H. Mansikka et A. Pertovaara, THE ROLE OF ALPHA(2)-ADRENOCEPTORS OF THE MEDULLARY LATERAL RETICULARNUCLEUS IN SPINAL ANTINOCICEPTION IN RATS, Brain research bulletin, 37(6), 1995, pp. 633-638
We attempted to find out the role of alpha(2)-adrenoceptors of the med
ullary lateral reticular nucleus (LRN) in antinociception in rats. Spi
nal antinociception was evaluated using the tail-flick test, and supra
spinal antinociception using the hotplate test. Antinociceptive effect
s were determined following local electric stimulation of the LRN, and
following microinjections of medetomidine (an alpha(2)-adrenoceptor a
gonist; 1-10 mu g), atipamezole (an alpha(2)-adrenoceptor antagonist;
20 mu g) or lidocaine (4%) into the LRN. The experiments were performe
d using intact and spinalized Hannover-Wistar rats with a unilateral c
hronic guide cannula. Electric stimulation of the LRN as well as of th
e periaqueductal gray produced a significant spinal antinociceptive ef
fect in intact rats. Medetomidine (1-10 mu g), when microinjected into
the LRN, produced no significant antinociceptive effect in the tail-f
lick test in intact rats. However, following spinalization, medetomidi
ne in the LRN (10 mu g) produced a significant atipamezole-reversible
antinociceptive effect in the tail-flick test. In the hot-plate test,
medetomidine (10 mu g) in the LRN produced a significant atipamezole-r
eversible increase of the paw-lick latency in intact rats. Microinject
ion of atipamezole (20 mu g) or lidocaine alone into the LRN produced
no significant effects in the tail-flick test. The results are in line
with the previous evidence indicating that the LRN and the adjacent v
entrolateral medulla is involved in descending inhibition of spinal no
cifensive responses. However, alpha(2)-adrenoceptors in the LRN do not
mediate spinal antinociception but, on the contrary, their activation
counteracts antinociception at the spinal cord level. The spinal anti
nociceptive effect of supraspinally administered medetomidine in spina
lized rats can be explained by a spread of the drug (e.g., via circula
tion) which then directly activates alpha(2)-adrenoceptors at the spin
al cord level.