Academic journal article Alcohol Health & Research World

Alcohol and Glutamate

Academic journal article Alcohol Health & Research World

Alcohol and Glutamate

Article excerpt

Excitatory neurotransmitters, the most important of which is glutamate, increase the activity of signalreceiving neurons and play a major role in controlling brain function. Glutamate exerts its effects on cells in part through three types of receptors that, when activated, allow the flow of positively charged ions into the cell. Of these, the N-methyl-D-aspartate (NMDA) receptor plays a particularly important role in controlling the brain's ability to adapt to environmental and genetic influences. Even low alcohol concentrations can inhibit the excitatory activity of the NMDA receptor. This inhibition of NMDA receptor function may be one of the mechanisms contributing to fetal alcohol syndrome and other more subtle developmental abnormalities. Moreover, alcohol-induced impairment of the NMDA receptor may contribute to alcohol-related learning disabilities, neuronal losses, and cognitive deficits as well as to some of the manifestations of alcohol withdrawal. KEY WORDS: glutamate receptors; NMDA receptors; neurotransmission; cell signaling; membrane channel; brain function; neuron; hereditary factors; environmental factors; AODE (alcohol and other drug effects); toxic drug effect; fetal alcohol syndrome; AOD withdrawal syndrome; cognitive process; learning; literature review

Nerve cells, or neurons, transmit signals from the environment to the central nervous system (CNS), among different regions of the CNS, and from the CNS back to other organs (i.e., the periphery). This signal transmission is mediated primarily by small molecules called neurotransmitters. In general, neurotransmitters can be classified as either excitatory or inhibitory. Excitatory neurotransmitters increase and inhibitory neurotransmitters decrease the activity (e.g., the firing rate) of the signalreceiving (i.e., postsynaptic) neuron. Neurons differ in their abilities to recognize, integrate, and pass on the signals conveyed by neurotransmitters. For example, some neurons continually fire at a certain rate and thus can be either excited or inhibited in response to environmental changes. Other neurons normally are at rest. Accordingly, any modification of their activity must occur in the form of excitation. As a result, neuronal excitation plays a fundamental role in controlling brain functioning, and substances that interfere with excitatory neurotransmitter systems can dramatically affect brain function and behavior. Alcohol is such a substance; it appears to interfere with the signal transmission mediated by the neurotransmitter glutamate.

Of the numerous molecules governing normal brain functioning, glutamate (also called glutamic acid) is one of the most important, and research on its functions has generated exciting advances in understanding how the brain works. This article briefly reviews glutamate's role in normal brain functioning and relates recent findings on how alcohol affects glutamate-mediated (i.e., glutamatergic) signal transmission.


Glutamate's role as an important signaling molecule has been recognized only within the past two decades. Glutamate is an amino acid; molecules of this type are the building blocks of proteins. Because all cells in the body, including neurons, produce proteins, glutamate is present throughout the brain in relatively high concentrations. Consequently, researchers initially considered glutamate primarily an intermediate metabolic product of many cellular reactions unrelated to neuronal signal transmission and thus did not interpret its presence in neurons as evidence of a potential role as a neurotransmitter.

Although the first indications of glutamate's excitatory function in the brain emerged in the 1950's, these findings initially were dismissed: Glutamate application to neurons elicited excitatory responses in virtually every brain area examined, suggesting that this excitation was not a specific response (Collingridge and Lester 1989). …

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