Amount Of Transmitter Research Articles

Cholinergic-dopaminergic relation in different brian structures

Publisher Summary This chapter elaborates the cholinergic–dopaminergic relation in different brain structures. Neostriatal neurons respond in an opposite manner to the iontophoretic application of dopaminergic and cholinergic compounds and to their respective antagonists. Thus, dopamine (DA) depresses, whereas acetylcholine (ACh) or physostigmine enhance the firing rate of caudate cells. A direct approach to the problem of the interconnection and the mutual regulation of striatal DA and ACh systems is provided by the measurement of drug-induced changes in the amounts of transmitters continuously released within the striatum. It is found that a striatal cholinergic system may be under a regulatory dopaminergic influence. It is possible that the nigro-striatal DA pathway modulates the activity and function of some cholinergic neurons by a tonic inhibitory input. It is found that impairment of dopaminergic transmission would result in an increased activity of cholinergic neurons, ACh release, and in the appearance of Parkinsonian symptoms. This is supported by the observations that anticholinergic drugs ameliorate rigidity, and tremor in Parkinson's disease, and extrapyramidal dysfunction caused by neuroleptic compounds.

Spreading activation of end-plate receptors by single transmitter quanta.

WHEN the contents of a synaptic vesicle are emptied into the synaptic space, the transmitter molecules not only diffuse radially, reaching the postsynaptic membrane, but tangentially as well. Although some of the quantitative aspects of tangential diffusion have been discussed1, the physiological significance of this process has not been sufficiently, emphasized. Indeed, we can assume that those molecules diffusing through the cleft interact with more receptors before reaching the extracellular space. In this manner, the surface area of activated postsynaptic membrane as well as the intensity and duration of the changes elicited by the transmitter-receptor interactions may be increased.

Some effects of nerve stimulation and hemicholinium on quantal transmitter release at the mammalian neuromuscular junction

1. Rat phrenic nerve-diaphragm preparations have been used to assess some effects of prolonged nerve stimulation on transmitter release.2. The amplitude of the end-plate potentials evoked by prolonged repetitive nerve stimulation fell gradually during stimulation. Most of this fall was due to a reduction in the number of transmitter quanta released by each nerve impulse; however there was also a small reduction in the muscle cell depolarization produced by each quantum of transmitter.3. Repetitive nerve stimulation also produced a small reduction in the amplitude of the miniature end-plate potentials. Recovery of amplitude occurred within about 7-8 min of ceasing stimulation.4. A much greater reduction in miniature end-plate potential amplitude accompanied prolonged nerve stimulation if hemicholinium was present in the bathing solution.5. Estimates of the ;readily available transmitter' (Elmqvist & Quastel, 1965b) were made at intervals following prolonged nerve stimulation. Readily available transmitter was reduced, and recovered over approximately 15 min.6. The relationship of these changes to the changes in nerve terminal synaptic vesicle numbers and volumes induced by similar prolonged nerve stimulation (Jones & Kwanbunbumpen, 1970) is discussed.

A new hypothesis on the mechanism by which temporary connections are formed

A new hypothesis is proposed on the mechanism by which temporary connections are formed. It is postulated that depolarization of the oligodendrocyte membrane serves as signal to its myelinizing function, and this process requires that there be, at the moment of oligodendrocyte depolarization, physicochemical "trace" of a preceding presynaptic excitation of the terminal in the intercellular clefts between its processes and these terminals. Contact of the presynaptic terminal with the glial process and enclosure by the myelin sheath create favorable conditions for the electrotonic propagation of the action potential, and the nerve impulse thus releases a larger amount of transmitter; the cerebro-cortical synapse changes from "potential" to "actual."

The escape of the renal blood flow response during sympathetic nerve stimulation.

Response of renal blood flow to regional sympathetic nerve stimulation has been studied in anesthetized cats. When the sympathetic nerves to the kidney are stimulated at frequencies within the ‘physiological range’, renal blood flow first decreases markedly and then increases over the next 3 to 5 min to a value slightly below the control level. A similar ‘escape’ of the resistance response is found when the renal nerves are stimulated under conditions of constant flow. If the frequency of renal nerve stimulation is gradually increased the onset of the escape is greatly delayed, indicating that failure of impulse transmission or severe depletion of transmitter is unlikely to be the cause of the escape phenomenon. Intraarterial infusion of noradrenaline produces increased flow resistance with little or no subsequent escape showing that the escape cannot be attributed to loss of responsiveness of the vascular smooth muscle to the adrenergic transmitter. A quantitative decrease in the amount of transmitter released per impulse and intrarenal vascular control mechanisms related to blood flow autoregulation are discussed as possible causes of the escape phenomenon.

Perfusion of the spleen with blood containing prostaglandin E1: transmitter liberation and uptake.

The cat’s spleen perfused with homologous blood containing prostaglandin E 1 provides an admirable preparation for the study of the liberation and uptake of the sympathetic transmitter. Obstruction of the circulation with platelet thrombi is eliminated; blood flow is high, and overflow of transmitter when the nerves are stimulated is higher than in other preparations. The high overflow of transmitter is attributed to adequate perfusion of a large mass of splenic tissue. There is no evidence that the amount of transmitter liberated per unit mass of tissue is increased. Uptake of liberated transmitter and of infused L-noradrenaline is no different from that observed in other preparations of the spleen.

Mechanism of neuromuscular blockade by tetraethylammonium.

ARTICLESMechanism of neuromuscular blockade by tetraethylammoniumRL ParsonsRL ParsonsPublished Online:01 Apr 1969https://doi.org/10.1152/ajplegacy.1969.216.4.925MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByPresynaptic calcium currents evoking quantal transmission from avian ciliary ganglion neuronsSynapse, Vol. 5, No. 4Tetraethylammonium ions and the potassium permeability of excitable cells21 June 2005Action of glucosamine on acetylcholine-sensitive channelsThe Journal of Membrane Biology, Vol. 56, No. 1Spontaneous synchronization by 4-aminopyridine of acetylcholine release in the neuromuscular junctionBulletin of Experimental Biology and Medicine, Vol. 88, No. 3Estimates of quantal content during 'chemical potentiation' of transmitter release1 January 1997 | Proceedings of the Royal Society of London. Series B. Biological Sciences, Vol. 205, No. 1160Depletion of synaptic vesicles at the frog (Rana pipiens) neuromuscular junctions by tetraphenylboronExperientia, Vol. 32, No. 11Transmission of Impulses from Nerve to MuscleNeuromuscular TransmissionTHE EFFECTS OF TETRAPHENYLBORON ON NEUROMUSCULAR TRANSMISSION IN THE FROG19 July 2012 | British Journal of Pharmacology, Vol. 54, No. 3Blockade by lobeline of potassium exchange in skeletal muscleNaunyn-Schmiedeberg's Archives of Pharmacology, Vol. 282, No. 4The influence of disulfide bond reduction and lanthanum on end-plate receptors1 June 1973 | Experientia, Vol. 29, No. 6Antinicotinic action of nicotine and lobeline on frog sartorius muscleNaunyn-Schmiedeberg's Archives of Pharmacology, Vol. 272, No. 3Influence of lanthanum on transmitter release at the neuromuscular junctionJournal of Neurobiology, Vol. 2, No. 3 More from this issue > Volume 216Issue 4April 1969Pages 925-931 Copyright & PermissionsCopyright © 1969 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1969.216.4.925PubMed4304760History Published online 1 April 1969 Published in print 1 April 1969 Metrics

Chemically mediated transmission at a giant fiber synapse in the central nervous system of a vertebrate.

The hatchetfish, Gasteropelecus, possesses large pectoral fin adductor muscles whose simultaneous contraction enables the fish to dart upwards at the approach of a predator. These muscles can be excited by either Mauthner fiber. In the medulla, each Mauthner fiber forms axo-axonic synapses on four "giant fibers," two on each side of the midline. Each pair of giant fibers innervates ipsilateral motoneurons controlling the pectoral fin adductor muscles. Mauthner fibers and giant fibers can be penetrated simultaneously by microelectrodes close to the synapses between them. Electrophysiological evidence indicates that transmission from Mauthner to giant fiber is chemically mediated. Under some conditions miniature postsynaptic potentials (PSP's) are observed, suggesting quantal release of transmitter. However, relatively high frequency stimulation reduces PSP amplitude below that of the miniature potentials, but causes no complete failures of PSP's. Thus quantum size is reduced or postsynaptic membrane is desensitized. Ramp currents in Mauthner fibers that rise too slowly to initiate spikes can evoke responses in giant fibers that appear to be asynchronous PSP's. Probably both spikes and ramp currents act on the same secretory mechanism. A single Mauthner fiber spike is followed by prolonged depression of transmission; also PSP amplitude is little affected by current pulses that markedly alter presynaptic spike height. These findings suggest that even a small spike releases most of an immediately available store of transmitter. If so, the probability of release by a single spike is high for any quantum of transmitter within this store.

Neuromuscular synapses of a crab motor axon

AbstractNeuromuscular transmission of the “fast” motor axon of a crab, Pachygrapsus crassipes, was investigated, using extracellular microeletrodes to record electrical events at individual synaptic regions, and intracellular microelectrodes to record simultaneously the postsynaptic potentials of the muscle fiber. At 1/sec stimulation of the motor axon, the transmitter quantum content per stimulus was estimated at about 2 for many synapses, with relatively slight facilitation at higher frequencies. At some synapses a lower quantum content was measured at 1/sec, and more facilitation was apparent at higher frequencies. Fatigue of transmission with maintained stimulation was rapid.Observations of time course and amplitude of extracellularly recorded potentials suggested heterogeneity of these events.Electron micrographs of synapse‐bearing nerve endings showed them to be in clefts or embedded beneath the surface of the muscle fiber. The presynaptic vesicles were usually present at relatively low density, which could account for the rapid fatigue of transmission. Calculated volume distributions of the vesicles did not correspond to amplitude distributions of extracellularly recorded spontaneous potentials; possible reasons for the lack of agreement are discussed.

Noradrenaline storage and release in the decentralized spleen.

Decentralization of the sympathetic postganglionic neurons of the cat’s spleen for 72 h had previously been shown to give rise to an increased liberation of transmitter when the nerves are stimulated. Measurement of the noradrenaline content of the spleen in terms of its deoxyribonucleic acid content shows that decentralization causes a 40% increase in the amount of transmitter in the organ. The proportion of this which is released by nerve stimulation is the same as in the normal spleen. A surgical operation under anaesthesia involving exposure of the left splanchnic nerves, without any direct interference with the nerves to the spleen, produces a reduction of 40% in the spleen’s noradrenaline content.