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Publication : Enhanced acetylcholine release in the hippocampus of cannabinoid CB(1) receptor-deficient mice.

First Author  Kathmann M Year  2001
Journal  Br J Pharmacol Volume  132
Issue  6 Pages  1169-73
PubMed ID  11250865 Mgi Jnum  J:289021
Mgi Id  MGI:6435826 Doi  10.1038/sj.bjp.0703987
Citation  Kathmann M, et al. (2001) Enhanced acetylcholine release in the hippocampus of cannabinoid CB(1) receptor-deficient mice. Br J Pharmacol 132(6):1169-73
abstractText  We examined whether acetylcholine release in the hippocampus and striatum and noradrenaline release in the hippocampus is altered in CB(1) receptor-deficient mice. The electrically evoked tritium overflow from hippocampal slices preincubated with [(3)H]-choline was increased by about 100% in CB(1)(-/-) compared to CB(1)(+/+) mice whereas the electrically evoked tritium overflow from striatal slices preincubated with [(3)H]-choline and from hippocampal slices preincubated with [(3)H]-noradrenaline did not differ. The cannabinoid receptor agonist, WIN 55,212-2, inhibited, and the CB(1) receptor antagonist, SR 141716, facilitated, the evoked tritium overflow from hippocampal slices (preincubated with [(3)H]-choline) from CB(1)(+/+) as opposed to CB(1)(-/-) mice. Both drugs did not affect the evoked tritium overflow from striatal slices (preincubated with [(3)H]-choline) and from hippocampal slices (preincubated with [(3)H]-noradrenaline) from CB(1)(+/+) and CB(1)(-/-) mice. The selective increase in acetylcholine release in CB(1)(-/-) mice may indicate that the presynaptic CB(1) receptors on the cholinergic neurones of the mouse hippocampus are tonically activated and/or constitutively active in vivo.
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