Impaired long-term potentiation and enhanced neuronal excitability in the amygdala of CaV1.3 knockout mice
Open accessAbstract
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.
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The L-type voltage gated calcium channel Cav1.3 decreases neuronal excitability.
“the L-type voltage gated calcium channel Cav1.3, which decreases neuronal excitability [55].”
From The molecular and cellular mechanisms of depression: a focus on reward circuitry (2019) · cites this paper as [55]
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- Authors
- McKinney, B. C., Sze, W., Lee, B., & Murphy, G. G.
- Affiliations
- University of Michigan (US)
- Corresponding author
- Murphy, Geoffrey G.
- Venue
- Neurobiology of Learning and Memory
- Publisher
- Elsevier BV
- Published
- 2009-11
- Volume
- 92
- Issue
- 4
- Pages
- 519-528
- ISSN
- 1074-7427 (ISSN-L)
- PMC
- PMC2747027
- OpenAlex
- W2051440962
- Cited by
- 63
- References
- 59
- Citations by year
- 2025: 2 · 2024: 3 · 2023: 4 · 2022: 3 · 2021: 9 · 2020: 8 · 2019: 5 · 2018: 2 · 2017: 3 · 2016: 2 · 2015: 5 · 2014: 6 · 2013: 3 · 2012: 5
- FWCI
- 1.29
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Neurobiology of Learning and Memory (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (RO1AG028488)
- National Institute of General Medical Sciences (5T32GM008322)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Keywords
- Cav1.3, L-type calcium channels, basolateral amygdala, long-term potentiation, neuronal excitability, fear conditioning, principal neurons, lateral amygdala, knockout mice
- MeSH terms
- Action Potentials, Amygdala, Animals, Electric Stimulation, Female, Male, Mice, Inbred C57BL, Neurons, Long-Term Potentiation, Mice, Knockout, Calcium Channels, L-Type, Mice, In Vitro Techniques
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