First Author | Ishida A | Year | 1994 |
Journal | Brain Res | Volume | 662 |
Issue | 1-2 | Pages | 60-8 |
PubMed ID | 7859091 | Mgi Jnum | J:21088 |
Mgi Id | MGI:69137 | Doi | 10.1016/0006-8993(94)90795-1 |
Citation | Ishida A, et al. (1994) An electrophysiological and immunohistochemical study of the hippocampus of the reeler mutant mouse. Brain Res 662(1-2):60-8 |
abstractText | The pyramidal cell layer in the CA1 subfield of the hippocampus of the reeler mouse is split into two laminae, the deep and the superficial. We examined the electrophysiological properties of double-layered CA1 pyramidal neurons in the reeler mouse hippocampal slice in vitro. We also studied cytoarchitectonic abnormalities in the hippocampus of this mutant by immunohistochemical methods using anti-parvalbumin and anti-F3/F11-protein antibodies. Laminar analysis of the postsynaptic field potentials in the CA1 subfield of the reeler hippocampus revealed broad negative field potentials with double negative peaks. In the CA1 subfield of the reeler mouse, tetanic stimulation of Schaffer collateral/commissural fibers induced long-term potentiation (LTP) in the majority of the deep layers (near alveus) examined, but very rarely in the superficial layer (near the molecular layer). Immunohistochemical study showed that parvalbumin-immunopositive neurons were densely concentrated in the hippocampus of the reeler mouse, especially in the stratum radiatum and the stratum lacunosum-molecular, in which only a few parvalbumin-immunoreactive neurons were seen in the normal mouse. Abnormal trajectories of axons arising from malpositioned pyramidal cells in the CA1 subfield of the reeler mouse were identified by F3/F11 immunohistochemistry. Interestingly, F3/F11-immunoreactive Schaffer collaterals were misdirected in the CA1 subfield of this mutant. The present electrophysiological and immunohistochemical data suggest that impairment of LTP in the superficial layer of the CA1 pyramidal neurons appears to be mainly due to strong inhibitory inputs to this malpositioned population of neurons. |