Impact of medullary lesions on Solenace-plant extract-induced 
alterations in pain responsitivity as measured in the tailflick, 
hotplate, and formalin tests

Like other members of the Solenace family, Hyoscyamus niger (henbane) has been used in folk medicine for its profound sedative and analgesic properties. Much of henbanes' action may reflect the high concentration (relative to other solenaceae) of the anticholinergic compound hyoscine (scopolamine) found in the leaves and roots. The present study examined the effects of electrolytic lesions of the rostral ventral medulla (RVM) on extract-induced nociceptive alterations in the tail flick, hotplate, and formalin tests of nociceptive responsivity. While multiple CNS sites are critically involved in the mediation of nociceptive responsivity, converging data strongly suggest a role of cholinergic (muscarinic) receptors specifically in the nociceptive circuitry of the RVM. Animals (experimental group) received radio frequency lesions (AP 
-1.5, ML 0, DV +.2 from interaural zero; 1.0mA, 10sec) or sham  lesions (control group; consisted simply of lowering the electrode  toward the site). Following a two-week post-operative recuperation period, animals were given subcutaneous injections of extract or equivolume saline. Nociceptive sensitivity was tested via hot plate, tail-flick, and formalin paradigms. Following testing, animals were euthanized via sodium pentobarbital overdose and perfused transcardially with 10% formalin. Histological verification of lesion extents in brain tissue is currently in progress. Our preliminary analysis of the results suggests that across the multiple experiments, animals receiving radio-frequency lesions of the RVM do not differ in their responsivity to the analgesic properties of a solenace plant extract (here henbane), delivered subcutaneously, and  dose adjusted to a standard of 1mg/ml/kg of scopolamine. While tentative at this time, this result suggests that the nociceptive effects seen with solenace extracts may not reflect mediation through well-established descending pain modulatory circuitry.