Amygdalar neuronal responses to peripheral nociceptive stimuli in rats.

Amygdala plays a very important role in the mediation of pain. In the present study the behaviour of the amygdalar neurons in response to various peripheral noxious stimuli was observed. Noxious mechanical, thermal, electrical, chemical and the non-noxious stimuli (touch) were applied individually to the animal and then the neuronal responses to these stimuli were recorded. Our results showed that the majority of amygdalar units recorded from medial, lateral and basolateral nuclei, responded to different peripheral noxious (thermal, electrical, chemical mechanical) and non-noxious stimuli by excitation. However few neurons decreased their activity on stimulation. Some of these neurons also exhibited after discharge following application of higher intensity of noxious stimuli.

Resiniferatoxin-induced loss of plasma membrane in vanilloid receptor expressing cells.

Resiniferatoxin (RTX), a potent analog of capsaicin, was evaluated electrophysiologically in dorsal root ganglion (DRG) cells and cell lines ectopically expressing the vanilloid receptor type 1 (VR1) to determine if cell phenotype influenced RTXs neurotoxic properties. Furthermore, capsaicin and heat activation of VR1 were evaluated in these cells to determine if cellular damage was unique to RTX activation of the receptors. RTX application to DRG cells identified as type 1, 2 or 5, cell types known to express VR1, induced large inward currents. RTX did not induce currents in DRG cells that do not express the receptor (type 4 cells). In cell lines ectopically expressing VR1, RTX-induced similar currents. RTX produced no effect in non-transfected cells. After exposure to RTX both DRG cells and transfected cells failed to respond to subsequent applications of the agonist. In addition, whole cell capacitance was reduced up to 70%. The decrease in capacitance was associated with the loss of plasma membrane, as determined by confocal microscopy. Cell phenotype, other than VR1 expression, did not influence the response to RTX. Interestingly, capsaicin and heat activation of vanilloid receptors also decreased cell capacitance, but the loss of membrane was not as great as with RTX and responses to these stimuli were not lost after the initial exposure. The loss of cell membrane required elevated intracellular levels of Ca2+. From these data it was concluded that the loss of cell membrane was dependent on the presence of both VR1 and intracellular Ca2+ accumulation, but not on cell phenotype.