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 levels 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,