Neuroscience 2000 Abstract
| Presentation Number: | 773.13 |
|---|---|
| Abstract Title: | Tolerance to, and precipitated withdrawal from, chronic cannabinoid effects on memory, is reflected in task-relevant encoding by ensembles of hippocampal neurons. |
| Authors: |
Deadwyler, S. A.*1
; Jordan, E. R.1
; Simeral, J. D.1
; Smulders, T. V.1
; Hampson, R. E.1
1Dept Physiol & Pharmacol, Wake Forest Univ Sch Med, Winston-Salem, NC |
| Primary Theme and Topics |
J. Disorders of the Nervous System and Aging - 146. Drugs of abuse: opioids and others |
| Secondary Theme and Topics | I. Neural Basis of Behavior<br />- 109. Learning and memory: pharmacology |
| Session: |
773. Drugs of abuse: miscellaneous compounds Poster |
| Presentation Time: | Wednesday, November 8, 2000 1:00 PM-2:00 PM |
| Location: | Hall G-J |
| Keywords: | delayed-nonmatch-to-sample, population |
This study complements a prior study of chronic delta-9-THC effects on memory during a delayed-nonmatching-to-sample task (Deadwyler et al 1995). Rats were exposed to a single high dose (3.75 mg/kg) of WIN 55,212-2 (WIN-2) before each DNMS session for a 35 day period. Tolerance to the memory debilitating effects of WIN-2 developed over 35 days, with eventual recovery of control performance despite initial impairment from the high dose. On day 36, withdrawal was precipitated with the CB1 receptor antagonist SR141617A (5.0 mg/kg, NIDA), producing frank behavioral withdrawal (Rubino et al. 1998), and depression of DNMS performance. These effects dissipated within 2-4 days and performance returned to normal. Simultaneous recording of ensembles of hippocampal neurons revealed that initial exposure to WIN-2 produced a >40% decrease in Sample and Delay phase ensemble coded firing (Heyser et al 1993), reflecting the selective suppression of functional cell types that preferentially fire during those phases of the DNMS task. Firing returned to control levels however, with the same timecourse as behavioral tolerance to the drug. SR141716A precipitated withdrawal produced a decrease in neural activity similar to acute injections of cannabinoids. Using this same paradigm we have shown that chronic exposure to cannabinoid receptor agonists (THC and WIN-2) decreases receptor coupling to Gi/o proteins (Breivogel et al. 1999) which may account for the remarkable tolerance of cannabinoid dependent hippocampal processes shown here.
Supported by NIH grants DA03502, DA00119 (S.A.D.) & DA08549 (R.E.H.)
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2000 Neuroscience Meeting Planner. New Orleans, LA: Society for Neuroscience, 2000. Online.
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