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 norepinephrine 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+ deregulation 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 over
stimulation 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 over excitation of neurons can create an abnormal
buildup of glutamate that kills neurons by over stimulating 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.