The Effect Of Hypothalamic Arcuate Nucleus Lesion On The Hyperalgesia Of Inflammatory Rats

Objective: To study the effect of hypothalamic arcuate nucleus(ARC) lesion on thehyperalgesia of inflammatory rats, as well as its effect on c-fos expression in spinal cordto investigate the descending modulation from ARC on hyperalgesia.Methods: The peripheral inflammation model was established by sub-plantarinjection of complete Freund’s adjuvant （CFA）in rats. The thermal pain threshold wasmeasured by radiant heat-withdrawal method and the mechanical pain threshold wasmeasured by von Frey method. The neuronal activation at L4and L5of spinal cordwas evaluated immunohistochemically by c-fos expression. The lesion of ARC wasproduced in rats electrolytically and by neonatal injection of monosodiumglutamate(MSG).Results:(1) Hyperalgesia (decrease of thermal and mechanical pain threshold)appeared after injection of CFA, the peak time was at3h, and the hyperajgesic statecould last for17days and returned to baseline at21thday.(2) In MSG-treated rats thethermal and mechanical pain threshold were decreased at3h after CFA injection, but theamplitude of decrement was significantly less as compared with that in thehyperosmotic saline–treated rats. As control, injection of saline in both MSG-treatedand hyperosmotic saline-treated rats did not produce any significant change of thermaland mechanical pain threshold. It was suggested that the CFA-produced hyperalgesiawas significantly attenuated after the neuronal damage induced by MSG neonatally.(3)At3h after CFA injection the number of Fos-immunoreactive positive neurons in I-IIand V-VI laminae of dorsal horn of spinal cord at L4and L5level was significantly lessthan that in hyperosmotic saline-treated rat, indicating that the neuronal excitability andthe inflammatory reactivity of dorsal horn of spinal cord was significantly deceasedafter neuronal damage induced by MSG..(4) In CFA-induced inflammatory rats boththermal and mechanical pain thresholds were increased significantly after ARC lesion ascompared with those in the sham lesioned rats, showing that ARC lesion could also attenuate the hyperalgesia induced by CFA.Conclusions: Under the condition of the existence of peripheral inflammation,ARC lesion induced by electrolytical method or by neonatal MSG injection couldattenuate the hyperalgesia. It suggested that ARC takes part in the hyperalgesia inducedby peripheral tissue inflammation. Both the hyperalgesia and the Fos expression inspinal cord were attenuated electrolytical lesion of ARC lesion, indicating that adescending facilitatory influence was elicited from ARC to spinal cord excitability andhyperalgesia in rats with peripheral inflammation.