Abstract:
:Previously, we demonstrated that mice in which the gene for the L-type voltage-gated calcium channel Ca(V)1.3 is deleted (Ca(V)1.3 knockout mice) exhibit an impaired ability to consolidate contextually-conditioned fear. Given that this form of Pavlovian fear conditioning is critically dependent on the basolateral complex of the amygdala (BLA), we were interested in the mechanisms by which Ca(V)1.3 contributes to BLA neurophysiology. In the present study, we used in vitro amygdala slices prepared from Ca(V)1.3 knockout mice and wild-type littermates to explore the role of Ca(V)1.3 in long-term potentiation (LTP) and intrinsic neuronal excitability in the BLA. We found that LTP in the lateral nucleus (LA) of the BLA, induced by high-frequency stimulation of the external capsule, was significantly reduced in Ca(V)1.3 knockout mice. Additionally, we found that BLA principal neurons from Ca(V)1.3 knockout mice were hyperexcitable, exhibiting significant increases in firing rates and decreased interspike intervals in response to prolonged somatic depolarization. This aberrant increase in neuronal excitability appears to be at least in part due to a concomitant reduction in the slow component of the post-burst afterhyperpolarization. Together, these results demonstrate altered neuronal function in the BLA of Ca(V)1.3 knockout mice which may account for the impaired ability of these mice to consolidate contextually-conditioned fear.
journal_name
Neurobiol Learn Memjournal_title
Neurobiology of learning and memoryauthors
McKinney BC,Sze W,Lee B,Murphy GGdoi
10.1016/j.nlm.2009.06.012subject
Has Abstractpub_date
2009-11-01 00:00:00pages
519-28issue
4eissn
1074-7427issn
1095-9564pii
S1074-7427(09)00136-1journal_volume
92pub_type
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