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.