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B Libet

Publications and source records attributed to B Libet.

54 records · Page 3Linked to original sources
PubMed1970

Dopamine as a synaptic transmitter and modulator in sympathetic ganglia: a different mode of synaptic action.

An analysis of the role of adrenergic transmission in mediating the hyperpolarizing, slow inhibitory postsynaptic potential has revealed that dopamine is apparently the specific synaptic transmitter for this response. An additional action of dopamine was discovered, namely the selective facilitation of another synaptic response, the slow excitatory postsynaptic potential. (This potential is a depolarizing response to the muscarinic action of acetylcholine.) This second, modulatory, role of dopamine has characteristics strikingly different from other known modes of synaptic action. After a brief initial action by dopamine, the facilitation of the slow excitatory postsynaptic potential response can persist for hours and is unaffected by a delayed blockade of the postsynaptic receptors for dopamine. This suggests that the modulation consists of a long-lasting metabolic and/or structural change induced in the postsynaptic neuron by dopamine. These conclusions are based on the demonstrated actions of dopamine and other catecholamines, as well as on effects (on dopamine actions and on slow postsynaptic potentials of alpha-adrenergic blockers, of blockade, of dopamine oxidase, of depletion of ganglionic catecholamine by muscarinic excitation, and of a selective re-uptake of dopamine after such depletion.

Acetylcholine↗
PubMed1970

Actions of noradrenaline and acetylcholine on sympathetic ganglion cells.

1. The responses of the post-synaptic membrane of sympathetic ganglion cells to noradrenaline (NA) and to acetylcholine (ACh) were studied in relation to the slow inhibitory post-synaptic potential (S-IPSP) and slow excitatory one (S-EPSP) respectively.2. NA produced an hyperpolarization of about 4 mV in cells of rabbit superior cervical ganglia.3. The hyperpolarizing response to NA was not accompanied by any detectable change in membrane resistance, and it was depressed by conditioning depolarization.4. NA also depressed all the post-synaptic potentials, presumably by an action on presynaptic function.5. ACh produced a large depolarization in ganglion cells of rabbit and of frog (paravertebral) ganglia, which was accompanied by a large decrease in membrane resistance.6. When ACh was applied during nicotinic blockade, achieved with high concentration of nicotine (frog ganglia) or D-tubocurarine (rabbit ganglia), it still produced a considerable depolarization. This response could be blocked by atropine, and is presumably a muscarinic type of action.7. The muscarinic-ACh response was not accompanied by a decrease in membrane resistance. Instead, the frog ganglion cells exhibited increased resistances of up to more than twice the resting value during both the muscarinic-ACh depolarization and the S-EPSP.8. The muscarinic-ACh depolarization and the S-EPSP were both depressed by conditioning hyperpolarization (in nicotinized frog cells). An initial hyperpolarizing phase now appeared in both of these responses.9. It is concluded that the hyperpolarizing response to NA and the depolarizing response to muscarinic-ACh action are not generated by increases in ionic mobilities in the post-synaptic membrane; and that these two responses are produced by the same electrogenic mechanisms which underlie the S-IPSP and the S-EPSP respectively.

Acetylcholine↗
PubMed1969

Generation of adrenergic and cholinergic potentials in sympathetic ganglion cells.

Norepinephrine elicited a hyperpolarizing response, and acetylcholine (during nicotinic blockade) elicited a depolarizing one. Both responses showed no increase in membrane conductance. The norepinephrine response was suppressed by initial depolarization; the acetylcholine response (frog cells); by hyperpolarization. These neurotransmitters apparently can activate electrogenic mechanisms which do not involve movement of ions down their electrochemical gradients.

Acetylcholine↗
PubMed1967

Responses of human somatosensory cortex to stimuli below threshold for conscious sensation.

Averaged evoked responses of somatosensory cortex, recorded subdurally, appeared with stimuli (skin, ventral posterolateral nucleus, cortex) which were subthreshold for sensation. Such responses were deficient in late components. Subthreshold stimuli could elicit sensation with suitable repetition. The primary evoked response was not sufficient for sensation. These facts bear on the problems of neurophysiological correlates of conscious and unconscious experience, and of "subliminal perception."

Consciousness↗
PubMedDate not supplied

Hyperpolarization following activation of K+ channels by excitatory postsynaptic potentials.

We have postulated that an excitatory postsynaptic potential (e.p.s.p.) may open voltage-sensitive K+ ('M') channels, in an appropriate depolarizing range, and that this could alter the e.p.s.p. waveform. Consequently, the fast e.p.s.p. in neurones of sympathetic ganglia, elicited by a nicotinic action of acetylcholine (ACh), could be followed by a hyperpolarization, produced by the opening of M channels during the depolarizing e.p.s.p. and their subsequent slow closure (time constant-150 mg). This introduces the concept that transmitter-induced p.s.ps may trigger voltage-sensitive conductances other than those initiating action potentials, and that in the present case this could produce a true post-e.p.s.p. hyperpolarization. (Some hyperpolarizations other than inhibitory postsynaptic potentials (i.p.s.ps) have been reported to follow e.p.s.ps.) We show here that this is so.

Animals↗