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The ventral portion of the anterior pretectal nucleus controls descending mechanisms that initiate neuropathic pain in rats
Author(s) -
Rossaneis Ana C,
Prado Wiliam A
Publication year - 2015
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12391
Subject(s) - neuropathic pain , pretectal area , sciatic nerve , medicine , anesthesia , lesion , inhibitory postsynaptic potential , stimulation , endocrinology , central nervous system , midbrain , pathology
Summary Stimulating the dorsal anterior pretectal nucleus ( dAPtN ) in rats is more effective than stimulating the ventral AP tN ( vAPtN ) at reducing tail‐flick latency, whereas stimulation of the vAPtN is more effective at reducing postoperative pain behaviour. This study examines whether a cell lesion caused by injecting N‐ methyl‐ D ‐aspartate into the dAPtN or vAPtN changes the withdrawal threshold of a rat hind paw during different phases of the tactile hypersensitivity induced by a chronic constriction injury ( CCI ) of the contralateral sciatic nerve. The number of Fos immunoreactive cells in the AP tN was also evaluated. The rats whose vAPtN was lesioned 2 days before CCI had more intense tactile hypersensitivity 2 days after CCI than that of the control group, but the groups were not different 7 days after the CCI . The rats whose vAPtN was lesioned 5 days after CCI had withdrawal thresholds that did not differ significantly 7 days after the CCI . The tactile hypersensitivity of the rats whose dAPtN was lesioned 2 days before or 5 days after CCI was not different from that of the control on the second and seventh days after the CCI . The number of Fos immunoreactive cells in the vAPtN and dAPtN increased 2 days after CCI , but did not differ from that in the control 7 days after CCI . We conclude that vAPtN and dAPtN cells are activated by nerve injury; the vAPtN exerts inhibitory control of the initial phase of neuropathic pain whereas the dAPtN does not appear to exert an inhibitory effect in neuropathic processing.