Conditional cannabinoid receptor type 1 mutants reveal neuron subpopulation-specific effects on behavioral and neuroendocrine stress responses.
Psychoneuroendocrinology. 2008-09-01; 33(8): 1165-1170
DOI: 10.1016/j.psyneuen.2008.06.004
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1. Psychoneuroendocrinology. 2008 Sep;33(8):1165-70. doi:
10.1016/j.psyneuen.2008.06.004. Epub 2008 Jul 23.
Conditional cannabinoid receptor type 1 mutants reveal neuron
subpopulation-specific effects on behavioral and neuroendocrine stress responses.
Steiner MA(1), Marsicano G, Wotjak CT, Lutz B.
Author information:
(1)Max Planck Institute of Psychiatry, Kraepelinstrasse 2-10, 80804 Munich,
Germany.
The complete genetic loss or pharmacological blockade of cannabinoid receptor
type 1 (CB1) in mice results in both altered behavioral performance and increased
stress hormone secretion in response to stressful encounters such as forced swim
test (FST) exposure. CB1 is expressed on nerve terminals belonging to different
neurotransmitter systems, including the glutamatergic and GABAergic system, where
it is able to suppress excitatory and inhibitory neurotransmission, respectively.
In the current study, we used the conditional mutagenesis approach in mice to
investigate the neurotransmitter systems involved in these behavioral and
neuroendocrine phenotypes in regard to CB1 signaling. Mice lacking CB1 in
cortical glutamatergic neurons (Glu-CB1(-/-)) showed decreased passive stress
coping (decreased immobility) in the FST, whereas mice lacking CB1 in principal
forebrain neurons (CaMK-CB1(-/-)) and GABAergic neurons (GABA-CB1(-/-)),
respectively, behaved as littermate controls. However, we found increased
FST-induced corticosterone secretion only in CaMK-CB1(-/-) mice, whereas
Glu-CB1(-/-) and GABA-CB1(-/-) mice exhibited normal corticosterone release as
compared to controls. Thus, behavioral and neuroendocrine acute stress coping in
response to the FST is mainly influenced by CB1 signaling on different
glutamatergic neuronal subpopulations, but not by CB1 on GABAergic neurons.
DOI: 10.1016/j.psyneuen.2008.06.004
PMID: 18653287 [Indexed for MEDLINE]