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Inhibitory effects of glutamate‐induced activation of thalamic nucleus submedius are mediated by ventrolateral orbital cortex and periaqueductal gray in rats
Author(s) -
Zhang Sun,
Tang JingShi,
Yuan Bin,
Jia Hong
Publication year - 1998
Publication title -
european journal of pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.305
H-Index - 109
eISSN - 1532-2149
pISSN - 1090-3801
DOI - 10.1016/s1090-3801(98)90008-8
Subject(s) - periaqueductal gray , nociception , glutamate receptor , inhibitory postsynaptic potential , chemistry , brainstem , stimulation , spinal cord , medicine , neuroscience , endocrinology , reflex , anesthesia , central nervous system , midbrain , biology , receptor
This study found that in lightly‐anesthetized rats a unilateral micro‐injection of glutamate (200 mm, 0.5 μ1) into the thalamic nucleus submedius (Sm) markedly depressed the radiant heat‐evoked tail flick (TF) reflex. After injection, the mean TFL increased 25.6 ± 6.5% ( n = 24) of the baseline at 5 min, up to a peak value (48.4 ± 7.2%) at 20 min, and recovered to the baseline level at 60 min. This inhibitory effect was dose‐related and repeatable over a time interval of 1.0–1.5 h in the same animal. Furthermore, micro‐injections of γ‐aminobutyric acid (GABA) (100 m m ) into the ipsilateral ventrolateral orbital cortex (VLO) (0.7μl), or bilaterally into the lateral or ventrolateral parts of the periaqueductal gray (PAG) (0.5 μ1 on each side), eliminated the Sm‐evoked inhibition. After GABA was injected into VLO or PAG, the Sm applications of glutamate failed to produce any significant changes in TFL, with the TFL changes being similar to the saline control ( p >0.05). These results confirmed our previous findings that electrical stimulation of Sm depressed the rat TF reflex and that this inhibitory effect was blocked by electrolytic lesion of the VLO or PAG. Therefore, the present study provides further support for the hypothesis that Sm plays an important role in modulation of nociception, and that its effects are mediated by the VLO‐PAG pathway, leading to activation of the brainstem descending inhibitory system and depression of the nociceptive inputs at the spinal cord level.