Final answer:
Alcohol particularly impacts the neurotransmitter glutamate, the CNS's main excitatory transmitter, by modulating NMDA receptor activity which affects cognitive functions. Acute alcohol use increases GABA's inhibitory effects and reduces glutamate's excitatory effects, leading to slowed cognition and motor skills. Chronic misuse can decrease GABA function and increase glutamate activity, risking excitotoxicity and neuronal damage.
Step-by-step explanation:
Despite affecting many neurotransmitters, alcohol has a particularly powerful effect on the neurotransmitter glutamate. Glutamate is the main excitatory neurotransmitter in the central nervous system (CNS), facilitating signals across the synaptic gap to increase neuron firing. It plays a key role in learning, memory, and brain development. Alcohol impacts glutamate's receptor activity, specifically interfering with NMDA (N-methyl-D-aspartate) receptors, which are critical for cognitive functions and synaptic plasticity.
Acute alcohol exposure increases the inhibitory effect of another neurotransmitter, GABA (gamma-aminobutyric acid), while simultaneously decreasing the function of excitatory neurotransmitters like glutamate. This effect is what translates behaviorally to the depressant effects of alcohol consumption, such as reduced motor skills and slower cognitive processes. However, prolonged drinking can lead to decreased GABA receptor function and a rebound increase in glutamate activity, contributing to excitotoxicity and cell death, which can be observed in disorders such as Parkinson's disease where there is an imbalance between glutamate and GABA neurotransmission.