Neuroscience 2005 Abstract
| Presentation Number: | 729.4 |
|---|---|
| Abstract Title: | Role of CB1 and novel cannabinoid receptors in the blockade of hippocampal long-term potentiation (LTP) following repeated exposure to δ<sup>9</sup>-THC. |
| Authors: |
Hoffman, A. F.*1,2
; Oz, M.1,2
; Lupica, C. R.1,2
1Cellular Neurobiology Branch, U.S. Dept. of Health and Human Services, National Inst. of Health, National Inst. on Drug Abuse, Intramural Research Program, Baltimore, MD 2Neurophysiology Section, U.S. Dept. of Health and Human Services, National Inst. of Health, National Inst. on Drug Abuse, Intramural Research Program, Baltimore, MD |
| Primary Theme and Topics |
Neural Excitability, Synapses, and Glia: Cellular Mechanisms - Synaptic Transmission -- Modulation |
| Secondary Theme and Topics | Neural Excitability, Synapses, and Glia: Cellular Mechanisms<br />- G-Protein Linked Receptors<br />-- Other |
| Session: |
729. Synaptic Modulation: Atypical Compounds Poster |
| Presentation Time: | Tuesday, November 15, 2005 4:00 PM-5:00 PM |
| Location: | Washington Convention Center - Hall A-C, Board # J4 |
| Keywords: | CANNABINOIDS, DRUG ABUSE, SLICE, SYNAPTIC PLASTICITY |
Memory deficits produced by marijuana are thought to arise, in part, via the interaction of the psychoactive component, Δ9-THC, with cannabinoid (CB) receptors located in the hippocampus. Whereas CBs acutely disrupt synaptic transmission and hippocampal long-term potentiation (LTP), a putative synaptic correlate of memory, the consequences of prolonged exposure to Δ9-THC on hippocampal function are less well understood. Sprague Dawley (SD) rats were treated once daily for 7 days with either a vehicle control solution or Δ9-THC (10 mg/kg). Hippocampal brain slices were prepared approximately 24 hours following the final treatment, and electrophysiological recordings were performed in the CA1 region. Relative to vehicle-treated controls, repeated Δ9-THC treatment completely blocked the LTP generated by both high-frequency stimulation(HFS, 100 Hz) and by a theta-burst stimulation protocol. Tolerance to the inhibitory effects of the CB agonist WIN55,212-2 was observed at GABAergic, but not glutamatergic, synapses. We have recently shown that CB-mediated inhibition of glutamate release in the hippocampus occurs through a novel, non-CB1 receptor that is expressed in SD rats but not in C57BL/6J mice (Lupica et al. Soc.Neurosci.Abst. 2005). Thus, to clarify the identity of the receptor responsible for the observed blockade of LTP, we examined the effect of repeated Δ9-THC treatment on LTP in C57BL/6J mice. In contrast to our findings in SD rats, this treatment did not significantly impair LTP in C57BL/6 wildtype (+/+) mice. These data suggest that prolonged exposure to Δ9-THC may block LTP through an interaction with a novel, uncloned non-CB1 cannabinoid receptor located on Schaffer collateral axon terminals.
Supported by NIDA-IRP
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2005 Neuroscience Meeting Planner. Washington, DC: Society for Neuroscience, 2005. Online.
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