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Morphine-induced changes in cerebral and cerebellar nitric oxide synthase activity
J C Leza1, I Lizasoain, O San-Martín-Clark
1Departamento de Farmacología, Facultad de Medicina, Universidad Complutense de Madrid, Spain.
European Journal of Pharmacology
|October 4, 1995
Summary
Morphine treatment increases nitric oxide (NO) synthase activity in the mouse cerebellum. This effect, observed with both acute and chronic administration, is blocked by naloxone, suggesting a link between opiates and the L-arginine: NO pathway.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Nitric oxide (NO) plays a crucial role in various physiological processes in the brain.
- Opiate drugs, like morphine, are known for their complex effects on the central nervous system.
- Understanding the interaction between opiates and NO signaling is important for elucidating neurobiological mechanisms.
Purpose of the Study:
- To investigate the impact of acute and chronic morphine administration on nitric oxide synthase (NOS) activity in the mouse brain.
- To determine if naloxone, an opioid antagonist, can block morphine-induced changes in NOS activity.
- To explore the relationship between opiate effects and the L-arginine: NO pathway.
Main Methods:
- Measurement of nitric oxide (NO) synthase activity by quantifying the conversion of [14C]arginine to [14C]citrulline.
- Administration of acute morphine and chronic morphine (via subcutaneous pellets) to mice.
- Co-administration of morphine with naloxone.
- Analysis of NOS activity in specific brain regions: cerebellum, frontal cortex, and forebrain.
Main Results:
- Acute morphine treatment significantly increased Ca2+-dependent NO synthase activity in the cerebellum.
- This increase in cerebellar NO synthase activity induced by acute morphine was completely blocked by co-administration with naloxone.
- Chronic morphine treatment also led to an elevation in cerebellar NO synthase activity, peaking on the second day of pellet implantation.
- No significant alterations in NO synthase activity were observed in the frontal cortex or forebrain following either acute or chronic morphine treatment.
Conclusions:
- Morphine administration, both acutely and chronically, enhances nitric oxide synthase activity in the mouse cerebellum.
- The involvement of the L-arginine: NO pathway is implicated in the central effects of opiates.
- Naloxone can antagonize the effects of morphine on cerebellar NO synthase, highlighting the opioid receptor-mediated nature of this response.