Benzodiazepines work by increasing the efficiency of a natural brain chemical, GABA, to decrease the excitability of neurons. This reduces the communication between neurons and, therefore, has a calming effect on many of the functions of the brain.
GABA controls the excitability of neurons by binding to the GABAA receptor.
Now, through years of use of benzodiazepines, you can restore the GABA back to the same level, if not even more than you normally had, by taking a couple of simple, OTC amino acids:
L-Glutamine
Vitamin B MEGA Complex
L-Glutamine converts to L-Glutamate which, when combined with PLP (Vitamin B6 complex), converts over to GABA.
(PLP plays a role in the conversion of dopa into dopamine, allows the conversion of the excitatory neurotransmitter glutamate to the inhibitory neurotransmitter GABA.)
Be careful though, as some people who are sensitive or taking other medications, should consult their doctors, due to risk of neurotoxicity. This is incorrect.
1. Long-term benzodiazapine use causes downregulation of GABA-a receptors, not depletion of intersynaptic GABA.
Dick head, what do you think is released when neurons are too excited? GABA. Benzodiazepines work by increasing the efficiency of GABA to calm down these excited neurons. Astrocytes express plasma membrane transporters such as glutamate transporters for several neurotransmitters, including glutamate, ATP, and GABA. More recently, astrocytes were shown to release glutamate or ATP in a vesicular, Ca2+-dependent manner.
Glutamate decarboxylase or glutamic acid decarboxylase (GAD) is an enzyme that catalyzes the decarboxylation of glutamate to GABA and CO2. GAD uses PLP as a cofactor.
In mammals, GAD exists in two isoforms encoded by two different genes - GAD1 and GAD2. These isoforms are GAD67 and GAD65 with molecular weights of 67 and 65 kDa, respectively.GAD1 and GAD2 are expressed in the brain where GABA is used as a neurotransmitter, GAD2 is also expressed in the pancreas.
Glutamate also serves as the precursor for the synthesis of the inhibitory GABA in GABA-ergic neurons. This reaction is catalyzed by glutamate decarboxylase (GAD), which is most abundant in the cerebellum and pancreas. Inhibitory GABA is released when benzodiazepines are taken. Once bound to the benzodiazepine receptor, the benzodiazepine ligand locks the benzodiazepine receptor into a conformation in which it has a greater affinity for the GABA neurotransmitter. This increases the frequency of the opening of the associated chloride ion channel and hyperpolarizes the membrane of the associated neuron. The inhibitory effect of the available GABA is potentiated, leading to sedatory and anxiolytic effects.
Acamprosate (calcium homotaurinate) is believed to block glutaminergicN-methyl-Daspartate receptors and activate 3-aminobutyric acid (GABA) type A receptors.
Oh yeah and also, Pregabalin increases neuronal GABA levels by producing a dose-dependent increase in glutamic acid decarboxylase activity.
2. Neither GABA nor glutamate pass the BBB, so the proposed methods wont increase the quantity of GABA synthesized.
Who the fuck said anything about GABA? GABA is a bunch of bullshit, like downregulation and upregulation, there's no scientific evidence to support these claims, so don't mention GABA again on my thread please.
L-glutamine does indeed bass the blood brain barrier. Because it converts itself to glutamic acid (glutamate) and with the aid of PLP, converts into GABA.
Myself Consequently, the
major (and direct) trigger for local glucose utilization would
remain glutamate. Consistent with this view is the fact that most
GABAergic neurons are locally acting interneurons activated by
glutamatergic inputs (34). Thus glutamate, by activating GABA
neurons, could lead to an overall inhibitory activity in a given
cortical area; yet glutamate release and uptake by astrocytes
would stimulate glycolysis in astrocytes and constitute a sufficient
signal coding for increased activity of GABAergic neurons
as well. It would therefore appear that the most relevant, and
possibly sufficient signal, linking neuronal activity (both excitatory
and inhibitory) with metabolism is glutamate, which would
mediate the appropriate metabolic coupling both for excitatory
and inhibitory neurons.
Sources:
Glutamine -
http://www.socialanxietysupport.com/...lements-30805/
