Alcohol and alcoholism associated neurological disorders: Current updates in a global perspective and recent recommendations

Figure 1 Schematic representation of the molecular mechanism of alcohol with gamma-aminobutyric acid and glutamate neuroreceptors. The electrical voltage across a membrane determines the responsiveness of a neuron. A cell with a higher positive charge is more responsive. When gamma-aminobutyric acid (GABA) binds to GABA receptors, ligand-gated Cl^- ions enter the neuron, making the inside more negative and less likely to respond to new stimuli. Furthermore, alcohol activates GABA receptors, which allows the channels to remain open for longer periods, exaggerating the inhibitory effect. On the other hand, glutamate opens to allow positively charged ions into the cell, causing it to become more positive and more likely to generate an electrical signal. DA: Dopamine; DOPA: Dihydroxyphenylalanine; MOAO: Multi-Object Adaptive Optics.

Figure 2 Schematic representation of dopaminergic reward pathway with alcohol. Alcohol inhibits the activity of monoamine oxidase, a protein that is responsible for the breakdown of dopamine. If dopamine is not degraded, it is transferred to the next neuron, confining its pleasurable effect. GABA: Gamma-aminobutyric acid.

Figure 3 Schematic representation and molecular mechanism of serotonin pathway in the presence of alcohol. During acute alcohol exposure, there is an increase in the 5-hydroxytryptamine (5-HT) extracellular level. Whereas during chronic alcohol exposure, there is a reduction in extracellular 5-HT level. This happens due to its reuptake from extracellular space through serotonin transporter. MOD: Moderate dysplasia; SER-1: Spherical equivalent refraction-1; 5-HT: 5-hydroxytryptamine.