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. |