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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

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