Neuroscience 2002 Abstract
| Presentation Number: | 545.2 |
|---|---|
| Abstract Title: | PROTEIN KINASE Cγ MEDIATES ETHANOL WITHDRAWAL HYPERRESPONSIVENESS IN SPINAL CORD MOTOR NEURONS: ELECTROPHYSIOLOGICAL AND IMMUNOCYTOCHEMICAL STUDY. |
| Authors: |
Li, H. F.*1
; Mochly-Rosen, D.1
; Kendig, J. J.1
1Dept. of Anesthesia, Stanford Univ Med Ctr, Stanford, CA |
| Primary Theme and Topics |
Synaptic Transmission and Excitability - Intracellular Signalling Pathways -- Protein phosphorylation |
| Secondary Theme and Topics | Neurological and Psychiatric Conditions<br />- Addiction and Drugs of Abuse<br />-- Alcohol, barbituates, and benzodiazepines |
| Session: |
545. Synaptic transmission: protein phosphorylation I Poster |
| Presentation Time: | Tuesday, November 5, 2002 2:00 PM-3:00 PM |
| Location: | Hall A2-B3 D-63 |
| Keywords: | PKCgamma, NMDA receptor, Alcohol, Spinal cord slices |
NMDA-evoked currents in motor neurons of spinal cord slices from rats 7-10 days old display ethanol (EtOH) withdrawal hyperresponsiveness, as a rebound of currents to levels above control after exposure to 100 mM EtOH and wash. The non-specific PKC inhibitor H7 decreased the occurrence of withdrawal (Li & Kendig, SFN 2001). In the present report, we carried out electrophysiological and immunocytochemical experiments to test the hypothesis that the PKCγ isoform mediates the EtOH withdrawal. Excitatory postsynaptic currents were evoked by picosprizing 2 mM NMDA onto single motor neurons using patch clamp techniques in slices taken from p7-10 rat spinal cord lumbar section. EtOH (100 mM, 20 min) depressed the area of currents to 70 ± 4% (n=11) of control. On washout, current area rebounded to 132 ± 6% (n=11) of control. A PKCγ isoform-specific peptide inhibitor, applied 30 min before EtOH, concentration dependently suppressed the withdrawal. Immunocytochemical analysis revealed that spinal cord motor neurons contain abundant PKCγ. In control slices, perfused by ACSF for 70 min, PKCγ immunoreactives were concentrated around motor neuron nuclei. However, in slices perfused by ACSF for 30 min followed by ACSF plus 100 mM EtOH for 20 min then wash for 20 min, PKCγ immunoreactives diffused to the cytoplasm, suggesting intracellular translocation of PKCγ isoform during EtOH withdrawal. This translocation of PKCγ isoform was prevented by the PKCγ isoform-specific peptide inhibitor. Our results support the hypothesis that activation of PKCγ isoform is required for ethanol withdrawal hyperresponsiveness. Supported by NIH Grant NS 13108 to JJK.
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2002 Neuroscience Meeting Planner. Orlando, FL: Society for Neuroscience, 2002. Online.
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