Post-ictal analgesia: involvement of opioid, serotoninergic and cholinergic mechanisms

Opioid-mediated pain sensitivity in mice bred for high voluntary wheel running

“…Each individual received all three treatments (saline, 5 mg/kg, and 10 mg/kg naloxone) in a randomly determined order over the course of 6 days, with 48 h between each injection to avoid carryover effects of the previous treatment. The doses of 5 and 10 mg/kg naloxone have been previously reported to maintain a physiologically effective blockade of opiate receptors in rats [45]. A mouse received treatment at approximately the same time of day for each injection.…”

“…Injections began 2 h after lights off, which is during peak wheel-running activity [36,40]. The acute locomotor response was measured as the total number of wheel revolutions in the period from 10 to 50 min postinjection [45]. The first 10 min were excluded because saline injection decreases wheel running during this period [34].…”

Ictal analgesia in temporal lobe epilepsy – The mechanism of seizure-related burns

“…The effect of serotonergic transmission in pain-inhibition was first described by Coimbra and colleagues [19,12]. Henceforth, efforts have been made to elucidate the impact of 5HT 2A/2C receptors in the organization of postictal antinociception [13,16,34,35] and the recruitment of 5-HT 1A/1B , 5-HT 6 , 5-HT 7 receptor subtypes has been demonstrated [36].…”

“…Later experiments clarified the central analgesic role of the PAG-brainstem-rostral ventromedullar system (including the dorsal raphe nucleus, raphe magnus, locus coeruleus and the nucleus reticularis gigantocellularis/paragigantocellularis complex), alleviating pain under physiologic circumstances [12]. Via the lateral funiculus as a descending neural pathway, this system inhibits the ascent of painful stimuli entering the posterior horn of the spine [18,14]; then the spread of pain from the brainstem up to the thalamus and sensory cortex, using endogenous opioid and cannabinoid, serotonergic and noradrenergic pathways [19,18,[20][21][22][23]. The inhibitory network is recruited by the primary somatosensory cortex-orbitofrontal-cingular-amygdalar network allowing the impact of emotional/cognitive changes [20].…”

Do endogenous opioids and nitric oxide participate in the anticonvulsant action of dipyrone?

“…In the electroshock model, the reversal of the anticonvulsant effect of dipyrone by naloxone was not observed. The dose of naloxone used was the same as that used by Coimbra et al (18). Using the same kind of seizures in BALB/c mice, Chen et al (19) reported that naloxone reversed the anticonvulsant effect of morphine.…”