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

Perfusion of the nucleus basalis magnocellularis (NBM) with histamine agoni sts and antagonists modulates the spontaneous release of cortical acetylcho line (ACh) in freely moving rats. Perfusion of the NBM with Ringer solution containing 100 mM K+ strongly stimulated the spontaneous release of cortic al ACh in freely moving rats, whereas perfusion with 1 muM tetrodotoxin red uced cortical ACh spontaneous release by more than 50%, Administration of h istamine to the NBM concentration-dependently increased the spontaneous rel ease of cortical ACh. Administration of H-1 (methylhistaprodifen) but not H -2 (dimaprit) or H-3 (R-alpha -methylhistamine) receptor agonists to the NB M mimicked the effect of histamine, Perfusion of the NBM with either H-1 (m epyramine or triprolidine) or H-2 (cimetidine) receptor antagonists failed to alter ACh spontaneous release from the cortex, however, H-1 but not H-3 receptor antagonists antagonized the releases of cortical ACh elicited by h istamine and methylhistaprodifen. Local administration of H-3 receptor anta gonists (clobenpropit and thioperamide) to the NBM increased the spontaneou s release of ACh from the cortex; this effect was antagonized by H-1 recept or 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 rel ease elicited by histamine. This study demonstrates that activation of hist amine H-1 receptors in the NBM increases ACh spontaneous release from the c ortex.Perfusion of the nucleus basalis magnocellularis (NBM) with histamine agonists and antagonists modulates the spontaneous release of cortical ace tylcholine (ACh) in freely moving rats. Perfusion of the NBM with Ringer so lution containing 100 mM K+ strongly stimulated the spontaneous release of cortical ACh in freely moving rats, whereas perfusion with 1 muM tetrodotox in reduced cortical ACh spontaneous release by more than 50%, Administratio n of histamine to the NBM concentration-dependently increased the spontaneo us release of cortical ACh. Administration of H-1 (methylhistaprodifen) but not H-2 (dimaprit) or H-3 (R-alpha -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 f ailed to alter ACh spontaneous release from the cortex, however, H-1 but no t H-2 receptor antagonists antagonized the releases of cortical ACh elicite d by histamine and methylhistaprodifen. Local administration of H-3 recepto r antagonists (clobenpropit and thioperamide) to the NBM increased the spon taneous release of ACh from the cortex; this effect was antagonized by H-1 receptor antagonism. Conversely local administration of MK-801, a noncompet itive receptor antagonist of the N-methyl-D-aspartate receptor, to the NBM failed to alter ACh spontaneous release from the cortex and to antagonize A Ch release elicited by histamine. This study demonstrates that activation o f histamine H-1 receptors in the NBM increases ACh spontaneous release from the cortex.