Effects of Ketamine and Three Other Anaesthetics on Spinal Reflexes and Inhibitions in the Cat

Abstract

The effects of ketamine, alphaxalone/alphadolone, methohexitone and di-isopropylphenol have been compared on synaptic excitations and inhibitions in the spinal cord of decerebrate or pentobarbitone-anaesthetized cats. Ketamine selectively and reversibly decreased polysynaptic reflexes over a wide dose range. With the other three anaesthetic drugs decreases in reflex activity were accompanied by increases in the prolonged inhibition of reflexes, and in the amplitude and time course of dorsal root potentials. It was concluded that ketamine decreases synaptic transmission at terminals of excitatory interneurones, whereas the other three anaesthetics enhance synaptic inhibitions mediated by gamma-aminobutyric acid. Such specific effects of anaesthetics on particular synaptic processes do not support a unitary hypotheses of anaesthesia.

The effects of sigma ligands and of neuropeptide Y on N‐methyl‐d‐aspartate‐induced neuronal activation of CA3 dorsal hippocampus neurones are differentially affected by pertussin toxin

“…Following the inactivation of Gj/0 proteins by PTX, the intravenous administration of DTG did not modify the neuronal response to NMDA and Quis, whereas the microiontophoretic application of DTG produced a slight but significant reduction of the excitatory effect of NMDA, but not of Quis, (Figures 2, 3 (Anis et al, 1983;Lodge & Anis, 1984;Malouf et al, 1988). This inhibitory effect of sigma ligands has been ascribed, however, to their low affinity for the PCP binding site (Lodge et al, 1988;Malouf et al, 1988;Church & Lodge, 1990;Monnet et al, 1992b).…”

Inhibition by propofol (2,6 di‐isopropylphenol) of the N‐methyl‐D‐aspartate subtype of glutamate receptor in cultured hippocampal neurones

“…Electrophysiological recordings from the cat spinal cord have previously shown that propofol attenuates glutamate-mediated polysynaptic reflexes, as does the noncompetitive NMDA receptor antagonist, ketamine (Lodge & Anis, 1984). Furthermore, propofol inhibits glutamate-stimulated entry of Ca2" into rat synaptosomes (Bianchi & Galzigna, 1991).…”

“…Recent studies indicate that propofol potentiates y-aminobutyric-acid (GABA)-mediated inhibitory synaptic transmission and directly activates the GABAA receptor (Hales & Lambert, 1992;Hara et al, 1993;Orser et al, 1994). In addition, several reports suggest that propofol may also inhibit glutamate receptor-mediated excitatory synaptic transmission (Lodge & Anis, 1984;Bianchi & Galzigna, 1991).…”

Spinal effects of four injectable anaesthetics on nociceptive reflexes in rats: a comparison of electrophysiological and behavioural measurements

“…It has been shown that anaesthetics exert direct influences on the spinal cord, on both dorsal and ventral horn neurones, so as to modulate spinal function in response to sensory stimuli (for reviews see Heavner, 1975;Davidoff & Hackman, 1983; see also Lodge & Anis, 1984). Although some similarities in modulation of transmitter action may be observed between compounds (e.g.…”