Increasing evidence suggests that not only
ammonia, but also its alkyl-derivatives, including
methylamine, may modulate neuron firing.
Methylamine occurs endogenously from
amine catabolism and its tissue levels increase in some pathological conditions, including diabetes. Interestingly,
methylamine and
ammonia levels are reciprocally controlled by a
semicarbazide-sensitive amine oxidase activity that deaminates
methylamine to
formaldehyde with the production of
ammonia and
hydrogen peroxide. As already described for
ammonia,
methylamine also targets the voltage-operated neuronal
potassium channels, probably inducing release of
neurotransmitter(s). From this interaction it has been observed that
methylamine is 1) hypophagic in mice without producing
amphetamine-like effects and 2) a stimulator of
nitric oxide release from rat hypothalamus.
Methylamine hypophagia is also maintained in genetically obese and diabetic mice and is increased when these animals are pre-treated with -amino
guanidine, an inhibitor of
methylamine oxidative deamination. The effect of -amino
guanidine suggests a potential beneficial effect of this drug, and other such inhibitors, in controlling food intake in animals with disturbed eating behavior. Moreover, the activity of
methylamine as an inducer of NO release suggests a role for the
amine and for the enzymatic activity that degrades it in
neurodegenerative diseases.