Excitatory neurotransmission central nervous system

Ionotropic glutamate receptors mediate fast excitatory neurotransmission in practically all areas of the central nervous system (CNS). They are also critical for both the induction and expression of synaptic plasticity, and have been implicated in diverse pathological conditions, such as epilepsy, ischemic brain damage, anxiety, and addiction. There are three subtypes of ionotropic glutamate receptors that are named after their high-affinity agonists as a-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA), N-1nethyl-D-aspartate (NMDA), and kainate (KA) receptors (1). 

Glutamate is a major excitatory neurotransmitter in the central nervous system. Theoretically, increased glutamater-gic neurotransmission may lead to excitatory neurotoxicity or excitotoxicity. The only two currently approved neuroprotective agents in the United States, riluzole for ALS and memantine for AD, may act to prevent glutamatergic excitotoxicity. 

Isopropanol is a potent central nervous system (CNS) depressant it is believed to exert this effect via a similar mechanism as ethanol by modulating ion transport at the cell membrane in excitatory and inhibitory neurons. Ethanol enhances inhibitory or antagonizes excitatory neurotransmission. The metabolite, acetone, may potentiate and lengthen the duration of CNS symptoms observed upon isopropanol exposure. Although early animal studies suggested that the CNS depressant effects of isopropanol is approximately twice that of ethanol, this increased CNS depressant activity is probably a result of the combined effects of isopropanol and acetone. 

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