scholarly journals An Atypical Role for Collapsin Response Mediator Protein 2 (CRMP-2) in Neurotransmitter Release via Interaction with Presynaptic Voltage-gated Calcium Channels

2009 ◽  
Vol 284 (45) ◽  
pp. 31375-31390 ◽  
Author(s):  
Joel M. Brittain ◽  
Andrew D. Piekarz ◽  
Yuying Wang ◽  
Takako Kondo ◽  
Theodore R. Cummins ◽  
...  
Keyword(s):  
Calcium Channels ◽  
Neurotransmitter Release ◽  
Collapsin Response Mediator Protein ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Mediator Protein

scholarly journals Functions of Presynaptic Voltage-gated Calcium Channels

Function ◽  
2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Annette C Dolphin
Keyword(s):  
Calcium Channels ◽  
Neurotransmitter Release ◽  
Action Potentials ◽  
Voltage Dependence ◽  
Kinetic Properties ◽  
Excitable Cells ◽  
Single Action ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Vesicular Release

Abstract Voltage-gated calcium channels are the principal conduits for depolarization-mediated Ca2+ entry into excitable cells. In this review, the biophysical properties of the relevant members of this family of channels, those that are present in presynaptic terminals, will be discussed in relation to their function in mediating neurotransmitter release. Voltage-gated calcium channels have properties that ensure they are specialized for particular roles, for example, differences in their activation voltage threshold, their various kinetic properties, and their voltage-dependence of inactivation. All these attributes play into the ability of the various voltage-gated calcium channels to participate in different patterns of presynaptic vesicular release. These include synaptic transmission resulting from single action potentials, and longer-term changes mediated by bursts or trains of action potentials, as well as release resulting from graded changes in membrane potential in specialized sensory synapses.

scholarly journals GABAB Receptors Couple to Potassium and Calcium Channels on Identified Lateral Perforant Pathway Projection Neurons

2000 ◽  
Vol 83 (2) ◽  
pp. 1073-1078 ◽  
Author(s):  
Xueyong Wang ◽  
Nevin A. Lambert
Keyword(s):  
Calcium Channels ◽  
Neurotransmitter Release ◽  
Granule Cells ◽  
Dorsal Hippocampus ◽  
Gabab Receptors ◽  
Projection Neurons ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Perforant Pathway ◽  
Inward Currents

Activation of presynaptic GABAB receptors inhibits neurotransmitter release at most cortical synapses, at least in part because of inhibition of voltage-gated calcium channels. One synapse where this is not the case is the lateral perforant pathway synapse onto dentate granule cells in the hippocampus. The current study was conducted to determine whether the neurons that make these synapses express GABAB receptors that can couple to ion channels. Perforant pathway projection neurons were labeled by injecting retrograde tracer into the dorsal hippocampus. The GABAB receptor agonist baclofen (10 μM) activated inwardly rectifying potassium channels and inhibited currents mediated by voltage-gated calcium channels in retrogradely labeled neurons in layer II of the lateral entorhinal cortex. These effects were reversed by coapplication of the selective GABAB receptor antagonist CGP 55845A (1 μM). Equivalent effects were produced by 100 μM adenosine, which inhibits neurotransmitter release at lateral perforant pathway synapses. The effects of baclofen and adenosine on inward currents were largely occlusive. These results suggest that the absence of GABAB receptor-mediated presynaptic inhibition at lateral perforant pathway synapses is not simply due to a failure to express these receptors and imply that GABAB receptors can either be selectively localized or regulated at terminal versus somatodendritic domains.

scholarly journals Presynaptic Paraneoplastic Disorders of the Neuromuscular Junction: An Update

2021 ◽  
Vol 11 (8) ◽  
pp. 1035
Author(s):  
Maria Pia Giannoccaro ◽  
Patrizia Avoni ◽  
Rocco Liguori
Keyword(s):  
Potassium Channels ◽  
Neuromuscular Junction ◽  
Calcium Channels ◽  
Myasthenia Gravis ◽  
Neuromuscular Transmission ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Immune Mediated ◽  
Recent Developments ◽  
Myasthenic Syndrome

The neuromuscular junction (NMJ) is the target of a variety of immune-mediated disorders, usually classified as presynaptic and postsynaptic, according to the site of the antigenic target and consequently of the neuromuscular transmission alteration. Although less common than the classical autoimmune postsynaptic myasthenia gravis, presynaptic disorders are important to recognize due to the frequent association with cancer. Lambert Eaton myasthenic syndrome is due to a presynaptic failure to release acetylcholine, caused by antibodies to the presynaptic voltage-gated calcium channels. Acquired neuromyotonia is a condition characterized by nerve hyperexcitability often due to the presence of antibodies against proteins associated with voltage-gated potassium channels. This review will focus on the recent developments in the autoimmune presynaptic disorders of the NMJ.

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