Benzodiazepines enhances the effects of the main inhibitory (calming) neurotransmitter in the central nervous: Gamma-Aminobutryic Acid (GABA):
GABA’s main function is to slow down activity in the brain, to prevent feelings of anxiety. GABA counteracts with the excitatory neurotransmitter: glutamate. Excessive inhibitory influences leads to sedation and incoordination while excessive excitatory influences leads to seizures and anxiety, therefore the brain balances both inhibitory and excitatory influences.
When GABA is activated it allows an influx of chloride ions (Cl−) to enter the brain cells, this influx of Cl− causes membrane hyperpolarization and inhibition of neuronal transmission (E/B). Cl− increases benzodiazepine receptor affinity, and it is necessary for the joint regulation of GABA and benzodiazepine binding. BZNs bind to the GABAa subunits: a and y. BZNs work by interacting with the specific GABAa subtype in opening chloride channels and increasing the frequency of Cl− to ender the neuron. This is in turn causes, sedation and reduces anxiety, thus the nerve becomes less excitable. (C) https://www.pointofreturn.com/benzodiazepines.html As GABA is initially enhanced by Benzodiazepines, excitatory neurotransmitters: Norepinephrine, Serotonin, Acetyl Choline and Dopamine are reduced. These neurotransmitters are necessary for alertness, muscle tone, coordination, memory, emotional responses, endocrine gland hormones, heart rate, blood pressure control and other functions. As a result, all these may be impaired by benzodiazepines.
Three groups of drugs which bind at the BDZ-binding site can be distinguished based on the type of modulation: positive allosteric modulators (agonists), negative allosteric modulators (inverse agonists) and antagonists. (D) %%
Positive agonists e.g. diazepam, potentiate the function of GABAa, this potentiating action is thought to be induced by a change in conformation that