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E Puil

Publications and source records attributed to E Puil.

84 records · Page 5Linked to original sources
PubMed1977

GABA and glycine actions on spinal motoneurons.

Applied microiontophoretically in the spinal cord of cats, glycine is consistently more powerful than gamma-aminobutyric acid (GABA) in raising the membrane conductance of lumbosacral motoneurons (mean ratio of equipotent iontophoretic currents tested on same cells is 5.6:1). This is the reverse of the situation in cerebral cortex. The effect of glycine is well maintained during applications lasting about 1 min, but that of GABA, after an early peak, drops to a much lower plateau (mean plateau-over-peak ratio is 0.23). The reversal potentials for the action of GABA and glycine are initially similar but they behave differently during a prolonged application; that for glycine usually remains constant or becomes more negative whereas that for GABA tends to shift in the positive direction. Various explanations of these phenomena are considered. It is suggested that a single process, electrogenic uptake of GABA, may account for both desensitization (by removing GABA from its site of action) and the positive shift in GABA reversal potential (became uptake is probably associated with an influx of Na+).

Action Potentials↗
PubMed1977

Bicuculline, benzyl penicillin, and inhibitory amino acids in the spinal cord of the cat.

Bicuculline methochloride (BMC), applied by microiontophoresis, tends to depolarize spinal motoneurons and lower their input resistance. With approximately equal iontophoretic currents of gamma-aminobutyric acid (GABA) and BMC, there is an almost equal chance of observing no change, a potentiation, or a depression of the GABA-evoked conductance increase. A block of the GABA action is seen consistently only when the iontophoretic current of BMC is at least double that of GABA. Under these conditions BMC can selectively antagonize GABA without blocking the effects of glycine, though the latter can also be blocked by larger amounts of BMC. BMC also regularly eliminates the usual apparent desensitization to GABA. This may be due to depression of GABA uptake by BMC, which would also account for its potentiating action at lower relative doses. Comparable effects are observed with iontophoretic applications of benzyl penicillin (BP); but even large doses of BP produce no definite change in membrane properties or in conductance increase evoked by GABA or glycine.

Action Potentials↗
PubMed1976

Intracellular Mg2+ increases neuronal excitability.

Injection of Mg2+ into spinal motoneurons of cats leads to a depolarization, associated with a fall in membrane conductance, diminution in post-spike hyperpolarization, and increased excitability. This action has an apparent reversal level substantially more negative than the resting potential, and can be ascribed to a fall in K+ membrane conductance. Since these effects are opposite to those produced by intracellular Ca2+, it is suggested that Mg2+ probably competes with Ca2+ at the Ca2+-activated K+ ionophoreal free ionophores. Neuronal excitability can be regulated by the ratio of internal free Ca2+/Mg2+.

Animals↗
PubMed1976

Is cyclic guanosine monophosphate the internal 'second messenger' for cholinergic actions on central neurons?

The most consistent effects produced by intracellular injections of guanosine 3',5'-cyclic monophosphate (cGMP) (but not 5'-guanosine 5'-monophosphate in spinal motoneurons of cats are a rise in membrane conductance, acceleration in time course of spike potentials, and accentuation of the post-spike hyperpolarization. Associated changes in resting potential are smaller, less constant, and more often in the depolarizing than hyperpolarizing direction, cGMP tends to increase electrical excitability but reduces excitatory post-synaptic potential amplitudes. Most of the effects of intracellular cGMP are quite different from, or indeed opposite to, those of either extra- or intracellular applications of acetylcholine and therefore not consistent with the proposal that cGMP is the internal mediator of muscarinic actions.

Acetylcholine↗
PubMed1975

Morphine excitation in the cerebral cortex.

Microiontophoretic administrations of morphine to cholino-excitable neurones in the cerebral cortex of decerebrate cats evoked a weak excitation which became more prominent upon repeated administrations of the alkaloid. This effect was not antagonized by naloxone. Iontophoresis of methylatropine prevented the excitation induced with acetylcholine and morphine, leaving that caused by glutamate relatively unaltered. Similar applications of morphine to neurones which were not excited by test applications of acetylcholine did not result in excitation but elicited mainly a depression of glutamate-evoked firing. It is suggested that the muscarinic effect of morphine in the cortex may be related to the excitation and convulsions, but not the analgesia, which occurs upon systemic administrations of the narcotic.

Acetylcholine↗
PubMed1975

Evidence for Ca2+-activated K+ conductance in cat spinal motoneurons from intracellular EGTA injections.

Ethylene glycol bis-(beta-aminoethyl ether)-N,N'-tetraacetic acid, injected by iontophoresis from triple-barrelled intracellular micropipettes, consistently raised the membrane resistance and depressed the post-spike after hyperpolarization (AHP), but did not slow the falling phase of the action potential. [Ca2+]i-activated K+ channels appear to play a significant role in the genesis of the AHP and in the control of the resting potential, but not in the repolarization phase of the action potential.

Action Potentials↗