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Biomedical subjects

G A Lambert

Publications and source records attributed to G A Lambert.

10 recordsLinked to original sources
PubMed1992

The spinal cord processing of input from the superior sagittal sinus: pathway and modulation by ergot alkaloids.

The effects of ergot alkaloids on field potentials and unit responses produced in the upper cervical spinal cord by stimulation of the superior sagittal sinus (SSS) were examined in 57 anesthetized cats. Electrical stimulation of the SSS produced field potentials and single-unit responses at latencies of 5-20 ms. Field potentials were abolished by section of the first division of the trigeminal nerve but were unaffected or increased by section of the upper cervical nerves. Field potentials were reduced or abolished by intravenous injection of ergotamine or dihydroergotamine (DHE). The evoked response of 41 units (34.4%) were suppressed by either i.v. or iontophoretic administration of ergotamine, DHE or ergometrine. The results suggest that ergot alkaloids exert an effect at a spinal cord relay centre which receives trigeminally mediated input from cranial blood vessels.

Action Potentials↗
PubMed1992

Craniovascular nociceptive pathways relay in the upper cervical spinal cord in the cat.

Units in the dorsolateral area of the upper cervical cord and the ventroposteromedial nucleus of the thalamus respond to stimulation of cranial vessels. To study the physiological role of the upper cervical cord in craniovascular transmission, we used a cryoprobe to interrupt reversibly neural transmission through the cord while recording in the thalamus. Twenty-one of 47 thalamic units tested showed reversible diminution in their response to superior sagittal sinus stimulation during cervical cord cooling. In contrast, receptive field responses and spontaneous thalamic activity were unaffected. These data suggest offt the cervical cord relays craniovascular nociceptive afferents.

Animals↗
PubMed1991

Craniovascular application of capsaicin activates nociceptive thalamic neurones in the cat.

In cats anaesthetized with alpha-chloralose and urethane, extracellular recordings were made in ventrobasal thalamus from cells responding to electrical stimulation of the superior sagittal sinus and middle meningeal artery. Capsaicin, but not vehicle, evoked an increase in the firing rate of nociceptive cells (5 of 6 wide dynamic range and the only nociceptive specific cell). Non-nociceptive cells did not respond to either capsaicin or vehicle. Cells with long latencies to electrical stimulation were excited by capsaicin but cells with short latencies were not. Capsaicin-responsive cells were found in the ventroposteromedial nucleus and the medial nucleus of the posterior complex and mostly had receptive fields involving the first trigeminal division.

Animals↗
PubMed1991

Cervical spinal cord neurons receiving sensory input from the cranial vasculature.

The superior sagittal sinus, middle meningeal artery or superficial temporal artery was stimulated electrically in anaesthetized cats. Field potential recordings were used to locate areas of maximum responses in the upper cervical cord, which were then further examined for responsive single units. Short latency units responded to stimulation of the superior sagittal sinus with a mean latency of 11.9 ms. Some units also responded at longer latencies in the 200-250 ms range. Spontaneous discharge rates of some units in a dorsolateral area of the cervical cord were accelerated by iontophoretic application of glutamic or homocysteic acid to these same units. Evoked action potentials were commonly multiphasic. Dorsolateral area units commonly received convergent input from two vessels and often had receptive fields on the face and limbs. Spontaneously active cells which respond to electrical stimulation were accelerated by the local application of bradykinin to the sinus and responses of dorsolateral area units could be reversibly blocked by local application of lignocaine to the sinus. It was concluded that the dorsolateral area is a relay area for the perception of pain from cranial vessels.

Action Potentials↗
PubMed1978

2,5-Dimethoxy-4-methylamphetamine (DOM)- a central component of its cardiovascular effects in rats; involvement of serotonin.

The hallucinogen DOM produces a rise in blood pressure and heart rate when injected into the cerebral ventricles of anesthetized rats. These effects are abolished in rats with transected spinal cords but are unaffected by prior treatment with hexamethonium. Central but not peripheral administration of the serotonin antagonist BOL reduces the response. Tachyphylaxis to the response develops rapidly and is accompanied by a decrease in the ability of 5-HT to induce a centrally mediated cardiovascular change. It is concluded that the response is mediated by direct stimulation of central 5HT receptors. Tachyphylaxis may be the result of irreversible binding of DOM to 5-HT receptors or to 5-HT receptor densensitization.

DOM 2,5-Dimethoxy-4-Methylamphetamine↗
PubMed1978

Pharmacological and biochemical properties of isomeric yohimbine alkaloids.

The stereochemical and pharmacological properties of yohimbine and some of its isomers are briefly reviewed. Several pharmacological and physical properties of a selection of the isomers have been determined with a view to elucidating which might be important in the elaboration of the known behavioral effects produced by them. Activity is not dependent upon lipid solubility or on the ease of access to the central nervous system. The isomers are weak inhibitors of rat-brain acetylcholinesterase and weak antagonists at muscarinic cholinergic receptors. In the rat brain in vitro they do not possess significant monoamine oxidase-inhibiting properties nor do they inhibit the uptake of serotonin. They are relatively potent antagonists of 5HT on the rat isolated fundus preparation and their potency in this preparation may be related to their ability to produce behavioral and cardiovascular effects in man and dogs.

Animals↗
PubMed1977

Interaction between yohimbine alkaloids and amphetamine in mice.

The toxicity (LD50) of the isomers yohimbine, beta-yohimbine, and corynanthine was determined in mice. The LD50 of amphetamine in the presence of a constant dose of a yohimbine isomer and that of the isomer in the presence of a constant dose of amphetamine were determined in aggregated mice. Isobolograms were constructed from these data and used to evaluate the interaction of the yohimbine alkaloids and amphetamine. Beta-yohimbine was found to be approximately twice as toxic as yohimbine and corynanthine about one fifth as toxic. There was a mutual potentiation between the toxicities of yohimbine and amphetamine. Potentiation of the toxicity of amphetamine occurred with beta-yohimbine but the effect was not as marked as with yohimbine. In contrast, corynanthine antagonized the toxicity of amphetamine. The interaction between yohimbine and amphetamine is unlikely to be due to noradrenergic mechanisms but could conceivably involve serotonergic or dopaminergic mechanisms.

Animals↗
PubMed1975

The role of the central nervous system in the cardiovascular responses to yohimbine.

Yohimbine injected intravenously or intracerebroventricularly in conscious dogs produced behavioural excitation accompanied by a rise in blood pressure and heart rate. The cardiovascular effects were reduced or abolished by hexamethonium, phenoxybenzamine and reserpine. In conscious cats intravenously administered yohimbine was depressor but intracerebroventricular administration in these animals caused a rise in blood pressure accompanied by behavioural depression. In anaesthetized or decerebrate cats yohimbine was always depressor. Yohimbine injected intracerebroventricularly produced a rise in blood pressure and heart rate in both conscious and anaesthetized rats. When administered intravenously to these animals there was a fall in blood pressure. It was concluded that the pressor action of yohimbine in conscious dogs was central in origin via the sympathetic nervous system. The different pattern of cardiovascular responses in the dog, cat and rat may be related to differences in the balance between medullary effects and effects on higher brain centres of the three species.

Adrenergic alpha-Antagonists↗