Cortical acetylcholine release elicited by stimulation of histamine H 1 receptors in the nucleus basalis magnocellularis: a dual‐probe microdialysis study in the freely moving rat

• Published in: The European journal of neuroscience Vol. 13; no. 1; pp. 68 - 78
• Main Authors: Cecchi, Marco, Passani, Maria Beatrice, Bacciottini, Lucia, Mannaioni, Pier Francesco, Blandina, Patrizio
• Format: Journal Article
• Language: English
• Published: 01.01.2001
• ISSN: 0953-816X; 1460-9568
• DOI: 10.1111/j.1460-9568.2001.01361.x

Abstract Perfusion of the nucleus basalis magnocellularis (NBM) with histamine agonists and antagonists modulates the spontaneous release of cortical acetylcholine (ACh) in freely moving rats. Perfusion of the NBM with Ringer solution containing 100 m m K + strongly stimulated the spontaneous release of cortical ACh in freely moving rats, whereas perfusion with 1 µ m tetrodotoxin reduced cortical ACh spontaneous release by more than 50%. Administration of histamine to the NBM concentration‐dependently increased the spontaneous release of cortical ACh. Administration of H 1 (methylhistaprodifen) but not H 2 (dimaprit) or H 3 (R‐α‐methylhistamine) receptor agonists to the NBM mimicked the effect of histamine. Perfusion of the NBM with either H 1 (mepyramine or triprolidine) or H 2 (cimetidine) receptor antagonists failed to alter ACh spontaneous release from the cortex, however, H 1 but not H 2 receptor antagonists antagonized the releases of cortical ACh elicited by histamine and methylhistaprodifen. Local administration of H 3 receptor antagonists (clobenpropit and thioperamide) to the NBM increased the spontaneous release of ACh from the cortex; this effect was antagonized by H 1 receptor antagonism. Conversely local administration of MK‐801, a noncompetitive receptor antagonist of the N ‐methyl‐ d ‐aspartate receptor, to the NBM failed to alter ACh spontaneous release from the cortex and to antagonize ACh release elicited by histamine. This study demonstrates that activation of histamine H 1 receptors in the NBM increases ACh spontaneous release from the cortex.