The Journal of Neuroscience, October 26, 2005, ():
Role of Hippocampal Cav1.2 Ca2+ Channels in NMDA Receptor-Independent Synaptic Plasticity and Spatial Memory
J. Neurosci. Moosmang et al.
25: 9883
Supplemantal data
Files in this Data Supplement:
- supplemental material -
Supplemental information.
- supplemental material
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Suppl. Fig. S1. Hippocampus and cortex restricted knockout of the CACNA1C gene.
(a) Schematic representation of the wild type (Wt), the knockout (L1) and the conditional Cav1.2 alleles (L2). The numbers indicate the exon number. Hippocampus specific activation of Cre recombinase (Nex-Cre) results in the deletion of Cav1.2 exons 14 and 15. Restriction sites are A, Acc65I; B, BamHI; C, ClaI; EI, EcoRI.
(b) Morphology of the Control (Ctr) and Cav1.2HCKO (KO) Brains. Nissl stains of sagittal sections through the hippocampus show no alteration in knockout animals.
(c,d) In-situ hybridization demonstrating Cav1.2 and Cav1.3 mRNA expression in murine brain.
(e) Western analysis of proteins from mouse brain using an anti-Cav1.2 antibody demonstrates strong reduction of Cav1.2 protein (arrow) in hippocampus (Hippo) and cerebral cortex (Cortex) of Cav1.2HCKO mice. Protein levels in cerebellum (Cereb) are unchanged. cGMP-dependent protein kinase I (cGKI; ~75 kd) was used as loading control.
(f) Immunoblot of NMDAR subunit NR1 and the Cav1.3 Ca2+ channel. ERK 1/2 and cGMP-dependent protein kinase I (cGKI; ~75 kd) were used as loading control, respectively.
(g) Expression level of the Cav1.2 protein in the hippocampal formation of young (2-3 weeks old) and adult (>6 weeks old) mice demonstrate the postnatal knockout of Cav1.2.
- supplemental material
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Suppl. Fig. S2. Labyrinth maze test. This spatial learning task consisted of a horizontal maze made from transparent acrylic glass tubes
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Suppl. Fig. S3. Mice with an inactivation of the CACNA1C gene in hippocampal pyramidal cells (Cav1.2HCKO) display a normal basal synaptic transmission in the CA1 region.
Panel a) Relation between the fEPSP slope and the fiber volley amplitude evoked by stimulation of the Schaffer collaterals in control (?) and Cav1.2HCKO (?) mice. The data points shown were pooled from experiments in 8 slices from 2 control mice and 7 slices from 2 Cav1.2HCKO mice.
Panels b and c) Representative fEPSPs and fiber volleys from control (ctr) and Cav1.2HCKO (ko) mice. fEPSP were recorded in normal aCSF (left). Fiber volleys were recorded in aCSF containing DNQX (10 µM) and APV (50 µM) (right). Scale bars for the fEPSPs on the left are 2.5 ms and 0.25 mV. Scale bars for fiber volleys on the right are 1 ms and 100 µV.
