Alcohol, or more specifically, ethanol, affects
brain functions in several ways. Alcohol is generally known as a DEPRESSANT
of the central nervous system; it INHIBITS brain activities, causing a range of physiological
effects such as impaired body movements and slurred speech. The pleasurable feeling associated with drinking,
on the other hand, is linked to alcohol-induced dopamine release in the brain’s reward pathway. Alcohol also increases levels of brain serotonin,
a neurotransmitter implicated in mood regulation. The brain is a complex network of billions
of neurons. Neurons can be excitatory or inhibitory. Excitatory neurons stimulate others to respond
and transmit electrical messages, while inhibitory neurons SUPPRESS responsiveness, preventing
excessive firing. Responsiveness or excitability of a neuron
is determined by the value of electrical voltage across its membrane. Basically, a neuron is MORE responsive when
it has more POSITIVE charges inside; and is LESS responsive when it becomes more NEGATIVE. A balance between excitation and inhibition
is essential for normal brain functions. Short-term alcohol consumption DISRUPTS this
balance, INCREASING INHIBITORY and DECREASING EXCITATORY functions. Specifically, alcohol inhibits responsiveness
of neurons via its interaction with the GABA system. GABA is a major INHIBITORY neurotransmitter. Upon binding, it triggers GABA receptors,
ligand-gated chloride channels, to open and allow chloride ions to flow into the neuron,
making it more NEGATIVE and LESS likely to respond to new stimuli. Alcohol is known to POTENTIATE GABA receptors,
keeping the channels open for a longer time and thus exaggerating this inhibitory effect. GABA receptors are also the target of certain
anesthetic drugs. This explains the SEDATIVE effect of alcohol. At the same time, alcohol also inhibits the
glutamate system, a major excitatory circuit of the brain. Glutamate receptors, another type of ion channel,
upon binding by glutamate, open to allow POSITIVELY-charged ions into the cell, making it more POSITIVE
and MORE likely to generate electrical signals. Alcohol binding REDUCES channel permeability,
LOWERING cation influx, thereby INHIBITING neuron responsiveness. GABA ACTIVATION and glutamate INHIBITION together
bring DOWN brain activities. Depending on the concentration of ethanol
in the blood, alcohol’s depressant effect can range from slight drowsiness to blackout,
or even respiratory failure and death. Chronic, or long-term consumption of alcohol,
however, produces an OPPOSITE effect on the brain. This is because SUSTAINED inhibition caused
by PROLONGED alcohol exposure eventually ACTIVATES the brain’s ADAPTATION response. In attempts to restore the equilibrium, the
brain DECREASES GABA inhibitory and INCREASES glutamate excitatory functions to compensate
for the alcohol’s effect. As the balance tilts toward EXCITATION, more
and more alcohol is needed to achieve the same inhibitory effect. This leads to overdrinking and eventually
addiction. If alcohol consumption is ABRUPTLY reduced
or discontinued at this point, an ill-feeling known as WITHDRAWAL syndrome may follow. This is because the brain is now HYPER-excitable
if NOT balanced by the inhibitory effect of alcohol. Alcohol withdrawal syndrome is characterized
by tremors, seizures, hallucinations, agitation and confusion. Excess calcium produced by overactive glutamate
receptors during withdrawal is toxic and may cause brain damage. Withdrawal-related anxiety also contributes
to alcohol-seeking behavior and CONTINUED alcohol abuse.
