The anterior pretectal nucleus (APtN) participates in nociceptive and antinociceptive mechanisms. Drugs were injected into the ventral APtN to evaluate how intrinsic mechanisms interact in the nucleus during persistent
allodynia produced by a
surgical incision in a rat hind paw.
Naloxone (1 and 10 ng/0.08 microl),
methysergide (0.037 and 3.7 ng/0.08 microl) or
atropine (0.1 and 10 ng/0.08 microl) increased the
allodynia. The effect of
methysergide was intensified by
naloxone or
atropine, the effect of
atropine was intensified by
naloxone or
methysergide, but the effect of
naloxone was not changed by
methysergide or
atropine.
DAMGO (1.5 microg/0.08 microl),
oxotremorine (5 microg/0.08 microl) or
serotonin (5 microg/0.08 microl) reduced the
allodynia. The effect of
DAMGO was less intense in
methysergide-treated rats but was not changed in
atropine-treated rats, the effect of
serotonin was not changed by
naloxone or
atropine, and the effect of
oxotremorine was not changed by
naloxone or
methysergide.
Baclofen (150 ng/0.08 microl) increased, whereas
phaclofen (300 ng/0.1 microl) reduced the
allodynia.
Bicuculline (50 ng/0.08 microl) increased the incision
pain, while
muscimol (50 ng/0.08 microl) did not change it.
Phaclofen was inhibited by
methysergide but was unchanged by
atropine. The effect of
DAMGO was reduced by
phaclofen (100 ng/0.1 microl). We interpret these results as indicative that noxious inputs utilize
cholinergic and serotonergic pathways in the vAPtN for the activation of descending
pain control mechanisms, the serotonergic pathway being under the control of GABAergic neurons which, in turn, are modulated negatively by
opioid nerve terminals.