Effects of elevated calcium and calcium antagonists on 6,7-benzomorphan-induced analgesia

Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence

“…These studies indicate that brief, phasic nociceptive tests, such as the tail-flick and hot-plate tests, are unaffected by Ca 2 + (Harris et al 1975;Chapman and Way 1982), Ca2+ chelators (Harris et al 1975;Ben-Sreti et al 1983), or Ca2+ channel antagonists (Benedek and Sikszay 1984;Contreras et al 1988), while tonic nociceptive tests, such as the formalin and acetic acid-induced writhing tests, are sensitive to Ca 2 +, Ca2+ ionophores and Ca 2 + channel agonists (Chapman and Way 1982;Coderre and Melzack 1992b) which increase nociceptive responses, or Ca 2 + chelators and Ca 2 + channel antagonists (Del Pozo et al 1987;Coderre and Melzack 1992b;Miranda et al 1992) which reduce nociceptive responses.…”

Buspirone-induced antinociception is mediated by l-type calcium channels and calcium/caffeine-sensitive pools in mice

“…Conversely, Ca 2+ chelators (e.g., EGTA and EDTA) administered by i.c.v. injections enhance opioid antinociceptive effects (Kakunaga et al 1966;Harris et al 1975;Ben-Sreti et al 1983).…”

Resveratrol-induced antinociception is involved in calcium channels and calcium/caffeine-sensitive pools

“…Ca 2+ and Ca 2+ vectors such as X-537A and A23187 will shift Ca 2+ from extracelluar to intracellular, thereby increasing the intracellular Ca 2+ concentration, decreased analgesic effect of opioids [30, 31]. Intracerebral injection of Ca 2+ chelator EGTA can enhance the analgesic effect of opioids [32, 33]. Ca 2+ is very easy to penetrate from the NMDA receptor channel into intracellular [34, 35].…”