Histamine in the regulation of wakefulness

Abstract

The histaminergic system is exclusively localized within the posterior hypothalamus with projection to almost all the major regions of the central nervous system. Strong and consistent evidence exist to suggest that histamine, acting via H 1 and/or H 3 receptor has a pivotal role in the regulation of sleep-wakefulness. Administration of histamine or H 1 receptor agonists induced wakefulness, whereas administration of H 1 receptor antagonists promoted sleep. The H 3 receptor functions as an auto-receptor and regulates the synthesis and release of histamine. Activation of H 3 receptor decreased histamine release and promoted sleep. Conversely, blockade of H 3 receptor promoted wakefulness. Histamine release in the hypothalamus and other target regions was highest during wakefulness. The histaminergic neurons displayed maximal activity during the state of vigilance, and cease their activity during NREM and REM sleep. The cerebrospinal levels of histamine were reduced in diseased states where hypersomnolence was a major symptom. The histamine deficient HDC KO mice displayed sleep fragmentation and increased REM sleep during the light period along with profound wakefulness deficit at dark onset, and in novel environment. Similar results were obtained when histamine neurons were lesioned. These studies strongly implicate the histaminergic neurons of the TMN to play a critical role in the maintenance of high vigilance state during wakefulness.

Histamine and H1-antihistamines: Celebrating a century of progress

“…It has anticonvulsant activity and contributes to regulation of vigilance (alertness and attention), cognition, learning, memory, and the circadian sleep-wake cycle, as well as to energy and endocrine homeostasis. 1,[18][19][20] Through its 4 receptor subtypes, histamine plays an important role in a complex system of immunoregulation and in acute and chronic allergic inflammation. 21 Through the H 1 -receptor, it increases antigen-presenting cell capacity, increases release of histamine and other mediators from mast cells and basophils, downregulates humoral immunity, and upregulates T H 1 priming, T H 1 proliferation, IFN-g production, cellular adhesion molecule expression, and chemotaxis of eosinophils and neutrophils (Table I).…”

Occurrence of sleep-related breathing disorders in patients with chronic urticaria at its asymptomatic or oligosymptomatic stages

“…SF36, DLQI, Skindex [18][19][20][21][22]. However, CU-Q2oL is a tool most recommended by the international expert panel under the auspices of the EAACI/GA2LEN/EDF/AAI/ WAO for patients with CU [23]. That questionnaire considers not only the occurrence of manifestations of the dermatological disease, but also its physical, mental and emotional results.…”

“…However, in spite of theoretical premises suggesting a possibility of the influence of mediators determining CU disseminations on various pathophysiological mechanisms and body functions, no papers have been found in the literature taking up the subject of SRBDs occurrence in patients with CU. It is known that histamine, the main mediator of acute urticaria, important also in chronic urticaria, participates under physiological conditions in the process of maintaining wakefulness through its effect on specific receptors in the central nervous system [23]. Its increased release in patients with CU may be responsible for the difficulties in falling asleep or awakenings, as well as for agitation or predisposition to depression [24].…”

Czy rzeczywiście znany jest efekt farmakodynamiczny środków stosowanych podczas znieczulenia ogólnego u noworodków, niemowląt i dzieci? Przegląd eksperymentalnych i klinicznych badań dotyczących działania neurodegeneracyjnego

“…The ventrolateral preoptic nucleus (VLPO) is responsible for the induction of sleep, whereas the tuberomammillary nucleus (TMN) activates the state of wakefulness. An essential role in activation of the switch on/off cycle is played by two neurotransmitters: γ-aminobutyric acid (GABA) from VLPO and histamine (HA) associated with activation of TMN, which is its only source in the CNS [7]. During sleep, the VLPO neurons are activated and stimulate the release of GABA to TMN, blocking the neurons of this centre and inducing sleep with the maximum activity during rapid eye movement (REM) and non-rapid eye movement (NREM) phases.…”