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V Kayser

Publications and source records attributed to V Kayser.

79 records · Page 5Linked to original sources
PubMed1983

Depressive effects of morphine and of an enkephalinase inhibitor on responses of ventro-basal thalamic neurones to noxious stimuli.

It has been shown that the responses of VB thalamic neurones to noxious mechanical and thermal stimuli are strongly depressed by low doses of Morphine (0,03; 0,1; 1 mg/kg i.v.) and to a lesser extent by ES 52 (a highly potent Thiorphan derivative) injected at higher doses (5; 10 mg/kg i.v). This last effect was less easily reversed by Naloxone than was the depressive effect of Morphine. Moreover, ES 52 can facilitate activity of some thalamic neurones induced by non-noxious mechanical stimuli.

Amino Acids, Sulfur↗
PubMed1983

Low dose of morphine strongly depresses responses of specific nociceptive neurones in the ventrobasal complex of the rat.

Effects of low intravenous doses of morphine (30, 100 and 1000 micrograms/kg) upon unitary responses of 22 'nociceptive' and 5 'non-nociceptive' units recorded in the ventrobasal (VB) complex of the rat were analyzed. The responses of the 'non-noxious' neurones were not depressed by morphine. By contrast, for all these doses there was a decrease of the total number of spikes and of the maximal firing rate of the responses of the noxious neurones. The depressive effect was significantly dose-related (with linear semi-logarithmic dose-response curve) and naloxone-reversible. Similar effects were observed upon responses to pinches and noxious heat. The ED50 which was close to 90 micrograms/kg for these thalamic responses to pinches is much more lower than that evaluated for spinal dorsal horn responses under the same anaesthetic conditions. Therefore the depressive effect of low doses observed for VB neurones seems to be mainly of supraspinal origin.

Animals↗
PubMed1982

Effects of systemic naloxone upon ventrobasal thalamus neuronal responses in arthritic rats.

This study deals with the effect of various doses of systemic naloxone (10 microgram, 300 microgram, 1 mg/kg) upon activities of 21 ventrobasa thalamus neurons recorded in 20 rats rendered arthritic by injection of Freund's adjuvant into the tail. These neurons presented reproducible responses to movement and/or mild lateral pressure on a joint and were recorded for at least 30 min after naloxone administration. Several neurons (5) were tested with two doses. After intravenous injection of naloxone at the dose of 10 microgram/kg (10 cases) there was a rapid decrease of the responses. The maximum effect occurred at 15 min when the mean value expressed as a percentage of the control was 46.20 +/- 8.51% (n = 10, P less than 0.001). Recovery could be considered as complete at 30 min. At the dose of 300 microgram/kg (9 cases), the decrease in the responses was less important, variable from one neuron to another but significant between 5 and 20 min (mean = 67.43 +/- 9.00% at 20 min, n = 7, P less than 0.01). At the dose of 1 mg/kg (7 cases), there was no significant modification of the response. Spontaneous firing rate of the neurons was slightly but significantly increased after injection of the two highest doses and unmodified after the lowest. The relationship between the depressive effect produced by low doses of naloxone upon the neuronal responses, and the 'bi-directional' analgesic-hyperalgesic action of the drug, demonstrated in these suffering rats, is discussed.

Action Potentials↗
PubMed1982

Aspirin clearly depresses responses of ventrobasal thalamus neurons to joint stimuli in arthritic rats.

This study dealt with the effect of aspirin upon activities of 17 ventrobasal thalamic neurons recorded in 17 rats rendered arthritic by injection of Freund's adjuvant into the tail. These neurons presented reproducible responses to mobilization and/or mild lateral pressure on a joint and were recorded for at least 40 min after aspirin administration. After intravenous injection of aspirin at the dose of 50 mg/kg (13 neurons tested), there was a progressive decrease in the number of spikes in the discharges. The maximum effect occurred at 30 min where the mean value of the response expressed as a percentage of the control was m = 34.62 +/- 7.5% (n = 13, p less than or equal to 0.001). Recovery was progressive and could be considered as complete at 60 min. By contrast, no significant modification of the spontaneous firing has been observed. With lower doses of aspirin (12.5 or 25 mg/kg tested with 4 neurons) there was respectively no clear depressive effect or only a transient decrease of the response.

Animals↗
PubMed1981

Dose-dependent analgesic and hyperalgesic effects of systemic naloxone in arthritic rats.

The effects of various i.v. naloxone doses (10 microgram, 300 microgram, 600 microgram, 1 mg/kg) were studied upon vocalization threshold to foot-pressure in 30 normal rats and 70 rats with Freund's adjuvant-induced arthritis. In arthritic rats, the lowest naloxone doses yielded a clear increase in pressure required to trigger vocalization (i.e. were analgesic) while the highest dose (1 mg/kg) was hyperalgesic. In normal rats, naloxone never induced significant changes in the vocalization threshold.

Animals↗
PubMedDate not supplied

Effects of ES52, an enkephalinase inhibitor, on responses of ventrobasal thalamic neurons in rat.

The effects of ES52, a highly potent derivative of Thiorphan, an inhibitor of enkephalinase, at doses of 5 and 10 mg/kg IV were studied on the responses to cutaneous stimuli of 18 "nociceptive" (N), 10 "convergent" (NNn) and 4 "non-nociceptive" (Nn) neurons recorded in the ventrobasal (VB) complex of the rat. The responses of neurons exclusively driven by noxious mechanical and thermal stimuli (N neurons) were depressed by 56% by ES52 15 min after the injection of 5 or 10 mg/kg IV. This depressive effect was reversed by naloxone for half the neurons. For the ten neurons driven by both noxious and non-noxious stimuli (convergent NNn neurons), the responses to noxious heat were decreased by 42% at 15 min. By contrast, there was a marked enlargement of their receptive fields to light tactile stimuli, which was not naloxone-reversible. The receptive fields of neurons exclusively driven by non-noxious stimuli (Nn neurons) were also greatly expanded by ES52. These results show that ES52 can depress the responses of VB thalamic neurons to noxious stimuli; the effects on receptive field size underlines the complexity of the endogenous opiate systems.

Amino Acids, Sulfur↗