scholarly journals The versatile synapse

1984 ◽  
Vol 112 (1) ◽  
pp. 199-224
Author(s):  
R. M. Pitman
Keyword(s):  
Ion Channels ◽  
Nerve Impulse ◽  
Synaptic Cleft ◽  
Ionic Species ◽  
Postsynaptic Membrane ◽  
Voltage Dependent ◽  
Biochemical Systems ◽  
Characteristics Analysis ◽  
Neurotransmitter Substances ◽  
Neurotransmitter Substance

‘Typically’ chemical synaptic transmission takes place when an influx of calcium ions during a presynaptic nerve impulse triggers exocytosis of neurotransmitter substance from synaptic vesicles. The neurotransmitter diffuses across the synaptic cleft and occupies receptors embedded in the subsynaptic membrane. This interaction (directly or via a second messenger) operates characteristic ion channels and produces an increase in the postsynaptic membrane permeability to particular ions. Depending on the ionic species to which the postsynaptic membrane becomes more permeable, the physiological response will be an excitatory or an inhibitory postsynaptic potential. The action of neurotransmitters may be terminated either by enzymic inactivation or by cellular uptake mechanisms. Over the last decade it has become clear that a neurotransmitter substance may exert a number of different actions on a single postsynaptic neurone. These may involve opening or closure of either voltage-independent or voltage-dependent ion channels. It is also possible that in some instances transmitters may act on neuronal biochemical systems to modify the physiology of postsynaptic cells without directly altering their electrical characteristics. Analysis of the postsynaptic actions of neurotransmitter substances has become further complicated by the increasing body of evidence which indicates that more than one transmitter substance (one of which may be a peptide) can be released from a single presynaptic neurone. The significance of such dual transmitter systems has yet to be fully elucidated. The efficacy of transmission across many synapses may be modified by either presynaptic or postsynaptic mechanisms; both transmitter release and postsynaptic responsiveness may depend on the recent history of a single synapse, on synaptic inputs from other neurones or on circulating neuroactive substances.

scholarly journals SIZES OF END PLATE COMPARTMENTS, DENSITIES OF ACETYLCHOLINE RECEPTOR AND OTHER QUANTITATIVE ASPECTS OF NEUROMUSCULAR TRANSMISSION

1973 ◽  
Vol 21 (9) ◽  
pp. 769-778 ◽  
Author(s):  
MIRIAM M. SALPETER ◽  
MOHYEE E. ELDEFRAWI
Keyword(s):  
Surface Area ◽  
Acetylcholine Receptor ◽  
Neuromuscular Transmission ◽  
Nerve Impulse ◽  
Synaptic Cleft ◽  
Postsynaptic Membrane ◽  
Optimal Response ◽  
End Plate

The area of the postsynaptic membrane and the volume of the synaptic cleft were calculated for the end plates of the diaphragm and sternomastoid of mouse and rat. From these dimensions we were able to extrapolate, from data given by others on acetylcholine (ACh) released during neuromuscular transmission and on ACh receptor per whole end plate, to densities in the postneural compartments. The concentration of ACh in the cleft per nerve impulse was found to be ~ 10–5 M and the density of ACh receptor was between 5 and 10 x l03/µ2 of postsynaptic membrane. (This is approximately a factor of 2 to 3 higher than that for acetylcholinesterase at this site.) From these values we conclude that the concentration of ACh receptor in the plane of the postsynaptic membrane is considerably higher than that of ACh in the cleft during neuromuscular transmission. In addition the ACh itself is present at considerably higher concentrations than necessary to give optimal response. We calculated that the acytelcholinesterase plus ACh receptor together would occupy about 25% of the surface area of the postsynaptic membrane.

scholarly journals Model of Postsynaptic Membrane Deactivation

2018 ◽  
Vol 63 (10) ◽  
pp. 919 ◽  
Author(s):  
A. N. Vasilev ◽  
O. V. Kulish
Keyword(s):  
Time Dependence ◽  
Time Distribution ◽  
Nerve Impulse ◽  
Synaptic Cleft ◽  
Postsynaptic Membrane ◽  
Space Time ◽  
Mediator Release ◽  
Activation Time

A model has been proposed to describe the deactivation of a postsynaptic membrane after its excitation by transmitting a nerve impulse across the synapse. In particular, the process of mediator release in the form of choline from the postsynaptic membrane and its diffusive excretion from the synaptic cleft are considered. The time dependence of the number of activated receptors, the dependence of the maximum number of activated receptors on the activation time, and the space-time distribution of the choline concentration in the synaptic cleft are calculated.

scholarly journals Transmembrane Auxiliary Subunits of Voltage-dependent Ion Channels

1996 ◽  
Vol 271 (45) ◽  
pp. 27975-27978 ◽  
Author(s):  
Christina A. Gurnett ◽  
Kevin P. Campbell
Keyword(s):  
Ion Channels ◽  
Auxiliary Subunits ◽  
Voltage Dependent

Control of secretion in anterior pituitary cells--linking ion channels, messengers and exocytosis

1988 ◽  
Vol 139 (1) ◽  
pp. 287-316
Author(s):  
W. T. Mason ◽  
S. R. Rawlings ◽  
P. Cobbett ◽  
S. K. Sikdar ◽  
R. Zorec ◽  
...  
Keyword(s):  
Ion Channels ◽  
Intracellular Calcium ◽  
Anterior Pituitary ◽  
Hormone Secretion ◽  
Cell Types ◽  
Pituitary Cell ◽  
Pituitary Cells ◽  
Calcium Activity ◽  
Anterior Pituitary Cells ◽  
Voltage Dependent

Normal anterior pituitary cells, in their diversity and heterogeneity, provide a rich source of models for secretory function. However, until recently they have largely been neglected in favour of neoplastic, clonal tumour cell lines of pituitary origin, which have enabled a number of studies on supposedly homogeneous cell types. Because many of these lines appear to lack key peptide and neurotransmitter receptors, as well as being degranulated with accompanying abnormal levels of secretion, we have developed a range of normal primary anterior pituitary cell cultures using dispersion and enrichment techniques. By studying lactotrophs, somatotrophs and gonadotrophs we have revealed a number of possible transduction mechanisms by which receptors for hypothalamic peptides and neurotransmitters may control secretion. In particular, the transduction events controlling secretion from pituitary cells may differ fundamentally from those found in other cell types. Patch-clamp recordings in these various pituitary cell preparations have revealed substantial populations of voltage-dependent Na+, Ca2+ and K+ channels which may support action potentials in these cells. Although activation of these channels may gate Ca2+ entry to the cells under some conditions, our evidence taken with that of other laboratories suggests that peptide-receptor interactions leading to hormone secretion occur independently of significant membrane depolarization. Rather, secretion of hormone and rises in intracellular calcium measured with new probes for intracellular calcium activity, can occur in response to hypothalamic peptide activation in the absence of substantial changes in membrane potential. These changes in intracellular calcium activity almost certainly depend on both intracellular and extracellular calcium sources. In addition, strong evidence of a role for multiple intracellular receptors and modulators in the secretory event suggests we should consider the plasma membrane channels important for regulation of hormone secretion to be predominantly agonist-activated, rather than of the more conventional voltage-dependent type. Likewise, evidence from new methods for recording single ion channels suggests the existence of intracellular sites for channel modulation, implying they too may play an important role in secretory regulation. We shall consider new data and new technology which we hope will provide key answers to the many intriguing questions surrounding the control of pituitary hormone secretion. We shall highlight our work with recordings of single ion channels activated by peptides, and recent experiments using imaging of intracellular ionized free calcium.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Proper Voltage-Dependent Ion Channel Function in Dysferlin-Deficient Cardiomyocytes

2015 ◽  
Vol 36 (3) ◽  
pp. 1049-1058 ◽  
Author(s):  
Lena Rubi ◽  
Vaibhavkumar S. Gawali ◽  
Helmut Kubista ◽  
Hannes Todt ◽  
Karlheinz Hilber ◽  
...  
Keyword(s):  
Ion Channels ◽  
Muscular Dystrophy ◽  
Ion Channel ◽  
Cardiac Electrophysiology ◽  
Cardiac Complications ◽  
Membrane Repair ◽  
Patch Clamp Technique ◽  
Cardiac Ion Channels ◽  
Ventricular Cardiomyocytes ◽  
Voltage Dependent

Background/Aims: Dysferlin plays a decisive role in calcium-dependent membrane repair in myocytes. Mutations in the encoding DYSF gene cause a number of myopathies, e.g. limb-girdle muscular dystrophy type 2B (LGMD2B). Besides skeletal muscle degenerative processes, dysferlin deficiency is also associated with cardiac complications. Thus, both LGMD2B patients and dysferlin-deficient mice develop a dilated cardiomyopathy. We and others have recently reported that dystrophin-deficient ventricular cardiomyocytes from mouse models of Duchenne muscular dystrophy show significant abnormalities in voltage-dependent ion channels, which may contribute to the pathophysiology in dystrophic cardiomyopathy. The aim of the present study was to investigate if dysferlin, like dystrophin, is a regulator of cardiac ion channels. Methods and Results: By using the whole cell patch-clamp technique, we compared the properties of voltage-dependent calcium and sodium channels, as well as action potentials in ventricular cardiomyocytes isolated from the hearts of normal and dysferlin-deficient (dysf) mice. In contrast to dystrophin deficiency, the lack of dysferlin did not impair the ion channel properties and left action potential parameters unaltered. In connection with normal ECGs in dysf mice these results suggest that dysferlin deficiency does not perturb cardiac electrophysiology. Conclusion: Our study demonstrates that dysferlin does not regulate cardiac voltage-dependent ion channels, and implies that abnormalities in cardiac ion channels are not a universal characteristic of all muscular dystrophy types.

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