinite factors involved in how readily we will be depleted of neurochemicals, hormones and other bodymind resources during the exhaustion phase: season/sunlight hours, emotional resourcefulness, heredity, trauma history, infancy-conditioning, diet-supplements-antioxidants, emotional processing ability, life circumstances, social community, intimate companionship, life purpose-vocation, education level, urban or rural, latitude, exercised or sedentary, life habits-samskaras...and much more.

The effectiveness of our spiritual practices obviously has a profound impact both on the awakening of kundalini and the rate that resources are depleted. While meditation makes the awakening of kundalini more likely to happen it also eases its passage and reduces the depletion-crash effect, by making the HPA axis less volatile. It does this by synchronizing neural nets to fire in more in sync thereby reducing energy wastage and improving nervous efficiency. It also stabilizes and amplifies the hormone production of the pituitary gland and reduces the spiking of the sympathetic fight flight response. Because various brain areas are neurologically enrichened by meditation there is also more prefrontal control over the limbic system. Meditation makes up for some of the deficits we may have in our primary matrix neuron growth.

The central functions of norepinephrine (NE) are: regulation of alertness and of the wakefulness/sleep cycle, maintenance of attention, memory and learning, cerebral plasticity and neuro-protection. Norepinephrine (NE) stimulates neural growth, significantly influences neuronal maturation and promotes neural plasticity and synaptic development during the early stages of fetal and infant development. NE is neuroprotective and when it's depleted, neurons are exposed to the debilitating effects of enkephalins and stress hormones released during the fight or flight response. In the infant NE may destabilize in response to even mild stress such as temporary separation from the mother. Consequently wildly fluctuating NE levels can lead to atrophied neural growth and aberrant neural networks (neuronal pools). These dysfunctional, deprivation and stress induced aberrant networks are especially pronounced within the amygdala, septal nuclei, and the hippocampus, and can lead to the propensity toward abnormal seizure-like activity, such as kindling. Neurons in the CNS are organized into definite patterns called neuronal pools; each pool differs from all others and has its own role in regulating homeostasis. A neuronal pool may contain thousands or even millions of neurons.

As well as abnormal growth of nerves unbalanced neurotransmitter leaves can lead to inferior firing patterns. Stress induced depletion of NE coupled with excessive secretion of corticosteroids and enkephalins can hyperactivate hippocampal pyramidal neurons and eliminate hippocampal theta and long term potentiation, thereby interfering with learning and memory. Depletion of neurotransmitters is countered by the use of Monoamine oxidase inhibitors. These relieve depression by preventing the enzyme monoamine oxidase (MAO) from breaking down the neurotransmitters norepinephrine, serotonin and dopamine in the brain. As you can imagine with such exaggerated activation of the adrenal/dopamine/cortisol systems we need to focus on building up our serotonin, GABA and acetylcholine systems, which get burnt out during the hyper-phase.

Current research on depression indicates increased deep limbic system activity and shut down in the prefrontal cortex, especially on the left side. In depression, the most important pathways are those of the serotonergic and noradrenergic neurons projecting to the prefrontal cortex, from the raphe nucleus and locus coeruleus, respectively. Extracellular Dopamine in the prefrontal cortex, as well as in the other cortices, may depend on Noradrenaline rather than Dopamine innervation and activity. High dopamine is involved in forebrain functions of thinking, planning, and problem solving. It is antidepressant and produces optimism and confidence, so is probably a key factor in ones sexual attractiveness and scoring ability. Dopamine has a major role in procreation also for it keeps one positive, focused and intent on the job of sex...thus ensure the continuation of the race. During the heating and peak phases dopamine is obviously high along with the sex hormones and growth hormone. It probably factors into both increased psychic and increased creative genius at this time, not to mention the increase sexual desire.

Suffers from anxiety or depression exhibit increased activity in their hypothalamic-pituitary-adrenocortical (HPA) axis. In these disorders there is a proposed link between noradrenaline and glutamate NMDA receptors. The NE system has alpha and beta types of adrenergic receptors. There is evidence that chronically depressed people have dysfunctional and atypical noradrenergic systems, particularly their alpha 2- and beta-adrenoceptors. It has also been suggested that noradrenaline (norepinephrine) is crucial in certain cognitive functions associated with the frontal lobes, particularly the prevention of distractibility by irrelevant stimuli (ADD/schizophrenia). The alpha 2-receptors of the prefrontal cortex appear to be of particular importance in this respect. In those who are depressed the "safety memory" mechanism of the prefrontal lobes might not be working well chronically overworking the HPA axis/fear response and burning out the catecholamines, adrenals, cortisol and thyroid, thereby generating depression.

As you will read in the Toxic Mind section the pilot of the limbic system is the orbitofrontal system, especially in the right hemisphere. Without adequate prefrontolimbic control our emotional regulatory system can become destabilized which in turn interferes with rational thought and thinking, planning, and problem solving. Without a balanced emotional system and healthy socioemotional life we are likely to burn out our HPA axis become depressed, put on weight and head toward contracting some sort degenerative disease. (See the Neuroendocrine Theory of Aging)

NERVE TRANSMISSION

Potential energy is stored in separated electrical charges of opposite polarity. Separation of opposite charges requires energy and uniting of opposite charges liberates energy for "work." Voltage the measure of potential difference generated by separated charges, and current is the flow of electrical charge from one point to another.

Insulators like fatty cell membranes have high electrical resistance while conductors such as membrane channels have low resistance to current flow. A higher current is achieved by either increasing voltage or decreasing resistance. In the body, charges are carried on charged particles or ions. Thus separation of charges in the body means separation of ions. The amount of current that can be produced depends on the voltage difference across the membrane and the resistance to flow of ions.

The cell membrane is a good insulator and can separate and maintain ions or electrical charges of different values. The difference of ions inside and outside of cells is controlled by channels, gates, and transport proteins. Higher concentration of Na+ outside than inside and higher [K+] inside than outside, but overall there is more Na+ outside than K+ inside. This makes the inside of nerve cells is negatively charged and the outside is positively charged.

The insulating capacity of the cell membrane allows for the production of an electrical or chemical concentration difference or gradient from one side of the membrane to the other. Current in the body is the flow of ions toward their opposite charge. Cations (+ ions) flow toward a negative charge, and anions (- ions) flow toward a positive charge.

Ions will flow down either their concentration or electrical gradients. Both types of gradients provide potential energy to power the movement of ions (charged particles) and thus produce an electrical current. An electrochemical gradient combines the effects of an electrical difference with a concentration difference.

Ion Channels: There are two basic types of ion channels by which ions flow through cell membranes, leakage channels and gated channels.

1. Passive Leakage channels (nongated) do not require energy and flow rate and directions is determined by electrical or concentration gradient direction and size. Leakage channels are more open to K+2 than to Na+. Since the electrical and concentration electrochemical gradients go up during kundalini we can assume that Leakage channels become more permeable.

2. Active Gated channels require ATP energy and open and close in response to some sort of stimulus such as voltage changes; specific chemical stimulus eg: neurotransmitters, ions, or hormones; and mechanical pressure. We can also expect gated channels to be more active during kundalini for voltage, chemical and mechanical reasons.

Synaptic Transmission occurs first with an action potential arriving at presynaptic membrane. A depolarizing phase then opens Na+ and Ca+2 channels and Ca+2 flows into synaptic terminal. The increase of intracellular Ca+2 produces exocytosis of synaptic vesicles, releasing transmitter into synaptic cleft. Then Ca+2 is removed from the cell by mitochondrial uptake with a Ca+2 pump. The transmitter then diffuses across cleft to postsynaptic membrane and binds to membrane receptors.

Excitatory neurotransmitters are those that can depolarize or make less negative the postsynaptic neuron's membrane, bringing the membrane potential closer to threshold, (ie: a depolarizing postsynaptic potential.) Although a single excitatory postsynaptic potential normally does not initiate a nerve impulse, the postsynaptic neuron does become more excitable (sensitized). Thus it is already partially depolarized and more likely to reach threshold when the next excitatory postsynaptic potential occurs.

Inhibitory neurotransmitters hyperpolarize the membrane of the postsynaptic neuron, making the inside more negative and generation of a nerve impulse more difficult, (ie:inhibitory postsynaptic potential). A hyperpolarizing potential can decrease the excitability of a resting neuron or counteract the effects of an excitatory postsynaptic potential.

Synaptic Potentiation Sensitization occurs as repeated release of neurotransmitter makes the postsynaptic cell more sensitive to neurotransmitters producing larger excitatory postsynaptic potentials. Thus repeated use of a synapse makes it more efficient thus contributing to conditioning and learning. Synaptic potentiation may also be produced by back propagating action potentials from the cell body to the dendrites. Synaptic sensitivity is also increased by NMDA (N-methly-D-aspartate) receptors in the postsynaptic membrane that increase Ca+2 entry. Elsewhere I mentioned that Isao Ito found more of a specific type of NMDA receptor on the tip of neurons in the right hemisphere of mice and in the left hemisphere these where on the base of the neurons.

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