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Chronic morphine increases calbindin D28k in rat striatum: possible NMDA receptor involvement
1Department of Otolaryngology, University School of Medicine, New Orleans, LA 70112-2699.
Neuroreport
|October 25, 1993
Summary
Chronic morphine treatment alters calbindin D28k expression in the rat striatum, particularly in the patch compartment. This change, linked to calcium signaling, may explain how NMDA receptor antagonists inhibit morphine tolerance.
Area of Science:
- Neuroscience
- Neuropharmacology
- Calcium Signaling
Background:
- Calbindin D28k is a neurochemical marker in the striatum, typically absent in the mu-opiate receptor-rich striosomal (patch) compartment.
- Chronic morphine administration is known to elevate calcium levels in rat striatal synaptosomes.
Purpose of the Study:
- To investigate the effects of chronic morphine treatment on calbindin D28k immunoreactivity (ir) in the rat brain.
- To explore the role of NMDA receptors in mediating these morphine-induced changes.
Main Methods:
- Immunocytochemistry was used to assess calbindin-ir in rat brain sections.
- Rats were treated with morphine for 5 days, with some receiving co-administration of the NMDA receptor antagonist MK-801.
Main Results:
- Morphine treatment increased calbindin-ir in both the striatal matrix and the patch compartment.
- The induced calbindin-ir in patches persisted for at least 14 days post-treatment.
- Co-administration of MK-801 blocked the morphine-induced increase in calbindin-ir in the patch compartment.
Conclusions:
- Chronic morphine treatment increases calbindin D28k levels in the striatum, suggesting a role for calcium and glutamatergic transmission.
- These findings provide a potential mechanism and anatomical basis for MK-801's ability to inhibit morphine tolerance.