Brain region-specific studies of the excitatory behavioral effects of morphine-3-glucuronide

Halliday, Andrew J., Bartlett, Selena E., Colditz, Paul and Smith, Maree T. (1999) Brain region-specific studies of the excitatory behavioral effects of morphine-3-glucuronide. Life Sciences, 65 2: 225-236. doi:10.1016/S0024-3205(99)00239-8

Author Halliday, Andrew J.
Bartlett, Selena E.
Colditz, Paul
Smith, Maree T.
Title Brain region-specific studies of the excitatory behavioral effects of morphine-3-glucuronide
Journal name Life Sciences   Check publisher's open access policy
ISSN 0024-3205
Publication date 1999-06-04
Sub-type Article (original research)
DOI 10.1016/S0024-3205(99)00239-8
Volume 65
Issue 2
Start page 225
End page 236
Total pages 12
Editor R. Bressler
S. Z. Langer
Place of publication New York
Publisher Elsevier B.V.
Collection year 1999
Language eng
Subject C1
730104 Nervous system and disorders
111501 Basic Pharmacology
Abstract This study was designed to determine in rats whether morphine-3-glucuronide (M3G) produces its neuro-excitatory effects most potently in the ventral hippocampus (as has been reported previously for subanalgesic doses of opioid peptides). Guide cannulae were implanted into one of seven regions of the rat brain: lateral ventricle; ventral, CA1 and CA2-CA3 regions of the hippocampus; amygdala; striatum or cortex. After a 7 day recovery period, rats received intracerebral injections of (i) M3G (1.1 or 11 nmol) (ii) DADLE ([D-Ala(2),D-Leu(5)]enkephalin), (45 nmol, positive controls) or (iii) vehicle (deionised water), and behavioral excitation was quantified over 80 min. High-dose M3G (11 nmol) evoked behavioral excitation in all brain regions but the onset, severity and duration of these effects varied considerably among brain regions. By contrast, low-dose M3G (1.1 nmol) evoked excitatory behaviors only when administered into the ventral hippocampus and the amygdala, with the most potent effects being observed in the ventral hippocampus. Prior administration of the nonselective opioid antagonists, naloxone and beta-funaltrexamine into the ventral hippocampus, markedly attenuated low-dose M3G's excitatory effects but did not significantly alter levels of excitation evoked by high-dose M3G. Naloxone given 10 min after M3G (1.1 or 11 nmol) did not significantly attenuate behavioral excitation. Thus, M3G's excitatory behavioral effects occur most potently in the ventral hippocampus as reported previously for subanalgesic doses of opioid peptides, and appear to be mediated through at least two mechanisms, one possibly involving excitatory opioid receptors and the other, non-opioid receptors.
Keyword Medicine, Research & Experimental
Pharmacology & Pharmacy
Ventral Hippocampus
Behavioral Excitation
Intracerebral Administration
Sensory Neurons
Q-Index Code C1

Document type: Journal Article
Sub-type: Article (original research)
Collections: School of Pharmacy Publications
Centre for Integrated Preclinical Drug Development Publications
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Citation counts: TR Web of Science Citation Count  Cited 23 times in Thomson Reuters Web of Science Article | Citations
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Created: Mon, 13 Aug 2007, 11:12:28 EST