Human presynaptic receptors

2017 ◽  
Vol 172 ◽  
pp. 1-21 ◽  
Author(s):  
Eberhard Schlicker ◽  
Thomas Feuerstein
Keyword(s):  
Presynaptic Receptors

scholarly journals Direct assessment of presynaptic modulation of cortico-striatal glutamate release in a Huntington’s disease mouse model

2018 ◽  
Vol 120 (6) ◽  
pp. 3077-3084 ◽  
Author(s):  
Ellen T. Koch ◽  
Cameron L. Woodard ◽  
Lynn A. Raymond
Keyword(s):  
Mouse Model ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
High Frequency ◽  
Glutamate Release ◽  
Presynaptic Receptors ◽  
High Frequency Stimulation ◽  
Presynaptic Modulation ◽  
Frequency Stimulation

Glutamate is the main excitatory neurotransmitter in the brain, and impairments in its signaling are associated with many neurological disorders, including Huntington’s disease (HD). Previous studies in HD mouse models demonstrate altered glutamate receptor distribution and signaling at cortico-striatal synapses, and some studies suggest that glutamate release is altered; however, traditional methods to study synaptic glutamate release are indirect or have poor temporal resolution. Here we utilize iGluSnFR, a modified green fluorescent protein reporter for real-time imaging of glutamate transmission, to study presynaptic modulation of cortical glutamate release in the striatum of the YAC128 HD mouse model. We determined that iGluSnFR can be used to accurately measure short- and long-term changes in glutamate release caused by modulation of extracellular Ca2+ levels, activation of presynaptic receptors, and high-frequency stimulation (HFS) protocols. We also confirmed a difference in the expression of HFS-induced long-term depression in YAC128. Together, this research demonstrates the utility of iGluSnFR in studying presynaptic modulation of glutamate release in healthy mice and disease models that display impairments in glutamate signaling. NEW & NOTEWORTHY We use iGluSnFR to directly assess presynaptic modulation of cortico-striatal glutamate release in brain slice and compare changes in glutamate release between wild type and a Huntington’s disease mouse model, YAC128. We observed reductions in glutamate release after low extracellular Ca2+ and activation of various presynaptic receptors. We also demonstrate a presynaptic mechanism of reduced glutamate release in high-frequency stimulation-induced long-term depression and show this to be altered in YAC128.

Influence of presynaptic receptors on neuromuscular transmission in rat

1982 ◽  
Vol 242 (5) ◽  
pp. C366-C372 ◽  
Author(s):  
D. F. Wilson
Keyword(s):  
Transmitter Release ◽  
Action Potentials ◽  
Physiological Function ◽  
Motor Nerve ◽  
Presynaptic Receptors ◽  
End Plate ◽  
Feedback Pathway ◽  
Partial Blockade ◽  
Ach Receptors

The presence and physiological significance of acetylcholine (ACh) receptors on motor nerve terminals was examined at the rat diaphragm neuromuscular junction. Intracellular recording techniques were used to monitor end-plate potentials (EPP), miniature end-plate potentials (MEPP), and resting potentials of the muscle fibers. Muscle action potentials were blocked by the cut-muscle technique. Quantal release was determined by the ratio EPP/MEPP, after correcting for nonlinear summation. Blockade of acetylcholinesterase with eserine and neostigmine was tested to determine the influence of residual ACh on transmitter release. Partial blockade of ACh receptors with curare was examined to further clarify the role of these presynaptic receptors. The experiments demonstrate that residual ACh inhibits transmitter release and that blockade of ACh receptors enhances transmitter release. It is concluded that presynaptic ACh receptors exist and that they serve an important physiological function. It is suggested that the presynaptic ACh receptors normally serve to limit transmitter release in a negative feedback pathway.

Potentiation of Neuromuscular Transmission by an Octopaminergic Neurone in the Locust

1979 ◽  
Vol 79 (1) ◽  
pp. 169-190 ◽  
Author(s):  
MICHAEL O'SHEA ◽  
PETER D. EVANS
Keyword(s):  
Indirect Effects ◽  
Neuromuscular Transmission ◽  
Time Course ◽  
Muscle Tone ◽  
Muscle Tension ◽  
Presynaptic Receptors ◽  
Extensor Muscle ◽  
Muscle Membrane ◽  
Muscle Fibres ◽  
Central Synapses

1. Spikes in the octopaminergic dorsal unpaired median (DUM) neurone which innervates the extensor tibiae muscle of the locust metathoracic leg (DUMETi) produce direct and indirect effects on muscle tension. 2. Direct effects include a slowing of an intrinsic rhythm of contraction and relaxation, a relaxation of muscle tone and a small hyperpolarization of the muscle membrane potential. The latter two effects are weak and variable. All three effects are mimicked by superfusion of octopamine and are mediated by octopamine receptors on the muscle fibres. 3. Indirect effects are found when the DUMETi neurone is stimulated at the same time as the motoneurones innervating the extensor muscle. They include (a) potentiation of tension generated in the extensor muscle by spikes in the slow excitatory motoneurone (SETi), (b) reduction in duration of each twitch contraction generated by SETi due to an increase in the rate at which the muscle relaxes, (c) increase in the amplitude of the synaptic potential generated by SETi. These various effects have a time course of several minutes and far outlast the duration of DUMETi stimulation. They can be mimicked by superfusion of octopamine. 4. The effect of DUMETi on neuromuscular transmission is mediated by receptors with a high affinity for octopamine located both on the muscle and on the terminals of the slow motoneurone. The presence of the presynaptic receptors is revealed by the increase in the frequency of spontaneous miniature end plate potentials recorded in the muscle in the presence of octopamine. 5. DUMETi is a member of a group of similar aminergic neurones and it is suggested that they may share a role in modulating transmission at peripheral neuromuscular synapses, and possibly central synapses.

Presynaptic inhibition by serotonin of nerve-mediated secretion of pancreatic amylase

1995 ◽  
Vol 268 (2) ◽  
pp. G339-G345 ◽  
Author(s):  
A. L. Kirchgessner ◽  
M. D. Gershon
Keyword(s):  
Presynaptic Inhibition ◽  
Cholinergic Neurons ◽  
Acinar Cells ◽  
Presynaptic Receptors ◽  
Amylase Secretion ◽  
Pancreatic Amylase ◽  
Inhibitory Receptor ◽  
Cholinergic Nerves ◽  
Positive Identification ◽  
Fos Expression

Enteric cholinergic and serotonergic neurons innervate pancreatic ganglia. Enteropancreatic cholinergic neurons are secretomotor, bu the function of the serotonergic cells is unknown and was investigated. Postganglionic cholinergic nerve-mediated amylase secretion was evoked by veratridine in isolated pancreatic lobules. This concentration-dependent response was inhibited by tetrodotoxin (1.0 microM), atropine (5.0 microM), 5-hydroxytryptamine (5-HT; 5.0 microM), 5-hydroxyindalpine (5-OHIP; 10.0 microM; a 5-HT1P agonist), and 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT; 0.1 microM), but not by hexamethonium (100.0 microM), 2-methyl-5-HT (10 microM), or 5-carboxyamidotryptamine (10 microM). The effects of 5-HT and 5-OHIP were blocked by the 5-HT1P antagonist N-acetyl-5-hydroxytryptophyl-5-hydroxytryptophan amide (5-HTP-DP; 100.0 microM). Carbachol (5.0 microM)-evoked secretion was not affected by 5-HT or 5-OHIP. Veratridine induced c-fos expression in pancreatic neurons and acinar cells. This expression was inhibited by tetrodotoxin, 5-HT, and 5-OHIP. These observations suggest that the serotonergic enteropancreatic innervation inhibits pancreatic secretion via presynaptic receptors on cholinergic nerves. Although the data are consistent with the hypothesis that the inhibitory receptor is a 5-HT1P site, positive identification awaits further study.

scholarly journals Differentially poised vesicles underlie fast and slow components of release at single synapses

2020 ◽  
Vol 152 (5) ◽  
Author(s):  
Kris Blanchard ◽  
Javier Zorrilla de San Martín ◽  
Alain Marty ◽  
Isabel Llano ◽  
Federico F. Trigo
Keyword(s):  
Action Potential ◽  
Laser Pulses ◽  
Presynaptic Receptors ◽  
Vesicular Release ◽  
Strong Stimulation ◽  
Subthreshold Laser ◽  
Presynaptic Calcium ◽  
Two Phases ◽  
Synaptic Vesicle Release ◽  
Selective Enhancement

In several types of central mammalian synapses, sustained presynaptic stimulation leads to a sequence of two components of synaptic vesicle release, reflecting the consecutive contributions of a fast-releasing pool (FRP) and of a slow-releasing pool (SRP). Previous work has shown that following common depletion by a strong stimulation, FRP and SRP recover with different kinetics. However, it has remained unclear whether any manipulation could lead to a selective enhancement of either FRP or SRP. To address this question, we have performed local presynaptic calcium uncaging in single presynaptic varicosities of cerebellar interneurons. These varicosities typically form “simple synapses” onto postsynaptic interneurons, involving several (one to six) docking/release sites within a single active zone. We find that strong uncaging laser pulses elicit two phases of release with time constants of ∼1 ms (FRP release) and ∼20 ms (SRP release). When uncaging was preceded by action potential–evoked vesicular release, the extent of SRP release was specifically enhanced. We interpret this effect as reflecting an increased likelihood of two-step release (docking then release) following the elimination of docked synaptic vesicles by action potential–evoked release. In contrast, a subthreshold laser-evoked calcium elevation in the presynaptic varicosity resulted in an enhancement of the FRP release. We interpret this latter effect as reflecting an increased probability of occupancy of docking sites following subthreshold calcium increase. In conclusion, both fast and slow components of release can be specifically enhanced by certain presynaptic manipulations. Our results have implications for the mechanism of docking site replenishment and the regulation of synaptic responses, in particular following activation of ionotropic presynaptic receptors.

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