Analgesia induced by 2- or 100-Hz electroacupuncture in the rat tail-flick test depends on the anterior pretectal nucleus

Aims

The anterior pretectal nucleus (APtN) and electroacupuncture (EA) activate descending mechanisms to modulate nociceptive inputs in the spinal dorsal horn. This study examines qualitatively whether mechanisms in the APtN participate in the EA-induced analgesia in rats.

Main methods

The tail-flick test was utilized to examine the changes produced by non-selective antagonists of serotonergic (methysergide, 37 pg), muscarinic (atropine, 10 ng) and opioid (naloxone, 10 ng) receptors; selective antagonists against μ (CTOP, 6.4 μg), δ (ICI174,864, 6.9 μg) or κ (nor-BNI, 7.3 μg); 5HT₁ (methiothepin, 0.47 μg), 5HT₂ (ketanserin, 5.4 μg), or 5HT₃ (MDL 72222, 15.7 μg); and GABA_A (bicuculline, 150 ng) receptors injected into the dorsal (d) or ventral (v) APtN on the antinociception induced by a 20-min EA applied at 2- or 100-Hz frequency to the Zusanli and Sanyinjiao acupoints.

Key findings

The 2-Hz EA-induced analgesia was blocked by naloxone, CTOP or atropine, was less intense after bicuculline, was shorter after methysergide or methiothepin in dAPtN, and was less intense after methysergide, methiothepin and bicuculline in vAPtN. The 100-Hz EA-induced analgesia was less intense after methysergide, methiothepin and CTOP in vAPtN, and remained unchanged after injection of the antagonists into the dAPtN.

Significance

The 2-Hz EA-induced analgesia utilizes cholinergic muscarinic, μ-opioid, GABA_A and 5-HT₁ mechanisms in the dAPtN and μ-opioid and 5-HT₁ mechanisms in the vAPtN, while 100-Hz EA-induced analgesia utilizes μ-opioid and 5-HT₁ mechanisms in the vAPtN but does not utilize them in the dAPtN.