Deletion of the L-type calcium channel Ca V 1.3 but not Ca V 1.2 results in a diminished sAHP in mouse CA1 pyramidal neurons
dc.contributor.author | Gamelli, Amy E. | en_US |
dc.contributor.author | McKinney, Brandon C. | en_US |
dc.contributor.author | White, Jessica A. | en_US |
dc.contributor.author | Murphy, Geoffrey G. | en_US |
dc.date.accessioned | 2011-02-02T17:58:40Z | |
dc.date.available | 2012-03-05T15:30:01Z | en_US |
dc.date.issued | 2011-02 | en_US |
dc.identifier.citation | Gamelli, Amy E.; McKinney, Brandon C.; White, Jessica A.; Murphy, Geoffrey G. (2011). "Deletion of the L-type calcium channel Ca V 1.3 but not Ca V 1.2 results in a diminished sAHP in mouse CA1 pyramidal neurons." Hippocampus 21(2): 133-141. <http://hdl.handle.net/2027.42/79416> | en_US |
dc.identifier.issn | 1050-9631 | en_US |
dc.identifier.issn | 1098-1063 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/79416 | |
dc.description.abstract | Trains of action potentials in CA1 pyramidal neurons are followed by a prolonged calcium-dependent postburst afterhyperpolarization (AHP) that serves to limit further firing to a sustained depolarizing input. A reduction in the AHP accompanies acquisition of several types of learning and increases in the AHP are correlated with age-related cognitive impairment. The AHP develops primarily as the result of activation of outward calcium-activated potassium currents; however, the precise source of calcium for activation of the AHP remains unclear. There is substantial experimental evidence suggesting that calcium influx via voltage-gated L-type calcium channels (L-VGCCs) contributes to the generation of the AHP. Two L-VGCC subtypes are predominately expressed in the hippocampus, Ca V 1.2 and Ca V 1.3; however, it is not known which L-VGCC subtype is involved in generation of the AHP. This ambiguity is due in large part to the fact that at present there are no subunit-specific agonists or antagonists. Therefore, using mice in which the gene encoding Ca V 1.2 or Ca V 1.3 was deleted, we sought to determine the impact of alterations in levels of these two L-VCGG subtypes on neuronal excitability. No differences in any AHP measure were seen between neurons from Ca V 1.2 knockout mice and controls. However, the total area of the AHP was significantly smaller in neurons from Ca V 1.3 knockout mice as compared with neurons from wild-type controls. A significant reduction in the amplitude of the AHP was also seen at the 1 s time point in neurons from Ca V 1.3 knockout mice as compared with those from controls. Reductions in both the area and 1 s amplitude suggest the involvement of calcium influx via Ca V 1.3 in the slow AHP (sAHP). Thus, the results of our study demonstrate that deletion of Ca V 1.3, but not Ca V 1.2, significantly impacts the generation of the sAHP. © 2009 Wiley-Liss, Inc. | en_US |
dc.format.extent | 375021 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.publisher | Wiley Subscription Services, Inc., A Wiley Company | en_US |
dc.subject.other | Life and Medical Sciences | en_US |
dc.subject.other | Neuroscience, Neurology and Psychiatry | en_US |
dc.title | Deletion of the L-type calcium channel Ca V 1.3 but not Ca V 1.2 results in a diminished sAHP in mouse CA1 pyramidal neurons | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Molecular, Cellular and Developmental Biology | en_US |
dc.subject.hlbsecondlevel | Neurosciences | en_US |
dc.subject.hlbsecondlevel | Public Health | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Molecular & Behavioral Neuroscience Institute, University of Michigan Medical School, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Medical Scientist Training Program, University of Michigan Medical School, Ann Arbor, Michigan ; Neuroscience Graduate Program, University of Michigan Medical School, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Molecular & Behavioral Neuroscience Institute, University of Michigan Medical School, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Molecular & Behavioral Neuroscience Institute, University of Michigan Medical School, Ann Arbor, Michigan ; Neuroscience Graduate Program, University of Michigan Medical School, Ann Arbor, Michigan ; Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan ; University of Michigan, 5037 Biomedical Science Research Building, 109 Zina Pitcher Place, Ann Arbor, MI 48109-2200 | en_US |
dc.identifier.pmid | 20014384 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/79416/1/20728_ftp.pdf | |
dc.identifier.doi | 10.1002/hipo.20728 | en_US |
dc.identifier.source | Hippocampus | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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