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
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
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
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.
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
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
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
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
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
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 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
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.
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
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
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 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 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
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
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
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.
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
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.
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
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)
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
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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