Lets talk GABA...
Posted 23 August 2004 - 06:18 PM
Posted 23 August 2004 - 06:24 PM
Posted 23 August 2004 - 07:18 PM
All benzodiazepines act by enhancing the actions of a natural brain chemical, GABA (gamma-aminobutyric acid). GABA is a neurotransmitter, an agent which transmits messages from one brain cell (neuron) to another. The message that GABA transmits is an inhibitory one: it tells the neurons that it contacts to slow down or stop firing. Since about 40% of the millions of neurons all over the brain respond to GABA, this means that GABA has a general quietening influence on the brain: it is in some ways the body's natural hypnotic and tranquilliser. This natural action of GABA is augmented by benzodiazepines which thus exert an extra (often excessive) inhibitory influence on neurons (Fig. 1).
The way in which GABA sends its inhibitory message is by a clever electronic device. Its reaction with special sites (GABA-receptors) on the outside of the receiving neuron opens a channel, allowing negatively charged particles (chloride ions) to pass to the inside of the neuron. These negative ions "supercharge" the neuron making it less responsive to other neurotransmitters which would normally excite it. Benzodiazepines also react at their own special sites (benzodiazepine receptors), situated actually on the GABA-receptor. Combination of a benzodiazepine at this site acts as a booster to the actions of GABA, allowing more chloride ions to enter the neuron, making it even more resistant to excitation. Various subtypes of benzodiazepine receptors have slightly different actions. One subtype (alpha 1) is responsible for sedative effects, another (alpha 2) for anti-anxiety effects, and both alpha 1 and alpha 2, as well as alpha 5, for anticonvulsant effects. All benzodiazepines combine, to a greater or lesser extent, with all these subtypes and all enhance GABA activity in the brain.
As a consequence of the enhancement of GABA's inhibitory activity caused by benzodiazepines, the brain's output of excitatory neurotransmitters, including norepinephrine (noradrenaline), serotonin, acetyl choline and dopamine, is reduced. Such excitatory neurotransmitters are necessary for normal alertness, memory, muscle tone and co-ordination, emotional responses, endocrine gland secretions, heart rate and blood pressure control and a host of other functions, all of which may be impaired by benzodiazepines. Other benzodiazepine receptors, not linked to GABA, are present in the kidney, colon, blood cells and adrenal cortex and these may also be affected by some benzodiazepines. These direct and indirect actions are responsible for the well-known adverse effects of dosage with benzodiazepines.
Posted 23 August 2004 - 07:31 PM
Posted 23 August 2004 - 08:44 PM
Posted 23 August 2004 - 08:53 PM
What do fellow benzo-bashers say about other drugs for epilepsy like Neurontin, Lamictal, Trileptal, etc?
"Bring on the Anti-Benzo Zealots!"
Posted 23 August 2004 - 09:11 PM
Posted 23 August 2004 - 09:18 PM
Posted 23 August 2004 - 09:22 PM
to oversimplify it greatly my serotonin levels are simultaneously being slowed (by klono) and increased (by celexa) ?
Posted 23 August 2004 - 09:32 PM
Posted 23 August 2004 - 09:48 PM
You got it! Most of the "experts" believe in the klono-ssri combo...I dont. I think they work against each other. As Ive said before, its like trying to make progress shoveling water up hill.
0 user(s) are reading this topic
0 members, 0 guests, 0 anonymous users