RT Journal Article
SR Electronic
T1 Influence of dynorphin (1-13) on spinal reflexes in the rat.
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 508
OP 513
VO 246
IS 2
A1 R M Caudle
A1 L Isaac
YR 1988
UL http://jpet.aspetjournals.org/content/246/2/508.abstract
AB Previously, we showed that intrathecal administration of dynorphin A (1-13) (dynorphin) in rats produced, within 5 min, a reversible inhibition of tail-shock vocalization, a reversible hind-limb paralysis and an irreversible loss of the tail-flick reflex. The selective loss of the tail-flick reflex was investigated using electrophysiologic methods and a dose of dynorphin effective in 90% of the rats. These studies revealed that intrathecal administration of dynorphin resulted in loss of the C-fiber initiated reflex when assayed 1 to 30 days after injection. On the other hand, reflexes initiated by Group I and III afferents were not obviously different from those seen in saline-injected animals. Application of dynorphin in situ on to the cord during stimulation of the dorsal root and recording of ventral root potentials demonstrated a rapid onset of peptide action. Initially the C-fiber evoked reflex was potentiated selectively with a decrease in conduction time. These responses were followed by inhibition of all reflexes for a short period of time after which the reflexes initiated by Group I and III afferents reappeared whereas the C-fiber reflex did not recover. This time course paralleled closely the time course of the loss of the tail-flick reflex suggesting that the two effects may be causally related. Furthermore, the selective N-methyl-D-aspartate antagonist DL-2-amino-5-phosphonovalerate applied directly to the spinal cord during recording resulted in a reversible inhibition of the C-fiber-initiated reflex.(ABSTRACT TRUNCATED AT 250 WORDS)