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S A Turkanis

Publications and source records attributed to S A Turkanis.

54 records · Page 3Linked to original sources
PubMed1975

The influence of delta9-tetrahydrocannabinol, cannabinol and cannabidiol on tissue oxygen consumption.

The mechanism of the hypothermia produced in mice by the naturally occurring cannabinoids, delta9-tetrahydrocannabinol, cannabinol, and cannabidiol, was investigated by evaluating the direct effect of these drugs on the oxygen consumption of tissue homogenates and isolated mitochondria. The tissues studied were brain, liver, skeletal muscle, and heart; the mitochondrial preparations were limited to brain and skeletal muscle. The in-vitro studies included a description of the influence of various cannabinoid vehicles containing Tween 80, ethanol, Pluronic F68, and albumin on the oxygen consumption of tissue preparations. Of these vehicles, only albumin was without effect on all tissues. The other vehicles produced diverse responses, including some that were qualitatively different; the data illustrate that the influence of each vehicle on oxygen consumption must be defined for each tissue employed. In spite of the different vehicle effects, delta9-tetrahydrocannabinol generally reduced oxygen consumption of all tissue preparations; however, the vehicles were capable of modifying the dose-effect relationship. The results of all three drugs prepared in Pluronic F68 on brain and skeletal muscle indicated that the cannabinoids generally cause a dose-related depression of oxygen consumption. The findings demonstrate that the cannabinoids can directly decrease oxidative metabolism of tissue and isolated mitochondria and that a marked response occurs in the concentration range of 1 X 10(-5) to 1 X 10(-4) M. Because these concentrations can exist in tissues following the in-vivo administration of delta9-tetrahydrocannabinol, the results suggest that the depressant effect of the cannabinoids on metabolic rate may contribute to the mechanism of the hypothermia produced by the drugs.

Animals↗
PubMed1973

Barbiturate-induced transmitter release at a frog neuromuscular junction.

1. The influence of barbiturates on neuromuscular transmission at end-plates of frog sartorius muscles was investigated electrophysiologically on preparations bathed in Ringer solution containing a low concentration of calcium and a high concentration of magnesium.2. Effects of a convulsant barbiturate, 5-(2-cyclohexylideneëthyl)-5-ethyl barbituric acid (CHEB), were compared with those of phenobarbitone.3. CHEB and phenobarbitone increased the mean quantum content of the end-plate potentials and decreased the mean amplitude of the miniature end-plate potentials.4. Both barbiturates enhanced the duration of the nerve-terminal action potential and had little or no effect on the effective resistance of the skeletal muscle membrane.

Action Potentials↗
PubMed1973

Effects of muscle stretch on transmitter release at end-plates of rat diaphragm and frog sartorius muscle.

1. Miniature end-plate potentials (m.e.p.p.s) and end-plate potentials were recorded intracellularly at neuromuscular junctions of the frog sartorius muscle and the rat diaphragm before, during and after muscle stretch.2. Stretch increased the frequency of the m.e.p.p.s and the mean quantum content (m) at end-plates of the sartorius muscle.3. Stretch enhanced m.e.p.p. frequency of the sartorius muscle in normal Ringer solution as well as in solutions high in magnesium and low in calcium content. In addition, an increase in frequency occurred in the presence of tetrodotoxin and in the absence of neostigmine methylsulphate.4. The magnitude of the increase in m.e.p.p. frequency in the sartorius muscle was negatively correlated with the control frequency.5. In contrast to the above findings at sartorius end-plates, muscle stretch did not affect the frequency of m.e.p.p.s or the m values at end-plates of the rat diaphragm.

Animals↗
PubMed1971

Correlation between nerve terminal size and transmitter release at the neuromuscular junction of the frog.

1. End-plate potentials were recorded intracellularly at the frog neuromuscular junction bathed in a solution containing a low concentration of calcium and a high concentration of magnesium.2. The muscle was subsequently subjected to ;cholinesterase staining', and the area of the individual end-plates, studied with intracellular electrodes, was measured.3. A positive correlation was found between the end-plate area and the diameter of muscle fibres.4. The mean quantum content (m) showed a positive correlation with the size of end-plates.5. The frequency of spontaneous miniature end-plate potentials was positively correlated with m as well as with end-plate area.6. It is concluded that the amount of transmitter released following nerve stimulation is related to the size of nerve endings.

Animals↗
PubMed1969

Some properties of the denervated anterior gracilis muscle of the rat.

1. Microdrops of acetylcholine (ACh) were topically applied to denervated, mammalian skeletal muscle in vivo, and ACh-evoked depolarization and contracture were recorded simultaneously.2. Contracture tension was directly proportional to the degree of ACh-elicited depolarization.3. Atropine and (+)-tubocurarine increased the amount of ACh required to produce a given amount of depolarization, but these anticholinergic agents did not alter the relationship between the degree of ACh-evoked depolarization and contracture tension.4. Topically applied catecholamines did not produce either depolarization or contracture, despite the fact that parenterally administered catecholamines elicited both responses.

Acetylcholine↗
PubMedDate not supplied

The cannabinoids as potential antiepileptics.

Comparative studies of the anticonvulsant properties of the cannabinoids and prototype antiepileptic drugs in numerous animal seizure models demonstrate that (1) as an anticonvulsant, cannabidiol (CBD), in contrast to delta 9-tetrahydrocannabinol (THC), is relatively selective in terms of both central nervous system (CNS), depressant and excitatory properties; (2) the potency of cannabidiol, unlike that of phenytoin and phenobarbital, varies greatly with the species; (3) the large potency difference between the cannabinoids and the antiepileptics in the mouse appears to be due to dispositional differences, because brain concentrations of all the drugs are very similar; (4) tolerance to the anticonvulsant properties of cannabidiol is not a prominent feature; in three seizure models, tolerance developed in one, but "reverse tolerance" developed in the other two; and (5) the results of a study of the electrophysiologic mechanisms of action indicate that cannabidiol produces some unique effects and that its spectrum of antiepileptic activity may be different from that of the prototype drugs. The anticonvulsant nature of cannabidiol suggests that it has a therapeutic potential in at least three of the four major types of epilepsy: grand mal, cortical focal, and complex partial seizures.

Acoustic Stimulation↗
PubMedDate not supplied

Electrophysiologic properties of the cannabinoids.

The effects of the psychoactive cannabinoid delta 9-tetrahydrocannabinol (THC) and the nonpsychoactive cannabinoid cannabidiol (CBD) were investigated comparatively on electrically caused transcallosal cortical evoked responses, electrically induced limbic after discharges, photically evoked cortical afterdischarges, spontaneous cortical focal epileptic potentials, and spinal monosynaptic reflexes. In each system, THC produced central excitation; for example, the drug's responses ranged from enhancement of synaptic transmission to precipitation of frank convulsions. In addition to central nervous system stimulation, THC usually elicited depression; the qualitative character of the effect of the drug was dependent upon the dosage and the test system. In contrast to THC, cannabidiol generated no CNS excitation: it was either depressant or inert in these test systems. The results clearly demonstrate the complexity of the CNS properties of THC and the selectivity of the depressant properties of cannabidiol; moreover, the data illustrate the wide range of neuropharmacologic responses that potentially any cannabinoid can effect.

Animals↗