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Biomedical subjects

A G Hayes

Publications and source records attributed to A G Hayes.

67 records · Page 4Linked to original sources
PubMed1983

Antinociceptive profile of dynorphin in the rat.

Morphine, bremazocine, dynorphin(1-17) and two of its fragments (1-13) and (1-8) all increased nociceptive pressure thresholds in the rat after intracerebroventricular administration. Morphine also increased nociceptive heat thresholds in the hotplate test at similar dose-levels. In contrast, bremazocine and the dynorphins were totally inactive against the noxious heat stimulus. This profile of antinociceptive activity is typical of kappa receptor agonists.

Analgesics↗
PubMed1983

Determination of receptors that mediate opiate side effects in the mouse.

The effects of mu and kappa-opiate receptor agonists were studied in a variety of tests in the mouse designed to correspond to clinical side-effects in man. These included sedation, decrease in pupil diameter, Straub tail, decrease in body temperature, decrease in respiratory rate and inhibition of gut propulsion. The mu-receptor agonists tested produced opiate side-effects in the mouse at doses between 2.4 and 34 times higher than their antinociceptive doses in the abdominal constriction test. Their ranked orders of potency in producing these effects were very similar to their order of antinociceptive potency. In contrast, the kappa-receptor agonists only produced opiate side-effects at doses between 29 and greater than 2500 times higher than their antinociceptive doses. There was no correlation between the potency ratios in these tests and in the abdominal constriction test. It is concluded that mu-receptor agonists may produce both their antinociceptive effects and opiate side-effects by interacting with the mu-receptor. The kappa-receptor agonists have previously been shown to produce antinociception via the kappa-receptor, but the opiate-like side-effects which appear with some of the drugs at much higher doses are probably due either to interaction with the mu-receptor or to some other non-specific action.

Analgesics↗
PubMed1982

Antinociceptive activity of clonidine in the mouse, rat and dog.

The antinociceptive activities of clonidine have been determined against several qualitatively different noxious stimuli in the mouse, rat and dog. In these tests clonidine given subcutaneously was 6 to 7 times more potent than morphine. Both clonidine and morphine were more potent against responses to heat induced nociceptive stimuli than against responses to heat induced nociception or that induced by electrical tail stimulation. However, unlike morphine the effects of clonidine in these latter tests were only seen at doses that also caused sedation and so these animals were less able to respond to the nociceptive stimuli. In contrast in pressure, chemical and tooth pulp stimulation tests clonidine produced increases in nociceptive thresholds at doses which caused no overt signs of behavioural depression. Comparisons of the relative potencies of clonidine and the less lipophilic analogue 4-hydroxyclonidine given subcutaneously and intracerebroventricularly indicate that clonidine induced antinociception is predominantly centrally mediated. However, a peripheral component may also be present in the inhibition of acetylcholine-induced abdominal constriction in the mouse.

Analgesics↗
PubMed1982

Agonist effects of [D-Pro2,D-Phe7,D-Trp9]substance P--evidence for different receptors.

[D-Pro2,D-Phe7,D-Trp9]substance P contracted guinea-pig ileum (GPI) indirectly, probably via substance P (SP) receptors on postganglionic parasympathetic neurones. It also depolarised rat superior cervical ganglion cells and contracted the rabbit external jugular vein, suggesting an agonist action on SP receptors in these tissues. In contrast, it had weak antagonist activity on smooth muscle SP receptors in GPI. This suggests that the receptor in GPI smooth muscle may differ from those in the other tissues.

Animals↗
PubMed1978

Effects of gamma-aminobutyric acid on nerve terminal excitability in a slice preparation of cuneate nucleus.

1 Superfusion of a slice preparation of the rat cuneate nucleus with gamma-aminobutyric acid (GABA) depolarized the afferent nerve fibres and increased their excitability. However, before the depolarization had reached its peak the increased excitability reversed to a decreased excitability, an effect which outlasted the depolarization. 2 Both components of the GABA excitability response were dose-related Cl--dependent and antagonized by bicuculline. 3 Possible mechanisms underlying the sequence of excitability changes are discussed.

Aminobutyrates↗