Modulators of consciousness: caffeine and alcohol
It is known that the modulation of synaptic transmission may affect the
level of consciousness. Effects produced by caffeine, a common
ingredient of tea and coffee are a good example. Using animal anesthesia
as a model, Fox et al (2020) reported that caffeine is able to reverse
the unconsciousness induced by light anesthesia in adult rats (Foxet al. , 2020). Subsequently, Fong et al (2018) showed that
caffeine injected intravenously accelerate human emergence from
isoflurane anesthesia (Fong et al. , 2018). These results provide
strong evidence that brain excitatory indeed play an important role in
the loss of consciousness during anesthesia, and it is possible to
explore the basic mechanisms of consciousness using pharmacological
approaches in both human and animals. Interestingly, they also found
that alteration of anesthesia and consciousness levels are correlated
well with brain electroencephalogram (EEG) activity, a common parameter
obtained in humans. At the cellular level, it is believed that caffeine
produced this effect by increasing intracellular cAMP level, triggering
immediate early genes, and regulation of the dopamine- and
cAMP-regulated phosphoprotein, M(r) 32 kDa (Lindskog et al. ,
2002; Fisone et al. , 2004) and inhibit neuronal adenosine A
receptors in the brain.
Alcohol is well known to cause unconsciousness or death when it is
consumed at higher dosages. At a low dose range, alcohol can cause
disinhibition and anxiolytic effects (Harrison et al. , 2017).
Cumulative evidence indicates that alcohol affects both excitatory and
inhibitory transmission in the brain (Zorumski et al. , 2014). One
of the key actions is that alcohol enhances the actions of
γ-aminobutyric acid (GABA) at certain GABAA receptors
and inhibits the function of NMDA receptors. Effects of alcohol on AMPA
as well as KA receptors have also been reported. It is thus predictable
that alcohol also affects central synaptic plasticity such as LTP. These
actions provide a basic mechanism of CNS dysfunction caused by alcohol
such as memory impairment, blackouts, and loss of consciousness.