Some of the conditions for the initiation of kundalini appear to be:
Hyperactivation of the thyroid and parathyroids.
Hyperactivation of estrogen and testosterone (plus metabolities of T. eg: Estradiol).
Hyperactivation of the sympathetic nervous system (adrenaline, norepinephrine).
Hyperactivation of the stress hormones (corticosteroids eg: cortisol,
DHEA) Hyperactivation of opiate systems (endorphins, enkephalins,
anandamide, phenylethylamine).
Repetitive or overwhelming circumstances and conditions create
cumulative resonance that increases in magnitude until the entire
organism is in sympathetic resonance. The barriers to unity are
penetrated so to speak. The increased charge and particular frequency
of neural firing opens up unique neural thresholds in crucial parts of
the brain. As the contagion of kundalini builds it pulls all bodymind
systems into its service.
Kundalini awakenings are likely if hyper-arousal of the nervous
system is kept going for several years and conditions of perpetual
irritation to the brain neurons occurs. The particular blend of
hormones and neurotransmitters reduces the threshold by which kundalini
passes through the body. Like a river of fire, kundalini forges its own
effluent cascade through the nerve tributaries and sustains itself
through the changes it induces. In recent years there has been some
attempt to correlate the phenomena of kindling with kundalini.
Kindling in epilepsy was first discovered accidentally by researcher
Graham Goddard in 1967, while he was studying learning in rats. He
found that a sustained, periodic, low-intensity stimulation of the
limbic region of mammalian brains eventually sets up a cumulative
resonance which increases in magnitude until the entire organism is in
sympathetic resonance. Eventually these bursts of electrical activity
induce similar patterns in nearby brain regions, and the seizure
threshold progressively lowered. While normally the electrical
stimulation he used was too low to cause any type of convulsing, he
discovered that repeated exposure of brain areas to small electric
shocks seem to make subsequent episodes of spontaneous seizure-like
electrical events more likely to occur. After repeated stimulation at
the same intensity, their brains had become sensitized to electricity,
and even months later the rat would convulse when stimulated.
The name kindling was chosen because the process was likened
to a log fire. While the log itself is very hard to set afire in the
first place, when surrounded by smaller, pieces of wood, kindling, soon
the log itself will catch fire. There is evidence that the more mood
episodes a person has, the harder it is to treat each subsequent
episode..." thus taking the kindling analogy one step further: that a
fire which has spread is harder to put out.
The kindling sensitization hypothesis suggests that initial seizure
episodes make it more likely that future seizure and depressive
episodes will occur. Spontaneous kindling is more likely if there has
been early damage to the brain through chemical exposure, childhood
sexual or emotional abuse, or if one has inherited a sensitive nervous
system. If reared in an abnormal, deprived, stressful and socially
isolated environment, the limbic system neurons will atrophy and the
septal nuclei, amygdala and hippocampus may develop seizure-like
activity, referred to as kindling. Trauma affects our capacity for
cortical control over the limbic system to regulate bodily
homeostatsis. This includes unusual patterns of cortisol,
norepinepherine, and dopamine metabolite excretion; the role of
serotonergic and opioid systems (arousal and numbing); receptor
modification by processes such as kindling; and involvement of central
pathways involved in the integration of perception, memory and arousal.
Kindling can start only in the limbic brain where it progresses from
the amygdala, then to the amygdala on the other side of the brain, to
the hippocampus, to the occipital cortex, and finally to the frontal
cortex. In fetal brain development the limbic or emotional brain
predates the development of the cortex or "seat of intelligence". The
brain's limbic system modulates emotions and memory organization
systems, balance, gastrointestinal motility, the autonomic nervous
system, and the auditory and visual integration of stimuli.
While kindling was originally thought to be a model of epilepsy,
John Gaito of York University has reported that a different mechanism
is apparently involved since the amino acid, taurine, which
suppresses epileptic seizures in laboratory animals, does not prevent
phenomena caused by kindling. Also, kindling apparently causes permanent changes in the neural circuitry.
Kundalini has elements similar to the kindling phenomena, and yet
runs through a very complicated sequence of "events." The article: "Kindling, once epilepsy model, may relate to kundalini,"
Brain/ Mind Bulletin, Vol. 2, No.7, February 21, 1977; pp. 1-2.)
reports on the convulsion-like phenomenon called kundalini. At the Max
Planck Institute in Germany, subjects reported "electrical sensations,
tingling, inner lights, even convulsions usually followed over a period
of time by a moderation of 'symptoms' and apparent alterations in the
central nervous system." This article says that the kundalini phenomena
typically occurs after a period of meditation in a setting that is
non-threatening. This report suggests that while meditating, the
individual tries to arrest all thought or cortical activity, thus
allowing the evolutionary more primitive areas of the brain to assert
itself. The Kindling Model is one of the current interpretations of
PTSD. The scientists concluded that those who experienced the kundalini
phenomenon were actually reexperiencing primal pain laid down before the brain has completely developed (See Toxic Mind Theory).
Periods of cycling may begin with an environmental stressor,
but if the cycles continue or occur unchecked, the brain becomes
kindled or sensitized. With repetitive use pathways inside the central
nervous system are reinforced so to speak--and future more frequent
episodes of depression, hypomania, or mania will occur by themselves
independent of an outside stimulus. Thus, to put it simply, brain cells
that have once been involved in an seizure episode are more likely to
do so again, and more cells will become sensitized over time. Goddard
demonstrated that it was possible to induce kindling chemically as well
through repeated small exposures to inhaled toxins; or single
overwhelming exposures of chemical, visual, auditory, electrical
stimulation. It has been shown that substances such as cocaine and
alcohol have their own kindling effects which can contribute to bipolar
kindling.
As a result of many studies involving the kindling model, many
researchers now believe that kindling contributes to both rapid mood
cycling and treatment-resistant bipolar disorder. This kindling model
also is consistent with cases where cycling began with definite mood
triggers, stressful or exciting events, and later became spontaneous.
Researchers concluded that there was a need for early and aggressive
treatment of bipolar disorder, to prevent the brain from becoming more
and more sensitized and going into rapid cycling or manic depression.
A seizure is a sudden involuntary alteration in perception or
behavior caused by an abnormal synchronized discharge of cortical
neurons in the central nervous system. Epilepsy, on the other
hand, refers to chronic recurrent seizures from a primary underlying
brain abnormality. Seizures can be attributed to a number of causes
including metabolic abnormalities, infections, nutritional
deficiencies, or trauma. Emotional stress and sleep deprivation also
increase the frequency of seizures, but most seizures occur due to
unknown reasons. Seizures can be broadly classified into two major
categories: partial, involving onset from a discrete area of the brain
that may or may not secondarily generalize to the rest of the brain,
and primary generalized, involving simultaneous onset from both
hemispheres.
What is really interesting is that pulsed repetitions of telepathic
senders have also been shown to increase the reception of telepathic
messages. Thus the kindling effect apparently applies to the paranormal
channel as well as to more orthodox transmission channels.
DISINHIBITION OF INHIBITION
The two primary regions of the brain that are involved in epilepsy
are the cerebral neocortex and the hippocampus. In the neocortex,
excitatory synapses are made primarily on the dendritic spines and
shaft. The release of neurotransmitters at these sites gives rise to
excitatory postsynaptic potentials. The inhibitory synapses are more
prominent on the soma or proximal dendrites, and give rise to
inhibitory postsynaptic potentials. Abnormal neuronal excitation is
thought to occur as a result of disruption of the depolarization and
repolarization mechanisms of the cell. Aberrant neuronal networks
develop abnormal synchronization resulting in the propagation of an
epileptic seizure.
The primary excitatory neurotransmitters in the central nervous
system are the amino acids glutamate and aspartate. The primary
inhibitory neurotransmitters in the central nervous system are
gamma-aminobutyric acid (GABA) and glycine. Excitatory
neurotransmitters usually act by opening Na+ or Ca2+ channels, whereas
inhibitory neurotransmitters usually open K+ or Cl- channels. Glial are
mainly responsible for K+ reuptake.
It seems that one of the mechanisms of kundalini may be the
overstimulation of the neuro-inhibitory glycine and GABA receptors in
the spine and brainstem, during the hyper-activation of the sympathetic
nervous system. This dis-inhibition means the hyper-charge is allowed
to continue like wild-fire because the "off switch" has essentially
been rendered ineffective. Simply upping one's glycine intake doesn't
return neuron inhibition back to normal. Kundalini abates when the
glycine receptors themselves become operational again, once the
hyper-charge of kundalini up the spine reduces, perhaps when the fire
runs out of fuel. Thus kundalini awakening ends when the "charge"
reduces and the "glycine receptors" are once more fully receptive and
able to do their neuro-inhibiting job.
Compounding this, it might be that when the free radical load goes
up with the onset of kundalini, glycine is pulled from all readily
available sources in order to make the antioxidant Glutathione
(ie: glycine + glutamic acid + cysteine). The cerebrospinal fluid (CSF)
would be one of those sources since it contains 100mg of glycine for
100ml of fluid. This reduction in CSF-glycine would further reduce the
inhibition of nerve firing up the spine. The wild fire would thus burn
until it burns itself out.
Glycine is an inhibitory neurotransmitter in the central nervous
system especially in the spinal cord. The cerebrospinal fluid contains
100 mg of glycine per 100 ml. When glycine receptors are activated,
chloride ions enter the neuron and the cell membrane undergoes
hyperpolarization, which inhibits the neuron. In seizures the brain
naturally accumulates more glycine at the seizure site in order to
protect itself by inhibiting neuron firing.
It may be that during the inner-conjunction the kundalini ignition
up the spine is so intense that the inhibitory neurotransmitter glycine
may have failed to stop the cascade of electro-chemical reactions that
constitutes the awakening. The force of the kundalini cascade may
overwhelm the normal nerve inhibition of glycine by rendering the
glycine receptors useless or "disinhibited." The poison strychnine
causes convulsions for this reason. B-alanine and taurine also activate
glycine receptors but with lower inhibitory capacity.
In the brain, glutamine is precursor to glutamate is a "on-switch"
neurotransmitter, it is also the precursor to GABA which is an
"off-switch" neurotransmitter. Lower GABA correspond to increased
seizures and epilepsy. Anti-seizure medications work by increasing
levels of the inhibitory neurotransmitter GABA in the temporal lobes,
calming neuronal activity and inhibit nerve cells from overfiring or
firing erratically. Glutamic acid decarboxylase (GAD) is the rate
limiting enzyme responsible for conversion of glutamate to
gamma-aminobutyric acid (GABA) regulating levels of glutamate and GABA
in the mammalian brain. GABA can be taken as a supplement
(L-Glutamine), produces a calming effect on people who struggle with
temporal lobe symptoms like temper, irritability, and anxiety.
Many people with temporal lobe problems also suffer from memory
problems, which can be helped with Phosphatidyl Serine (PS), Gingko
Biloba and Vitamin E. Brain GABA levels depend on both zinc and vitamin
B6. Consequently, zinc deficiency may increase the risk of seizures by
reducing brain GABA.
Glutamate concentrations in the brain are higher in some seizure
patients, and these concentrations can increase to potentially
neurotoxic concentrations during seizures causing cell death. One study
showed that with a higher dose of B6 (10 mg/kg), the CSF glutamic acid
was normalized. It was concluded that the optimal dose of B6 for
epileptics should be the dose that normalizes CSF glutamate levels, not
just the control of seizures.
Glutamate is the principal excitatory neurotransmitter in the brain
thus it inevitably plays a role in the initiation and spread of seizure
activity. The process of "kindling" limbic seizures in rodents by
repeated electrical stimulation is dependent on activation of
N-methyl-D- aspartate (NMDA) receptors. The function of these receptors
is enhanced in the hippocampus of kindled rats and in the cerebral
cortex of patients with focal epilepsy.
It is probable that the adrenocorticotrophin releasing
hormone system in the central nervous system is mainly distributed in
the limbic system, and glutamate might be one of the trigger factors to
induce excessive stress response in the hypothalamus-pituitary-adrenal
axis. Acute mania is accompanied by elevated glutamate/glutamine levels
within the left dorsolateral prefrontal cortex. Glutamate and aspartate
NMDA receptor antagonists are one potential mechanism for
anticonvulsants.
Psychosis could result from AMPA receptor activation caused by
overactivity of the glutamatergic system, due to reduced GABAergic
inhibitory control. Expression of messenger RNA for the GABA
synthesizing enzyme in the prefrontal cortex and the number of
GABAergic neurons in the hippocampus are reduced in schizophrenia and
bipolar disorder. GABAa receptor drugs, which activate Cl-, appear more
effective as anticonvulsants than GABAb receptor agents, which activate
K+. Apparent the GABAa receptor is involved in epilepsy due to its role
in the synchronization or desynchronization of thalamus-cortical
pathways. The oscillatory and burst-firing of these circuits is
attributed to neurons in the thalamus and leads to synchronization and
desynchronization of the EEG.
Dr. Stephen Lasley found that brains of rats that are genetically prone to seizures also have reduced levels of taurine as well as increased levels of aspartate.
Therefore, I believe that avoidance of aspartame should be a key
element in an anti-seizure diet. Also, taurine, in doses of 1-3 grams
per day may be helpful.
ENERGY GENERATION
If kundalini starts and you really don't want it then cut all carbs
from your diet for 2 weeks, and this should suspend the cascade of
change. If stopping the consumption of carbohydrates stops or lessens
the progression of kundalini metabolism, this then points to the
mechanism of kundalini itself. It is therefore apparent that kundalini
is fueled it seems by the burning of glucose "glycolosis" and
less so or not at all by ketosis or the burning of fat. Glucose is
taken up by glial cells and metabolized by glycolysis to lactate and
pyruvate, which are then released as substrates for oxidative phosphorylation in
the neurons. Within the brain, glycogen is primarily stored in glial
cless, Glycogen stores in the brain are low compared to liver and
muscle however the glycogen turnover is very rapid.
Glycolysis is the conversion of glucose to pyruvate and
lactate resulting in the net production of only 2 mol of ATP. Pyruvate
can enter the Krebs cycle and produce 30 mol of ATP via the
mitochondrial oxidative phosphorylation cascade. Hence the
energetic value of oxidative phosphorylation over glycolysis is
obvious. In the early stages of activation the increased energy demand
is met by glycolysis rather than oxidative phosphorylation. It was
found with PET scans that glucose utilization in activated cortical
areas was not matched by an equivalent increase in oxygen consumption,
because Glycolysis does not require oxygen to function.
Glucose is the energy fuel for the brain and is almost entirely
oxidized to CO2 and H2O. A quarter of the total body's glucose is
utilized by the brain although the brain only represents 2% of the body
weight. Glucose can be incorporated into lipids, proteins and glycogen,
and it is also the precursor to certain neurotransmitters such as GABA,
glutamate and acetylcholine. GABA and glutamate serve to regulate the
excitability of virtually all neurons in the brain. GABA and glycine
are the most important inhibitory neurotransmitters in the brainstem
and spinal cord. The neurotransmitter glutamate is derived from
glucose, and I think that glutamate is probably the primary
neurotransmitter involved in the changes in the conveyance of energy
through the nerves.
I propose that Nitric Oxide is produced in excess during certain
hyper-kundalini events causing a hypersensitivity to glutamate NMDA
receptors and this produces the most radical peak experiences and
pivotal height of the awakening cycle itself. Energy metabolism may be
controlled by specific neurotransmitters such as norepinephrine (NE).
Cell bodies of NE-containing neurons are localized in the brainstem
from which axons project to various regions of the brain including the
cerebral cortex. Hence the noradrenergic system could regulate energy
homeostasis globally in the
brain.
Polarity is vitally important for living cells, hence they
continually work to generate and maintain regions of differing
electrical properties against continual leakage of charge. In fact, the
ceaseless work involved in achieving and maintaining these electrical
needs consumes some 50Ð60% of the metabolic activity of the cell.
"When our cells are functioning normally, a proton (H+, a
hydrogen atom with its positive charge) gradient exists across the
oxygen-using parts of our cells, which keep out calcium and sodium
ions. But when these oxygen-using parts, the mitochondria, are unable
to make ATP, they cannot keep up the gradient. Sodium and calcium ions
rush into the cell in a fatal process of cell damage called necrosis.
(269) If damage caused by these [oxidative] reactants is not reversed
to normal, there will be decreases in the capacity to generate ATP,
lower global biochemical activity, and reduced use of free energy. The
oxidative poisoning can lead to cell damage or trigger the mechanism of
cell self-destruction call apoptosis. (271) Levels of the intracellular
antioxidant glutathione fall when ATP is not around. Lowered ATP thus
reduces the cell's ability to make more of the ATP it needs more than
ever." 270, Eric Schneider & Dorion Sagan, Into the Cool: Energy Flow, Thermodynamics and Life. University of Chicago, 2005
THE COMBUSTION OF FAT
Ketogenesis is the process by which ketone bodies are
produced as a result of fatty acid breakdown. Ketogenesis may or may
not occur, dependent on how many carbohydrates are available. Ketone
body formation occurs as an alternative energy source during times of
prolonged stress e.g. starvation. The initiating event is a change in
the ratio of glucagon:insulin in the blood. Insulin deficiency triggers
the lipolytic process in adipose tissue with the result that free fatty
acids pass into the plasma for uptake by liver and other tissues.
Glucagon appears to be the primary hormone involved in the induction of
fatty acid oxidation and ketogenesis in the liver. It insures that
long-chain fatty acids can be transported through the inner
mitochondrial membrane to the enzymes of fatty acid oxidation and
ketogenesis.
Ketone bodies are produced mainly in the mitochondria of liver cells
when carbohydrates are so scarce that energy must be obtained from
breaking down fatty acids. Fatty acids are long chains of carbons with
an acid group on one end. The body gets energy from fatty acids by
breaking the carbon chain down into pieces that contain only two carbon
atoms. These pieces are in the form of acetyl-CoA. When the body has no carbohydrates
available, fat instead must be broken down into acetyl-CoA in order to
get energy. CoA is not being recycled through the citric acid cycle: it
is being attached to more and more acetyl groups. You need more CoA to
keep breaking down fats, and the only place to get it is from all those
acetyl-CoA molecules, by attaching them to each other to get the CoA to
fall off. A large amount of energy is released during this process,
which can be used for muscle contraction and all of the other
activities in the cell.
L-carnitine acts to increase energy by carrying fat across the cell
membrane and into the mitochondria. Energy is then stored as ATP. It
reduces the metabolites of fats (ketones) in the blood from incomplete
fat metabolism and reduces hyperammonemia.
GLYCOSIS AND KETOGENESIS AND SEIZURES
The Ketogenic or high-fat
diet was found to reduce epileptic seizures by a 50 to 70%. Dr. John M.
Freeman, in The Epilepsy Diet Treatment recommends a stringent diet
consisting of high fat, low protein, low carbohydrate foods. Generally
the ketogenic diet consists of 4 parts fat to 1 part
protein/carbohydrate. Notice that protein also is low, the theory being
that the body can turn protein into sugars also. This extreme measure
might be necessary for epileptics to reduce seizure, but it is simply
no way to be generally healthy. Complications can include nutrient
deficiency, kidney stones, abnormal liver function, high cholesterol,
weight gain, dehydration and bone thinning. Not to mention all the
extra free radicals generated from such a high fat diet.
Such extreme measures are perhaps not necessary for a kundalini
awakening, however there is much to learn from the ketogenic diet about
how we might modify our diet to best serve our awakening. Of paramount
importance however is to prevent the spiking of blood sugar to concerve
the integrity of protein structures and prevent glycation, so you can
convey a deeper more focused consciousness. This is achieved by
ensuring that our carbohydrate quotient consists of low glycemic,
non-starchy, high fiber to prevent blood sugar spiking. I also find
that raw carbohydrates are much easier on the body and on de-fogging
and lucidity than all forms of cooked carbohydrate. Reduce the blood
sugar and kundalini doesn't spark up to an all-consuming flame.
During a kundalini awakening the body is in a mode of hyper-energy
generation. The cells are producing more energy (via hyperactivated
mitochondria)…what energy is not converted to ATP is given off as heat.
This extra cellular energy in the nerves causes certain glutamate
receptors (NMDA) to be hyperactive increasing the action potential and
release of neurotransmitters in the synapses. Thus the sympathetic
nervous system is in hyperdrive, and the off switch receptors
(parasympathetic, glycine, GABA) are over stimulated hence cannot
perform their normal inhibitory functions.
The heat of kundalini itself further exacerbates the excitation of the
nerves by facilitating ion movement and increasing neurotransmitter
release. Researchers from St Louis School of Medicine have
discovered that ‘cooling’ the neurons responsible for focal epileptic
seizures can stop the seizure from ever happening without doing any
harm to the brain cells. Cold seemed to prevent the nerve cells firing
probably through interfering with the movement of ions in the cells and
preventing the release of neurotransmitters.
As the kundi-fired body is in a HPA axis activated state, the liver
generates and releases more glycogen to fuel this fire. Cell apoptosis
(cell death) occurs through excess free radicals and high glutamate and
Ca2+ levels and body tissues are catabolically dismantled and turned
into glycogen. The hyperactivity of the limbic brain turns on the
pleasure centers generating copious endogenous opiates and
cannaboids…and these increase compulsivity so that the individual is
attracted to eating carbohydrates (sugar) to fuel the increased energy
demand. The body is asking for more energy, and this can be achieved by
drinking water (ie: hydroelectric energy). Giving in to sugar cravings
while in kundalini will cause blood sugar spiking that can severely
damage tissues and turn the body toward insulin resistence and
down-regulate other receptors as well.
Besides the reduction of excess glutamate and Ca2+ release, perhaps
another reason why the ketogenic diet works could be the actual
physical blocking of insulin receptors with cholesterol due to the high
fat content of the diet. This blocking would reduce sugar/glucose
uptake by the cells and prevent the energy surge that initiates
kindling of seizures. Since the ketogenic diet is so low on
carbohydrates the usual blood sugar spiking that initates excessive
levels of inslin and leptin and associated down-regulation of receptors
is avoided.
By eliminating the majority of cooked/high-gylcemic/starchy carbohydrates from one’s diet the fog of bliss can be lifted. Avoid
sugars, honey, artificial sweeteners, grains, fruit and anything
starchy or sweet except perhaps sativa. Green vegetables, tomatoes and
avocados can be eaten but avoid “starchy” plants like rice, potatoes,
corn, and “sweet” ones like carrots and beets. You will find that after
less than three days of eliminating sweet and starchy foods the
bliss-fog significantly clears. I experienced less magnetic activity
around my head, probably due to reduced “kindling” or firing of the
nerves in the brain. Body pain did not increase, although there was a
little tiredness from the rapid cutoff of carbohydrates.
By reducing carbohydrates in our diet kundalini still remains but
greatly subdued. Even during peak estrogen day of the month, if not
given its glycogen fuel kundalini did not rise significantly. That is,
even if all the other triggers are available (thyroxin, sex hormones,
DHEA, adrenaline etc…) if there is not a surplus of glucose available
in the blood, then kundalini does not increase its fire. Knowing
this is a radical boon for people going through kundalini awakenings,
and for seizure, epilepsy, psychosis and probably bipolar depression
etc.. You might find that during and after a kundalini awakening you
may want or need to adopt a low carb diet indefinitely.
One of the contributing factors to my spontaneous kundalini awakening
of 1989 was that I had eaten 3 pieces of very rich Xmas cake packed
with coconut sugar and dried fruit. After eating this I could feel the
blood curse through my veins like speed. This combined with being in a
car, playing bongo drums and singing, a biblical New Zealand Christmas
evening under the stars, catalyzed my first 10,000 org spontaneous rush
up the spine...after which I felt like Jesus Christ.
One possibility why the ketogenic diet controls epilepsy is that
the diet alters brain handling of glutamate, the major excitatory
neurotransmitter and a probable factor in evoking and perpetuating a
convulsion. Researchers found that brain metabolism of ketone bodies
can furnish as much as 30% of glutamate and glutamine carbon. Ketone
body metabolism also provides acetyl-CoA to the citrate synthetase
reaction, in the process consuming oxaloacetate and thereby diminishing
the transamination of glutamate to aspartate. Relatively more glutamate
then is available to the glutamate decarboxylase reaction, which
increases brain GABA. Ketosis also increases brain GABA by increasing
brain metabolism of acetate, which glia convert to glutamine.
GABA-ergic neurons readily take up the acetate and use it as a
precursor to GABA.
Ketosis also may be associated with altered amino acid transport at the
blood-brain barrier. Specifically, ketosis may favor the release of
glutamine from the brain, through transporters at the blood-brain
barrier exchanging it for blood leucine. Since brain glutamine is
formed in astrocytes (glial) from glutamate, the overall effect will be
to favor the release of glutamate from the nervous system.
Astrocytes are glial cells which make up 80% of the mass of the brain
and communicate with neurons via changes in Ca2+. Intracellular Ca2+
mediates changes in membrane proteins to initiate transmitter release
and ion channel opening; it also activates enzymes to allow neurons to
cover or uncover receptor sites that alter neuronal sensitivity.
Several studies indicate that following the rise of calcium, astrocytes
release the amino acid glutamate, which helps them talk to the neurons.
The communication flows both ways, with neurons also being able to talk
to the astrocytes through their own glutamate release. Signaling
molecules, such as ATP and prostaglandins, also appear to promote the
cell-to-cell communication.
Communication between astrocytes and neurons may aid memory. Adding
glutamate to cell samples of astrocytes prompts them to produce special
molecules that nourish neurons, known as neurotrophins, that are key to
memory function. In one recent study, injections of trophic factors
into the brains of rats boosted the biological mechanisms known to
relate to memory and improved the rats' performance in a memory task.
This all may mean that glutamate release from neurons triggers
astrocytes to produce neurotrophic factors, which then help neurons
process information for memory.
High blood sugar (hyperglycemia) is implicated in increasing the
likelihood of seizure. Ordinarily, insulin prods the liver to decrease
its production of glucose. It also helps the body's fat and muscle
tissues use glucose in the blood for energy. Insulin has many roles
including stimulating and balancing immune function, stimulating
revascularization, stimulating neuron and oligodendrocyte growth,
reducing cell death, stimulating myelination and re-myelination of
neurons, stimulating differentiation and proliferation of neural stem
cells, increasing permeability and transport of nutrients and wastes
across cell membranes and the blood-brain barrier. (Oligodendrocyctes
are the structures responsible for myelination. The presence of NMDA
receptors in oligodendrocyte processes presents a mechanism by which
demyelination might occur under excessive glutamate/Ca2+ conditions.)
LACK OF GLUTAMATE CLEARING
Patients suffering from temporal lobe epilepsy (TLE), experienced
increased extracellular glutamate levels in the hippocampus both during
and after clinical seizures. These increased glutamate levels could be
the result of malfunctioning and/or downregulation of glutamate
transporters, indicating impaired clearance of glutamate released by
neurons. Glutamate is predominantly cleared by glial cells through the
excitatory amino acid transporter 2 (EAAT2) and its subsequent
conversion to glutamine by the glial enzyme glutamine synthetase.
Cerebrospinal Fluid, limbic, temporal and striatum glutamine
concentrations are implicated in schizophrenia, bipolar disorder and
major depression. The answer, it appears, is by cleaning up their
synapses. For LTP to occur, a presynaptic neuron must release
the glutamate in a continuous manner. Normally, glutamate is removed
from the synaptic cleft by housekeeping proteins, known as glutamate
transporters, in the postsynaptic neuron. Suspecting that this
glutamate-removal system might play a role in maintaining input
specificity,
An increase in the extracellular concentration of glutamate and
aspartate before or during seizure onset, suggesting that either
enhanced amino acid release or impaired uptake contributes to seizure
initiation. Glutamate antagonists are potent anticonvulsants and
provide significant protection against brain damage following stroke or
traumatic injury, but can have cognitive side effects. Anticonvulsant
compounds which act on sodium channels and reduce ischemia-induced
glutamate release, are cerebroprotective but are free from the
cognitive side effects of NMDA-receptor antagonists.
In developing a supplemental protocol for kundalini we would do well to consider Ward Deans article Seizures: A Nutritional Approach at www.vrp.com/
©2006
Biology of Kundalini by Jana Dixon