Ali Ladkani WKSHP5 309185424
Difference between alcohol and drug mechanism of actions
After partying Joe has become ill. As a paramedic i need to distinguish between alcoholic effects or
drug effects.
Alcoholic beverages contain the active ingredient ethanol. This ethanol binds to ACh, GABA,
serotonin and NMDA receptors.
Mechanism of Action of Alcohol:
Both lipid and water soluble àcan cross the blood brain barrier
Acts as a CNS depressor by affecting three different membrane receptors:
Receptor Normal Mechanism
GABA a Increase flow of Cl- across
membrane
Prevents
depolarisation
NMDA
Allows Ca2+ to enter the
cell
Causes
Depolarisation
Dopamine Excites neurones responsible for
memory and pleasure
Effects of alcohol
Indirect agonist
Increases GABA activity
Symptoms
Loss of Coordination
Indirect antagonist
Inhibits Ca2+ transport
Drowsiness
Reduction in clear
thought
Increases dopamine
release
dopamine reuptake
Reduced memory
Inhibits
Once ingested, the ethanol within the alcohol is oxidised by the enzyme alcohol dehydrogenase in
the liver. However, within the body this is limited. Thus the removal of large amounts of alcohol
from the blood follows zero order kinetics (Trujillo, 2008). This means that alcohol leaves the body at
a constant rate rather than having an elimination half life.
However the actual definite mechanism of action of alcohol has not been determined mainly due to
the fact that ethanol acts at so many neurotransmitter sites. Ethanol appears to act by modifying cell
membranes rather than by binding to specific receptor sites on neurons like other compounds
(Trujillo, 2008). Alcohol dissolves in the lipid layer of cellular membranes, causing an increase in its
fluidity. This change may modify the actions of specific receptors or ion channels, resulting in the
many behavioral effects of ethanol (Argawal, 1992).
Specific receptors that have been associated with the effects of alcohol include gamma aminobutyric
acid (GABA) and N-methyl-D-aspartate (NMDA). The inhibitory effects of ethanol may result from an
enhancement of GABAA receptor function, increasing the effects of this inhibitory receptor which
causes most of the effects such as relaxation, relief from anxiety, ataxia, and lowering of inhibitions
(Argawal, 1992). A blockade of NMDA receptor function interferes with the effects of this excitatory
receptor. However, pinpointing a site of action or single mechanism of alcohol effects is difficult
because the drug affects virtually all neurochemical and endocrine systems (Argawal, 1992).
Illicit drugs or psychoactive drugs are drugs that are taken for recreational purposes. Psychoactive
drugs are a class of chemical substances that act on the central nervous system and can alter
behavior and cognition . All psychoactive drugs are highly fat-soluble and thus cross the blood-brain
barrier readily (Fisher et. al.,2000). Psychoactive drugs alter synaptic transmission by altering neurotransmitter amounts and availability or by affecting receptor activity. In addition to the drug's
primary effects on behaviors such as arousal, thought processes, mood, perception, and
Ali Ladkani WKSHP5 309185424
consciousness, psychoactive drugs can produce a variety of nonbehavioral effects that may more
directly affect health and, in some instances, can lead to death.
Because most illicit drugs have the same pathways/ mechanism of action, whilst only differing at the
receptor they act on, which may also overlap, i will describe the mechanism of action of a common
illicit drug, Ecstacy. MDMA does not act by directly releasing serotonin but, rather, by binding to, and
thus blocking, the transporter involved in its reuptake (Fisher et. al.,2000). In a study, rats, trained to
discriminate between the effects of saline and those of serotonin in an operant task, responded to
MDMA as if it were serotonin (Fisher et. al.,2000). A similar, but weaker, action is also exerted on the
reuptake of dopamine. The physiological effects of MDMA and MDA in mice are the same as those of
amphetamine, which is known to act as a releaser of dopamine and noradrenaline (Green et. al.,
1995). There is a small amount of experimental evidence that the net release of acetylcholine may
also be increased by MDMA, but the importance of this effect in humans is unknown. It is clear,
however, that the increase in the net release of serotonin (and possibly dopamine) is the major
mechanism of action underlying the distinctive mental effects of MDMA, whereas the increased
release of noradrenaline is mainly responsible for the physical effects that it shares with
amphetamine (Huether et. al., 1997).
Therefore, as a paramedic, i believe that Joe was under the influence of an illicit drug as opposed to
alcohol. Unfortunately his death could be due to overdose.
References:
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Agarwal DP, Goedde HW (1992). "Pharmacogenetics of alcohol metabolism and alcoholism".
Pharmacogenetics 2 (2): 48
Fischer HS, Zernig G, Schatz DS, Humpel C, Saria A. MDMA (‘ecstasy’) enhances basal
acetylcholine release in brain slices of the rat striatum. Eur J Neurosci 2000;12:1385-90
Green AR, Cross AJ, Goodwin GM. Review of the pharmacology and clinical pharmacology of
3,4-methylenedioxymethamphetamine (MDMA or "ecstasy"). Psychopharmacology (Berl)
1995;119(3):247-60
Huether G, Zhou D, Rüther E. Causes and consequences of the loss of serotonergic
presynapses elicited by the consumption of 3,4-methylene-dioxymethamphetamine
(MDMA, "ecstasy") and its congeners. J Neural Transm 1997;104:771-94.
Shulgin AT. The background and chemistry of MDMA. J Psychoactive Drugs 1986; 18:291304.
Trujillo, Keith A. and Andrea B. Chinn. "Drugs and the Brain: Ethanol. California State
University. 20 FEB 2008.