Alcohol consumption and central nervous system

Question

After alcohol intake, the cerebrum related functions like vision and speech is affected first and later on there's problem with the cerebellar functions like balancing and hand-eye coordination. My question is- why is it so? Why do they appear in that order? Like does it have anything to do with differential rate of absorption in cells, or anything else like related to anatomy rather than physiology.

Answer 1

After alcohol intake, the cerebrum related functions like vision and speech is affected first and later on there's problem with the cerebellar functions like balancing and hand-eye coordination. My question is- why is it so? Why do they appear in that order?

It is and it isn't complicated. When you include what each does, it's an interesting question.

We know from experience (and even research, though the ethics of carrying out such research is questionable) that of the noticeable effects on the brain, the first part of the brain (that we can see the effects of) are on the cerebrum. At relatively low doses, the drinker feels more relaxed, more talkative, less inhibited. (there is also a measurable decrease in information processing and reaction time, as well as other less obvious effects.) All these are under the control of the cerebrum.

At this stage, the cerebellum is affected as well, but not grossly (in a manner that we can observe as change in behavior.) The cerebrum is critical to functioning; the cerebellum is critical to survival. Although it's presented as a teleological argument, the simple fact is that effects of alcohol and other sedatives on various parts of the brain are dose-dependent.

First, dose-dependent functional magnetic resonance imaging (fMRI) changes were revealed in orbitofrontal (OF) and motor (but not cerebellar) regions; visual and medial frontal regions were unaffected. Second, cerebellar regions were significantly associated with driving behavior in a dose-dependent manner. Finally, a global disruptive effect of alcohol on the ICA time courses was observed with highly significant differences in OF and motor regions. Alcohol thus demonstrated some behavioral effects and unique, disruptive, dose-dependent effects on fMRI signal within several brain circuits. The fMRI data also suggest that the deficits observed in alcohol intoxication may be modulated primarily through OF/anterior cingulate, motor and cerebellar regions as opposed to attentional areas in frontoparietal cortex.

If you want to know why different parts of the brain require higher doses to become impaired, that is easy in theory but very complicated in reality. In theory, the brain is no different than any other complex organ in the body: it's made up of different cells. Sure, they're all neurons (excluding glial/etc cells), but not every neuron is the same, just like not every cardiac myocyte is the same. In reality, the answer is unknown.

Neuronal mechanisms underlying alcohol intoxication are unclear. We find that alcohol impairs motor coordination by enhancing tonic inhibition mediated by a specific subtype of extrasynaptic GABAA receptor (GABAR), α6β3δ, expressed exclusively in cerebellar granule cells. In recombinant studies, we characterize a naturally occurring single-nucleotide polymorphism that causes a single amino acid change (R100Q) in α6 (encoded in rats by the Gabra6 gene). We show that this change selectively increases alcohol sensitivity of α6β3δ GABARs. Behavioral and electrophysiological comparisons of Gabra6100R/100R and Gabra6100Q/100Q rats strongly suggest that alcohol impairs motor coordination by enhancing granule cell tonic inhibition. These findings identify extrasynaptic GABARs as critical targets underlying low-dose alcohol intoxication and demonstrate that subtle changes in tonic inhibition in one class of neurons can alter behavior.

The above sounds like a reason, but it is debated still. I think it's safe to say that like so many cellular reactions, the answer will come down to receptors and their activation or inhibition, be it for GABA/NMDA, combinations or others.

_{Alcohol impairment of behavior in men and women
Differential effects of ethanol on motor coordination in adolescent and adult rats
Alcohol Intoxication Effects on Simulated Driving: Exploring Alcohol-Dose Effects on Brain Activation Using Functional MRI
Modulation of GABA A receptors in cerebellar granule neurons by ethanol: a review of genetic and electrophysiological studies
Ethanol affects NMDA receptor signaling at climbing fiber-Purkinje cell synapses in mice and impairs cerebellar LTD}