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Neuroscience 2004 Abstract

Presentation Number: 690.1
Abstract Title: Cannabinoid receptor activation modulates frontal cortical norepinephrine efflux in rat brain.
Authors: Oropeza, V. C.*1 ; Page, M. E.2 ; Mackie, K.3 ; Van Bockstaele, E. J.1
1Dept of Neurosurgery, Thomas Jefferson Univ, Phila, PA
2PA, 900 Walnut St, 19107-6799,
3USA, 900 Walnut St, 19107-6799,

Primary Theme and Topics Neurological and Psychiatric Conditions
- Addiction and Drugs of Abuse
-- Cannabinoids
Secondary Theme and Topics Neurological and Psychiatric Conditions<br />- Addiction and Drugs of Abuse<br />-- Addiction: neurobiology
Session: 690. Drugs of Abuse: Cannabinoids
Poster
Presentation Time: Tuesday, October 26, 2004 8:00 AM-9:00 AM
Location: San Diego Convention Center - Hall A-H, Board # EEE10
Keywords: CANNABINOIDS, NOREPINEPHRINE, MICRODIALYSIS, IMMUNOHISTOCHEMISTRY
Δ9-tetrahydrocannabinol (THC), the main psychoactive ingredient in marijuana, exerts complex actions on modulatory neurotransmitters involved in attention and cognition. Though it is known that these effects are mediated via the cannabinoid (CB1) receptor, the precise pharmacological and anatomical mechanisms underlying these effects are poorly understood. Several of the cognitive and autonomic functions affected by cannabinoid administration are modulated by the noradrenergic brainstem nucleus locus coeruleus (LC) and its efferent projections to the frontal cortex (FC). Previous research performed in our laboratory has demonstrated that systemic administration of cannabinoid agonists alters norepinephrine (NE) release in the frontal cortex in a dose-dependent manner. Direct effects on noradrenergic neurons are supported by our previous electron microscopy studies showing that the receptor is present within somatodendritic processes in the LC. To further elucidate sites of action of cannabinoids in the coeruleo-cortical pathway, we utilized in vivo microdialysis coupled with direct reverse perfusion of WIN 55,212-2(WIN, 100 µM) into the FC. Direct application of WIN into the FC elicited an increase in extracellular NE (57% above baseline). To determine cellular sites of CB1 receptor activation, immunohistochemical analysis of CB1 receptor and dopamine-β-hydroxylase (DBH) was conducted in the same section of tissue in the FC. Confocal fluorescence and immunoelectron microscopy confirmed that axonal processes exhibited both CB1 and DBH immunoreactivity. Taken together, these data indicate that cannabinoid agonists may directly modulate the release of NE in the FC by acting on presynaptically distributed CB1 receptors that are located on noradrenergic axon terminals.
Supported by Jefferson Intramural Research Award A71501

Sample Citation:

[Authors]. [Abstract Title]. Program No. XXX.XX. 2004 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2004. Online.

Copyright © 2004-2025 Society for Neuroscience; all rights reserved. Permission to republish any abstract or part of any abstract in any form must be obtained in writing by SfN office prior to publication.

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