Effects of H₂‐receptor antagonists on the central nervous system

Abstract

Histamine functions as a neurotransmitter in the central nervous system (CNS), and H,-receptor activation can modulate the activity of the CNS. H2-receptor antagonists are known to penetrate the blood-brain barrier and to cause neuropsychiatric effects. It appears that interactions with CNS H,-receptors may account for many of these effects, although receptor interactions unique to certain H,-antagonists may also play a role.

Medications and their effects on sleep

“…Somnolence and lethargy at conventional doses, however, have been documented in the elderly and patients with renal impairment. Slow wave sleep is increased by cimetidine [19,[49][50][51].…”

Potential immunological consequences of pharmacological suppression of gastric acid production in patients with multiple sclerosis

“…Because activation of H2R appears to be a key mechanism for histamine-mediated immunosuppression, it raises the question of whether H2R antagonists aggravate disease activity in patients with MS. H2R is expressed by a variety of cells, including endothelial and systemic inflammatory cells [ 7 ], and H2R is expressed in EAE by CNS inflammatory infiltrates and possibly microglia and astrocytes [ 13 ]. Because H2R antagonists have been shown to gain access to the brain [ 14 ], they can exert effects on inflammatory cells within the CNS as well as systemically.…”