Gama-氨基丁酸（GABA）是主要的快速抑制神经递质。GABA在GA

Gama-aminobutyric acid (GABA) is the main fast-inhibiting neurotransmitter. GABA opens Cl-channels (ligand gate ion channels) in GABAA receptors, causing hyperpolarization of cells. BDZs enhance the ability of GABA to open the Cl- channel, allowing more Cl- to enter. <br><br>GABAA receptor is a gated receptor of chloride ion channels, and has a GABA binding site on its β subunit. When GABA binds to it, the Cl- channel opens and Cl- flows in, leading to hyperpolarization of nerve cells and postsynaptic inhibition (binding to G protein). <br>There are benzodiazepine binding sites on the α subunit. The combination of benzodiazepine and α subunit will cause the conformational change of the receptor protein, promote the binding of GABA and GABAA receptors, increase the opening frequency of CI channels, and increase cl-internal flow. <br>Enhance GABA neurotransmission function and synaptic inhibition. <br>BDZ must rely on the release of GABA to function.

Gama-amino butyric acid (GABA) is the main fast-suppressing neurotransmitter. GABA opens the Cl-channel (licular gate ion channel) in the GABAA complex, causing cell hyperpolarization. BDZs enhance GABA's ability to open the Cl-channel, allowing more Cl-access.<br><br>GabAA is a gated subject of the chlorine ion channel, with gaba binding β on its sub-base. When GABA binds to it, the Cl-channel opens and Cl-inflows, causing neurocellular hyperpolarization and post-synapse inhibition (binding to the G protein).<br>α the binding site of benzodiazepines on the sub-base, the binding of benzodiazepines with α sub-base will lead to changes in the composition of the receptor protein, promote the binding of GABA and GABAA receptors, increase the open frequency of the CI channel, and increase the cl-internal flow.<br>Enhance GABA nerve transfer and synact inhibition.<br>BDZ must rely on GABA's release to function.

Gama aminobutyric acid (GABA) is the main fast inhibitory neurotransmitter. GABA opens Cl – channel (ligand gate ion channel) in GABAA receptor, resulting in cell hyperpolarization. BDZs enhances GABA's ability to open Cl – channels, allowing more Cl – to enter.<br>GABAA receptor is a gated receptor of chloride channel and has GABA binding site on its β subunit. When GABA binds to GABA, Cl - channels open and Cl - flows in, leading to hyperpolarization and postsynaptic inhibition (binding to G protein).<br>There are benzodiazepine binding sites on α subunit. The binding of benzodiazepine to α subunit will lead to conformational changes of receptor protein, promote the binding of GABA to GABAA receptor, increase the opening frequency of CI channel and increase the internal flow of Cl -.<br>GABA can enhance the neurotransmission function and synaptic inhibition of GABA.<br>BDZ has to rely on the release of GABA to function.<br>