Histaminergic perikarya are found exclusively in the tuberomammillary nucleus of the posterior hypothalamus from where they project to all parts of the brain [1]. Histaminergic efferents to the basal forebrain modulate the activity of the nucleus basalis magnocellularis (NBM) neurons [2], which provide cholinergic innervation to the cortex, and play a pivotal role in learning and memory processes [3]. Indeed, intra-NBM administration of H3 antagonists increased cortical ACh release; this effect was blocked by H1 antagonists [4]. Likely, blockade of H3 autoreceptors released endogenous histamine that impacted on postsynaptic H1 receptors. This modulation seems functionally relevant, as H3 receptor blockade in the NBM improves place recognition memory [5], and H1 receptor stimulation ameliorates time-dependent deterioration in memory in a rat object recognition test [6]. Betahistine acts both as a partial histamine H1 receptor agonist, and as a histamine H3 receptor antagonist [7] and the current study focuses on the effects of betahistine upon NBM-cortical cholinergic neurons.

Betahistine increases ACh release from the cortex, but not histamine release from the nucleus basalis magnocellularis of freely-moving rats / G. Cenni; M.B. Passani; P.F. Mannaioni; P Blandina. - In: INFLAMMATION RESEARCH. - ISSN 1023-3830. - STAMPA. - 55:(2006), pp. S28-S29.

Betahistine increases ACh release from the cortex, but not histamine release from the nucleus basalis magnocellularis of freely-moving rats

PASSANI, MARIA BEATRICE;MANNAIONI, PIER FRANCESCO;BLANDINA, PATRIZIO
2006

Abstract

Histaminergic perikarya are found exclusively in the tuberomammillary nucleus of the posterior hypothalamus from where they project to all parts of the brain [1]. Histaminergic efferents to the basal forebrain modulate the activity of the nucleus basalis magnocellularis (NBM) neurons [2], which provide cholinergic innervation to the cortex, and play a pivotal role in learning and memory processes [3]. Indeed, intra-NBM administration of H3 antagonists increased cortical ACh release; this effect was blocked by H1 antagonists [4]. Likely, blockade of H3 autoreceptors released endogenous histamine that impacted on postsynaptic H1 receptors. This modulation seems functionally relevant, as H3 receptor blockade in the NBM improves place recognition memory [5], and H1 receptor stimulation ameliorates time-dependent deterioration in memory in a rat object recognition test [6]. Betahistine acts both as a partial histamine H1 receptor agonist, and as a histamine H3 receptor antagonist [7] and the current study focuses on the effects of betahistine upon NBM-cortical cholinergic neurons.
2006
55
S28
S29
G. Cenni; M.B. Passani; P.F. Mannaioni; P Blandina
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Utilizza questo identificatore per citare o creare un link a questa risorsa: https://hdl.handle.net/2158/403131
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