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R Pumain

Publications and source records attributed to R Pumain.

50 records · Page 3Linked to original sources
PubMed1971

Actions of dinitrophenol and some other metabolic inhibitors on cortical neurones.

1. In cats under methoxyflurane, DNP and other metabolic inhibitors were tested on cortical neurones by iontophoresis from micropipettes.2. DNP, dinitro-o-cresol, iodoacetate, pentachlorophenol and oligomycin (uncouplers or inhibitors of oxidative phosphorylation), as well as moderate anoxia, blocked selectively and reversibly spontaneous firing and discharges evoked by ACh; responses evoked by glutamate were facilitated by moderate doses of DNP and blocked only by large amounts.3. Azide, cyanide, ouabain and strophanthidine had a mainly excitatory effect; the cardiac glycosides tended to depress more strongly responses to glutamate.4. Intracellular observations showed that DNP causes a sharp fall in electrical excitability, associated with a hyperpolarization and fall in membrane resistance.5. The hyperpolarizing action of DNP had a mean reversal level (E(DNP)) nearly 30 mV more negative than the resting potential; E(DNP) was identical with the mean reversal level for the depolarizing action of ACh, measured on the same cells.6. DNP had its usual hyperpolarizing effect on neurones whose IPSPs had been made positive by raising the internal [Cl]; the mean E(IPSP) was over 30 mV more positive than E(DNP).7. It is concluded that DNP lowers excitability by raising the membrane conductance to K(+) (g(K)) and that it blocks ACh responses selectively because ACh has a precisely opposite action on these neurones.8. In the Discussion, it is suggested that the rise in g(K) is mediated by an increase in internal free Ca(2+), caused by a slowing of mitochondrial activity, and that a similar mechanism may play a significant role in general anaesthesia.

Acetylcholine↗
PubMed1971

Effects of Ba2+ and tetraethylammonium on cortical neurones.

1. Ba(2+), applied by micro-iontophoresis, excites most cortical neurones that are excitable by ACh; other neurones tend to be depressed.2. The discharges evoked by Ba(2+) resemble those evoked by ACh, but they have an even slower time course and are characterized by firing in high frequency bursts.3. The excitatory action of Ba(2+), unlike that of ACh, is not abolished by muscarine antagonists; but it can be prevented with dinitrophenol.4. The depolarizing effect of Ba(2+) is associated with a rise in membrane resistance and it has a reversal level 24 mV more negative than the resting potential.5. These observations suggest that, as in other tissues, Ba(2+) reduced the K(+) conductance by a direct action on the cell membrane. Some diminution in Na(+) inactivation is indicated by the repetitive firing at high frequency.6. TEA has a predominantly depressant effect on all neurones tested. Like Ba(2+), it often increases greatly the duration of spikes, but there is no regular change in resting membrane resistance and no tendency to repetitive firing. TEA probably reduces only the delayed K(+) current.7. Even in large doses neither Ba(2+) nor TEA interferes with the conductance increase that generates the typical prolonged IPSPs recorded in cortical neurones.

Acetylcholine↗
PubMed1971

The mechanism of excitation by acetylcholine in the cerebral cortex.

1. The muscarinic depolarizing action of ACh on cortical neurones is associated with an increase in membrane resistance (mean DeltaV/DeltaR = 3.16 mV/MOmega).2. ACh also promotes repetitive firing by slowing repolarization after spikes.3. The depolarizing effect has a mean reversal level of -86.7 mV (with mean resting potential -56 mV).4. It is concluded that as a muscarinic excitatory agent, ACh probably acts by reducing the resting K(+) conductance of cortical neurones, and also the delayed K(+) current of the action potential.5. These results are discussed in relation to the possible role of ACh in cortical function.

Acetylcholine↗
PubMedDate not supplied

Laminar analysis of the origin of the various components of evoked potentials in slices of rat sensorimotor cortex.

In slices of rat sensorimotor cortex, extracellular field potentials evoked by electrical stimulation of the white matter were recorded at various cortical depths. In order to determine the nature of the various components, experiments were performed in 3 situations: in a control perfusion medium, in a solution in which calcium ions had been replaced by magnesium ions to block synaptic transmission, and in cortices in which the pyramidal neurons of layer V had been previously induced to degenerate. In the control situation, the response at or near the surface was a positive-negative wave. From a depth of about 150 microns downwards, the evoked response consisted usually of 6 successive components, 3 positive-going, P1, P3 and P6 and 3 negative-going, N2, N4 and N5. P1 and N4 were apparent in superficial layers only. The amplitude of the remaining waves was variable in the cortex but all diminished near the white matter. The early part of the surface positive wave arises from a non-synaptic activation of superficial elements, probably apical dendrites. The late part of the surface positive wave and the negative wave are due to the synaptic activation of neurons located probably in layer III. The large negative wave N2 represents principally the antidromic activation of cell bodies and possibly of proximal dendrites of neurons situated in layers III, IV and V, though the compound action potentials of afferent and efferent fibers may contribute to a reduced part to its generation. The late components N4 to P6 are post-synaptic responses. The negative component N5, the amplitude of which is largest in layers III and IV, represents excitatory responses of neurons located at various depths in the cortex. The nature of the positive component P6 is less clear, although the underlying mechanism might be inhibitory synaptic potentials.

Animals↗