Gabaergic and cholinergic mediation in the antinociceptive action of homotaurine

Serrano, Isabel; Ruiz, Rosa María Ávila; Serrano, Juan Bautista Vivero; Fernández, Ana

doi:10.1016/0306-3623(92)90105-s

Cited by 10 publications

(2 citation statements)

References 35 publications

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“…GABAergic and opioid mechanisms activated by homotaurine might be involved in the interaction of the amino acid with K + ‐channels, because CGP 35348 – a highly selective GABA B antagonist – and naloxone inhibited the antinociceptive effect of homotaurine, and morphine at subanalgesic doses potentiated it [3]. CGP 35348 inhibits the antinociceptive effect of homotaurine both in the acetic acid and tail flick test, while baclofen – an agonist to GABA B receptors – potentiates homotaurine effect in the acetic acid test but it does not modify tail flick results [2,3]. It has been shown that agonists at these receptors increase K + current through voltage‐dependent channels that are usually inactivated in the resting membrane [32].…”

Section: Discussionmentioning

confidence: 99%

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Role of K⁺‐channels in homotaurine‐induced analgesia

Serrano

Asadi

et al. 2001

Fundamemntal Clinical Pharma

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In previous articles, antinociceptive activity for homotaurine has been demonstrated to be mediated by opioid, GABAergic and cholinergic mechanisms. GABAB‐agonists affect K+‐channels and it is known that K+‐channels modulate specific activation of opioid receptors. In this study, we examined the involvement of K+‐channels in the antinociceptive activity of homotaurine (22–445 mg/kg). Antinociceptive response was obtained after icv pretreatment with the channel specific blockers 4‐aminopyridine (voltage‐dependent channels), tetraethylammonium (Ca++ and voltage‐dependent) and gliquidone (ATP‐dependent). The nociceptive tests performed were acetic acid induced abdominal constriction (mice) and tail flick (rats) tests. Acetic acid responses to homotaurine were inhibited by tetraethylammonium (5 μg) and gliquidone (16 μg). Tail flick response to homotaurine was inhibited by tetraethylammonium (50 μg), gliquidone (40 and 80 μg) and 4‐aminopyridine (25 and 250 ng). These results suggest an involvement of the three types of K+‐channels in antinociception by homotaurine, depending on specific homotaurine and blocker doses. At a spinal level, they appear to be involved together with GABAB and opioid mechanisms. Peripherally, only tetraethylammonium channels would be substantially activated during homotaurine antinociceptive effect.

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Section: Discussionmentioning

confidence: 99%

“…Homotaurine (3‐APS) exerts an antinociceptive action in chemical and thermal nociceptive tests, where cholinergic, opioid and GABAergic mechanisms are involved [1–3]. Homotaurine may act as an agonist to GABA A receptors [4–6] and as a partial agonist to GABA B receptors [7,8].…”

Section: Introductonmentioning

confidence: 99%