both ultrastructural and functional levels suggest that this nucleus may play an important role in
the morphine-induced analgesia. This study was designed to determine neuronal activity and
responsiveness to peripheral morphine administration in the nucleus coneiformis of rat.
Materials and Methods: In this study, neural activity of cuneiform neurons in response to
peripheral administration of morphine was recorded by extracellular single unit recording
technique. Firing rate of neurons was recorded in four groups: intact group (n=19) to determine
the spontaneous (baseline) activity, saline group (n=20), morphine group (n=39) and morphine +
naloxone group (n=12), before and after drug administration.
Results: Our findings showed that the firing rate in majority of cuneiform neurons decreased
after morphine (3.8 mg/kg; SC) administration. Activity of neurons (n=39) in the cuneiform neurons
was reduced significantly (P<0.01) after morphine injection (6.66±0.67 spike/sec) in comparison
with pre-injection time (12.47±1.84 spike/sec) and the saline group (11.6±1.58 spike/sec). The
firing rate and response pattern of many of neurons in response to peripheral application of
morphine were reversed after naloxone injection (2 mg/kg; SC) in this nucleus.
Conclusion: Based on the above findings, we suggest that the changes of activity pattern in
spontaneous activity of cuneiform neurons in response to peripheral administration of morphine
maybe resulted from direct action of morphine on opioid receptors in the nucleus cuneiformis.
Nevertheless, the role of pain transmission and modulation pathways are still important in the
antinociceptive effect of morphine as well.
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