Pain is a complex phenomenon and not completely understood. Understanding how the body modulates pain may lead to better care for patients in pain. Stimulation of the lateral hypothalamus (LH) produces analgesia in part through connections with the ventrolateral periaqueductal gray (vPAG), an area in the brainstem known to produce endogenous analgesia. However, the specific neurotransmitters involved have not been clearly defined. Substance P (subP) containing neurons have been identified in the LH and subP receptors have been identified on neurons in the vPAG. To test the hypothesis that LH-induced analgesia is mediated in part by a subP connection with the vPAG, the cholinergic agonist carbachol (125 nmol) was microinjected into the left LH of lightly anesthetized female Sprague-Dawley rats (250-350g), and moderate analgesia was obtained on the tail flick test . Cobalt Chloride (23µg/0.5µl), which blocks all synaptic activity in the area of injection, was microinjected into the left vPAG and partially blocked analgesia compared to controls (3.11 ± 0.18 vs. 4.96 ± 0.14 sec., respectively, p<0.05). The subP receptor antagonist L-703,606 (2µg/5µl) was then microinjected into the left PAG and also partially blocked LH-induced analgesia compared to controls (3.12 ± 0.16 vs. 4.96 ± 0.14 sec., respectively, p<0.05). Neither cobalt chloride nor L-703,606 produced a significant effect when microinjected into the vPAG alone. These data suggest that analgesia from LH stimulation is partially mediated subP connections with the vPAG, but this connection is not tonically active. Support Contributed By: USPHS grant NR04778 and T32-NR07075 from the National Institute of Nursing Research, and a predoctoral fellowship from the National Science Foundation
Session #1199 - Pain
The 29th Annual MNRS Research Conference (April 1-4, 2005)