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Biomedical subjects

A Dray

Publications and source records attributed to A Dray.

At least 145 records · Page 8Linked to original sources
PubMed1976

Observations on the pharmacology of cholinoceptive neurones in the rat brain stem.

The pharmacology of spontaneously active cholinoceptive neurones in the brain stem of rats anaesthetized with urethane has been investigated using microiontophoresis to administer muscarinic and nicotinic agonists and antagonists. 2. Acetylcholine (ACh) excited most cells but occasionally depressed their activity. Muscarine, and the muscarinic agonists methacholine and bethanechol produced prolonged excitation or inhibition of cells whereas nicotine produced prolonged excitations but no inhibitions. 3 Atropine selectively antagonized ACh excitations and both excitation and inhibition of neuronal activity produced by muscarine and muscarinic agonists, but not the excitations produced by nicotine, glutamate or DL-homocysteic acid. 4 Dihydro-beta-erythroidine (DHBE) and tubocurarine antagonized both ACh and nicotine excitations but not those induced by glutamate or DL-homocysteic acid. Inhibitions by ACh or muscarine were not affected. 5 It is concluded that excitations of cholinoceptive neurones in the rat brain stem may be mediated by activation of both muscarinic and nicotinic receptors whereas inhibitions are mediated by activation of a muscarinic receptor.

Acetylcholine↗
PubMed1976

Caudate stimulation and substantia nigra activity in the rat.

1. The responses of spontaneously active single neurones in the substantia nigra and overlying mesencephalic reticular formation have been analysed during the electrical stimulation of the ipsilateral caudate nucleus. Experiments were performed in rats anaesthetized with urethane or pentobarbitone. All recordings were made extracellularly with multi-barrelled glass micropipettes which were also used to test neuronal responsiveness to electrophoretically administered substances. The micropipette tip position was marked and the distribution of neurones studied has been analysed. 2. Single shock stimulation of the caudate nucleus inhibited neuronal activity in the substantia nigra (270/320 cells: mean latency 5-4 msec) and in the mesencephalic reticular formation (62/72 cells: mean latency 16-6 msec). However, these effects were often accompanied by periods of excitation. In pentobarbitone anaesthetized animals the latency and duration of these substantia nigra inhibitions was increased. 3. Compared with the zona reticulata, fewer neurones in the zona compacta of the substantia nigra responded to caudate stimulation in both urethane or pentobarbitone anaesthetized animals. 4. The activity of most cells was depressed by electrophoretically administered GABA or glycine and increased by acetylcholine or glutamate. Neurones of the mesencephalic reticular formation were less sensitive to GABA and glycine than substantia nigra neurones. Within the substantia nigra, both zona compacta and zona reticulata neurones were more sensitive to GABA than to glycine. Over-all, glutamate was a more potent excitant than acetylcholine (ACh). 5. Electrophoretic bicuculline methochloride (BMC) consistently reduced GABA but not glycine depression of substantia nigra neurones. Approximately twice as much BMC was required to reduce the endogenous inhibition of the same substantia nigra neurones and the amplitude of concomitantly evoked positive field potential as was required to abolish exogenous GABA responses. Some evoked substantia nigra inhibitions were resistant to BMC. 6. Electrophoretic strychnine consistently reduced glycine but not GABA depression of substantia nigra neurones, and did not modify caudate evoked inhibition of these neurones or the accompanying field potential. 7. The results support the concept of a slowly conducting caudato-nigral pathway which has both facilitatory and inhibitory components. The inhibitory pathway uses GABA as the neurotransmitter. The identity of the possible excitatory transmitter is unknown. The monosynaptic nature of this pathway is uncertain and the possible contribution of other bicuculline insensitive nigral inhibitory processes is discussed.

Action Potentials↗
PubMed1974

Morphine and neurotransmitter substances: Microiontophoretic study in the rat brain stem.

1 The effects of microiontophoretically applied morphine and its interactions with the effects of microiontophoretic applications of either acetylcholine, (-)-noradrenaline or 5-hydroxytryptamine have been studied on single neurones in the brain stem of rats anaesthetized with urethane.2 Morphine excited or inhibited most neurones tested and the effects, especially excitation, were often extremely powerful. However, the time course of the excitatory and inhibitory effects were somewhat different.3 Desensitization to the excitation produced by morphine was seen after repeated or prolonged applications and it is suggested that this phenomenon may be related to the tolerance which develops after chronic administration of morphine. No desensitization was observed to inhibition of neuronal activity by morphine.4 Morphine usually reduced the excitation of neurones by acetylcholine, noradrenaline or 5-hydroxytryptamine but sometimes potentiated the effect, although not always on the same neurones. Inhibition of neuronal activity by these compounds was never modified by morphine and neither were the effects of glutamate or D,L-homocysteic acid when used as control agonists.5 The in vitro release of morphine from six micropipettes was determined and the transport number was calculated to be 0.051 (s.d. 0.021).6 The implications of these observations in explaining the pharmacological actions of morphine are discussed.

Acetylcholine↗
PubMed1974

The effects of microiontophoretically applied morphine and transmitter substances in rats during chronic treatment and after withdrawl from morphine.

The effects of microiontophoretically applied acetylcholine, noradrenaline, 5-hydroxytryptamine and morphine were studied on single brain stem neurones of rats during chronic morphine pretreatment and 24 h after its withdrawal. No significant changes were observed in the initial spontaneous neuronal firing rate or in the qualitative or quantitative effects of acetylcholine, noradrenaline or 5-hydroxytryptamine. However, in chronically treated animals there was a significant decrease in the number of neurones excited by morphine or showing tachyphylaxis to morphine on repeated microiontophoretic applications.We suggest that some of the cellular central nervous system changes which occur during chronic morphine treatment are reflected by the decrease in sensitivity of neurones to morphine excitation.

Acetylcholine↗
PubMed1973

Modification of the responses of brain stem neurones to transmitter substances by anaesthetic agents.

1. The effects of microiontophoretic applications of acetylcholine (ACh), (-)-noradrenaline ((-)-NA) and 5-hydroxytryptamine (5-HT) have been investigated on spontaneously active brain stem neurones in decerebrate unanaesthetized rats and in rats anaesthetized with either tribromoethanol, urethane or pentobarbitone.2. Four types of responses to both (-)-NA and 5-HT were seen. These were: simple excitation; excitation preceded by a short-lasting inhibition; short-lasting inhibition and prolonged inhibition. Three types of responses to ACh were seen: an excitation with long latency of onset; excitation with short latency of onset, resembling the response to an excitant amino acid, and a short-lasting inhibitory response.3. The types of responses to microiontophoretically applied ACh, (-)-NA or 5-HT in anaesthetized and unanaesthetized animals were similar.4. The number of ACh excitatory responses with short latency of onset were significantly reduced in the pentobarbitone-anaesthetized group and a small but significant increase in the number of 5-HT inhibitory effects were observed in each anaesthetized group of animals.5. A significantly greater proportion of slower firing neurones (less than 10 spikes/s) were found in the pentobarbitone-anaesthetized animals.6. The effects of microiontophoretically applied and i.v. administered pentobarbitone were studied on spontaneously active neurones which responded consistently to ACh and a control agonist.7. Pentobarbitone administered by either route reduced the firing rate of most neurones studied and was shown to antagonize specifically the excitation of neurones by exogenously applied ACh.8. It is suggested that postsynaptic antagonism of endogenously released ACh may be a contributing factor in the mechanism of action of pentobarbitone.

Acetylcholine↗