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Histamine H2 receptors mediate morphine-induced locomotor hyperactivity of the C57BL/6J mouse
Abstract:
Morphine-induced locomotor hyperactivity of the C57BL/6J mouse was challenged with intracranial injections of antihistamines or the opiate antagonist naloxone. When cimetidine (H2 receptor blocker) was injected into the nucleus accumbens/stria terminalis, it significantly reduced opiate-stimulated locomotion. However, ventricular injections of cimetidine did not significantly alter either morphine or amphetamine hyperactivity, nor did cimetidine depress spontaneous locomotion. Although naloxone eliminated morphine-induced locomotion when injected into either the nucleus accumbens or the ventricles, chlorpheniramine (H1 receptor blocker) failed to reduce this behavior. These data suggest that opiate-stimulated locomotion of the C57BL/6J mouse may be partially mediated by histamine H2 receptors of the nucleus accumbens or closely adjacent structures.
Insights
Histamine H2 receptors in the brain may play a role in morphine-induced hyperactivity in mice. Blocking these receptors in specific brain regions reduced the stimulant effects of morphine.
Area of Science:
- Neuroscience
- Pharmacology
Background:
- Opioid drugs like morphine cause hyperactivity in mice.
- The exact brain mechanisms underlying this effect are not fully understood.
Purpose of the Study:
- To investigate the role of histamine receptors in morphine-induced locomotor hyperactivity.
- To determine if blocking histamine H1 or H2 receptors affects opioid-stimulated movement.
Main Methods:
- Intracranial injections of antihistamines (cimetidine, chlorpheniramine) and naloxone were administered to C57BL/6J mice.
- Injections targeted specific brain regions (nucleus accumbens/stria terminalis) or the ventricles.
- Locomotor activity was measured following drug administration.
Main Results:
- Cimetidine (H2 receptor blocker) injected into the nucleus accumbens/stria terminalis significantly reduced morphine-induced locomotion.
- Ventricular cimetidine injections did not affect morphine or amphetamine hyperactivity.
- Chlorpheniramine (H1 receptor blocker) did not reduce morphine-induced locomotion.
- Naloxone, an opiate antagonist, blocked morphine-induced locomotion.
Conclusions:
- Histamine H2 receptors, particularly in the nucleus accumbens or adjacent areas, may partially mediate morphine-stimulated locomotion in C57BL/6J mice.
- Histamine H1 receptors do not appear to play a significant role in this specific behavioral response.