Neuroscience 2002 Abstract
| Presentation Number: | 812.14 |
|---|---|
| Abstract Title: | Cannabinoids inhibit Nucleus Accumbens neuronal responses to baso-lateral amygdala and prefrontal cortex stimulation. |
| Authors: |
Pistis, M.*1
; Pillolla, G.1
; Muntoni, A. L.2
; Melis, M. R.1
; Argiolas, A.1
; Perra, S.1
; Gessa, G. L.1
1Dept. of Neuroscience, Univ. of Cagliari, Cagliari, Italy 2C.N.R. Inst. of Neurogen. Neuropharm., Cagliari, Italy |
| Primary Theme and Topics |
Neurological and Psychiatric Conditions - Addiction and Drugs of Abuse -- Basic Mechanisms |
| Secondary Theme and Topics | Synaptic Transmission and Excitability<br />- Synaptic Transmission<br />-- Postsynaptic mechanisms: Excitatory |
| Session: |
812. Addiction and drugs of abuse: basic mechanisms II Poster |
| Presentation Time: | Wednesday, November 6, 2002 2:00 PM-3:00 PM |
| Location: | Hall A2-B3 AA-18 |
| Keywords: | electrophysiology, accumbens shell, rat |
The Nucleus Accumbens (NAc) represents a critical site for the rewarding properties of drugs of abuse. Glutamatergic afferents to the NAc are involved in the actions of psychostimulants and opioids, while the potentiation of dopaminergic neurotransmission in the NAc is a common feature of abused drugs, including cannabinoids. Cannabinoid receptors (CB1) are densely expressed in regions that provide excitatory innervation to the NAc, such as the amygdala, the cortex and the hippocampus. In this study we recorded extracellularly from neurons in the shell of the NAc which responded to the stimulation of the baso-lateral amygdala (BLA) or the medial prefrontal cortex (PFC) in urethane anaesthetized rats. The generation of action potentials in NAc neurons induced by BLA or PFC stimulation was strongly inhibited by the synthetic cannabinoid agonists WIN 55212,2 (0.062-0.25 mg/kg, i.v.) and HU-210 (0.125-0.25 mg/kg, i.v.) or the psychoactive principle of Cannabis Δ9-tetrahydrocannabinol (1.0 mg/kg, i.v.). Neither the D1 or D2 dopamine receptor antagonists (SCH23390 0.5-1.0 mg/kg, sulpiride 5-10 mg/kg, i.v.) or the opioid antagonist naloxone (1.0 mg/kg, i.v.) were able to reverse the action of cannabinoids, while the selective CB1 receptor antagonist/reverse agonist SR141716A (0.5 mg/kg, i.v.) fully suppressed the action of cannabinoid agonists, whereas per se had no significant effect. These results provide evidence that cannabinoids, in common with other drugs of abuse, strongly inhibit the excitability of neurons in the shell of the NAc.
Supported by C.N.R Young investigator award
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2002 Neuroscience Meeting Planner. Orlando, FL: Society for Neuroscience, 2002. Online.
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