scholarly journals A Transient Receptor Potential-Like Channel Mediates Synaptic Transmission in Rod Bipolar Cells

2009 ◽  
Vol 29 (19) ◽  
pp. 6088-6093 ◽  
Author(s):  
Y. Shen ◽  
J. A. Heimel ◽  
M. Kamermans ◽  
N. S. Peachey ◽  
R. G. Gregg ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Bipolar Cells ◽  
Transient Receptor ◽  
Rod Bipolar Cells

scholarly journals Differential epitope masking reveals synapse-specific complexes of TRPM1

2018 ◽  
Vol 35 ◽  
Author(s):  
MELINA A. AGOSTO ◽  
IVAN A. ANASTASSOV ◽  
THEODORE G. WENSEL
Keyword(s):  
Binding Site ◽  
Transient Receptor Potential ◽  
Transmembrane Domain ◽  
Receptor Potential ◽  
Transient Receptor Potential Channel ◽  
Bipolar Cells ◽  
Mouse Retina ◽  
Binding Partners ◽  
Transient Receptor ◽  
Quantitative Immunoblotting

AbstractThe transient receptor potential channel TRPM1 is required for synaptic transmission between photoreceptors and the ON subtype of bipolar cells (ON-BPC), mediating depolarization in response to light. TRPM1 is present in the somas and postsynaptic dendritic tips of ON-BPCs. Monoclonal antibodies generated against full-length TRPM1 were found to have differential labeling patterns when used to immunostain the mouse retina, with some yielding reduced labeling of dendritic tips relative to the labeling of cell bodies. Epitope mapping revealed that those antibodies that poorly label the dendritic tips share a binding site (N2d) in the N-terminal arm near the transmembrane domain. A major splice variant of TRPM1 lacking exon 19 does not contain the N2d binding site, but quantitative immunoblotting revealed no enrichment of this variant in synaptsomes. One explanation of the differential labeling is masking of the N2d epitope by formation of a synapse-specific multiprotein complex. Identifying the binding partners that are specific for the fraction of TRPM1 present at the synapses is an ongoing challenge for understanding TRPM1 function.

scholarly journals TRPV1 channels contribute to spontaneous glutamate release in nucleus tractus solitarii following chronic intermittent hypoxia

2019 ◽  
Vol 121 (3) ◽  
pp. 881-892 ◽  
Author(s):  
David D. Kline ◽  
Sheng Wang ◽  
Diana L. Kunze
Keyword(s):  
Synaptic Transmission ◽  
Intermittent Hypoxia ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Nucleus Tractus Solitarii ◽  
Chronic Intermittent Hypoxia ◽  
Excitatory Postsynaptic Currents ◽  
Epsc Amplitude ◽  
Postsynaptic Currents ◽  
Transient Receptor

Chronic intermittent hypoxia (CIH) reduces afferent-evoked excitatory postsynaptic currents (EPSCs) but enhances basal spontaneous (s) and asynchronous (a) EPSCs in second-order neurons of nucleus tractus solitarii (nTS), a major area for cardiorespiratory control. The net result is an increase in synaptic transmission. The mechanisms by which this occurs are unknown. The N-type calcium channel and transient receptor potential cation channel TRPV1 play prominent roles in nTS sEPSCs and aEPSCs. The functional role of these channels in CIH-mediated afferent-evoked EPSC, sEPSC, and aEPSC was tested in rat nTS slices following antagonist inhibition and in mouse nTS slices that lack TRPV1. Block of N-type channels decreased aEPSCs in normoxic and, to a lesser extent, CIH-exposed rats. sEPSCs examined in the presence of TTX (miniature EPSCs) were also decreased by N-type block in normoxic but not CIH-exposed rats. Antagonist inhibition of TRPV1 reduced the normoxic and the CIH-mediated increase in sEPSCs, aEPSCs, and mEPSCs. As in rats, in TRPV1+/+ control mice, aEPSCs, sEPSCs, and mEPSCs were enhanced following CIH. However, none were enhanced in TRPV1−/− null mice. Normoxic tractus solitarii (TS)-evoked EPSC amplitude, and the decrease after CIH, were comparable in control and null mice. In rats, TRPV1 was localized in the nodose-petrosal ganglia (NPG) and their central branches. CIH did not alter TRPV1 mRNA but increased its protein in NPG consistent with an increased contribution of TRPV1. Together, our studies indicate TRPV1 contributes to the CIH increase in aEPSCs and mEPSCs, but the CIH reduction in TS-EPSC amplitude occurs via an alternative mechanism. NEW & NOTEWORTHY This study provides information on the underlying mechanisms responsible for the chronic intermittent hypoxia (CIH) increase in synaptic transmission that leads to exaggerated sympathetic nervous and respiratory activity at baseline and in response to low oxygen. We demonstrate that the CIH increase in asynchronous and spontaneous excitatory postsynaptic currents (EPSCs) and miniature EPSCs, but not decrease in afferent-driven EPSCs, is dependent on transient receptor potential vanilloid type 1 (TRPV1). Thus TRPV1 is important in controlling nucleus tractus solitarii synaptic activity during CIH.

scholarly journals Brain-derived Neurotrophic Factor (BDNF)-induced Mitochondrial Motility Arrest and Presynaptic Docking Contribute to BDNF-enhanced Synaptic Transmission

2013 ◽  
Vol 289 (3) ◽  
pp. 1213-1226 ◽  
Author(s):  
Bo Su ◽  
Yun-Song Ji ◽  
Xu-lu Sun ◽  
Xiang-Hua Liu ◽  
Zhe-Yu Chen
Keyword(s):  
Synaptic Transmission ◽  
Neurotrophic Factor ◽  
Hippocampal Neurons ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Brain Derived Neurotrophic Factor ◽  
High Energy ◽  
Mitochondrial Transport ◽  
Mitochondrial Motility ◽  
Transient Receptor

Appropriate mitochondrial transport and distribution are essential for neurons because of the high energy and Ca2+ buffering requirements at synapses. Brain-derived neurotrophic factor (BDNF) plays an essential role in regulating synaptic transmission and plasticity. However, whether and how BDNF can regulate mitochondrial transport and distribution are still unclear. Here, we find that in cultured hippocampal neurons, application of BDNF for 15 min decreased the percentage of moving mitochondria in axons, a process dependent on the activation of the TrkB receptor and its downstream PI3K and phospholipase-Cγ signaling pathways. Moreover, the BDNF-induced mitochondrial stopping requires the activation of transient receptor potential canonical 3 and 6 (TRPC3 and TRPC6) channels and elevated intracellular Ca2+ levels. The Ca2+ sensor Miro1 plays an important role in this process. Finally, the BDNF-induced mitochondrial stopping leads to the accumulation of more mitochondria at presynaptic sites. Mutant Miro1 lacking the ability to bind Ca2+ prevents BDNF-induced mitochondrial presynaptic accumulation and synaptic transmission, suggesting that Miro1-mediated mitochondrial motility is involved in BDNF-induced mitochondrial presynaptic docking and neurotransmission. Together, these data suggest that mitochondrial transport and distribution play essential roles in BDNF-mediated synaptic transmission.

scholarly journals The Absence of the Transient Receptor Potential Vanilloid 1 Directly Impacts on the Expression and Localization of the Endocannabinoid System in the Mouse Hippocampus

2021 ◽  
Vol 15 ◽  
Author(s):  
Jon Egaña-Huguet ◽  
Itziar Bonilla-Del Río ◽  
Sonia M. Gómez-Urquijo ◽  
Amaia Mimenza ◽  
Miquel Saumell-Esnaola ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Transient Receptor Potential ◽  
Acid Amide ◽  
Endocannabinoid System ◽  
Receptor Potential ◽  
Perforant Path ◽  
Transient Receptor Potential Vanilloid ◽  
Excitatory Synapses ◽  
Selective Ligand ◽  
Transient Receptor

The transient receptor potential vanilloid 1 (TRPV1) is a non-selective ligand-gated cation channel involved in synaptic transmission, plasticity, and brain pathology. In the hippocampal dentate gyrus, TRPV1 localizes to dendritic spines and dendrites postsynaptic to excitatory synapses in the molecular layer (ML). At these same synapses, the cannabinoid CB1 receptor (CB1R) activated by exogenous and endogenous cannabinoids localizes to the presynaptic terminals. Hence, as both receptors are activated by endogenous anandamide, co-localize, and mediate long-term depression of the excitatory synaptic transmission at the medial perforant path (MPP) excitatory synapses though by different mechanisms, it is plausible that they might be exerting a reciprocal influence from their opposite synaptic sites. In this anatomical scenario, we tested whether the absence of TRPV1 affects the endocannabinoid system. The results obtained using biochemical techniques and immunoelectron microscopy in a mouse with the genetic deletion of TRPV1 show that the expression and localization of components of the endocannabinoid system, included CB1R, change upon the constitutive absence of TRPV1. Thus, the expression of fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) drastically increased in TRPV1−/− whole homogenates. Furthermore, CB1R and MAGL decreased and the cannabinoid receptor interacting protein 1a (CRIP1a) increased in TRPV1−/− synaptosomes. Also, CB1R positive excitatory terminals increased, the number of excitatory terminals decreased, and CB1R particles dropped significantly in inhibitory terminals in the dentate ML of TRPV1−/− mice. In the outer 2/3 ML of the TRPV1−/− mutants, the proportion of CB1R particles decreased in dendrites, and increased in excitatory terminals and astrocytes. In the inner 1/3 ML, the proportion of labeling increased in excitatory terminals, neuronal mitochondria, and dendrites. Altogether, these observations indicate the existence of compensatory changes in the endocannabinoid system upon TRPV1 removal, and endorse the importance of the potential functional adaptations derived from the lack of TRPV1 in the mouse brain.

scholarly journals mGluR6 deletion renders the TRPM1 channel in retina inactive

2012 ◽  
Vol 107 (3) ◽  
pp. 948-957 ◽  
Author(s):  
Ying Xu ◽  
Anuradha Dhingra ◽  
Marie E. Fina ◽  
Chieko Koike ◽  
Takahisa Furukawa ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
G Protein ◽  
Transient Receptor Potential ◽  
Metabotropic Glutamate Receptor ◽  
Receptor Potential ◽  
Bipolar Cells ◽  
Wild Type ◽  
Protein Subunit ◽  
Transient Receptor Potential Melastatin ◽  
Rod Bipolar Cells

In darkness, glutamate released from photoreceptors activates the metabotropic glutamate receptor 6 (mGluR6) on retinal ON bipolar cells. This activates the G protein Go, which then closes transient receptor potential melastatin 1 (TRPM1) channels, leading to cells' hyperpolarization. It has been generally assumed that deleting mGluR6 would render the cascade inactive and the ON bipolar cells constitutively depolarized. Here we show that the rod bipolar cells in mGluR6-null mice were hyperpolarized. The slope conductance of the current-voltage curves and the current noise were smaller than in wild type. Furthermore, while in wild-type rod bipolar cells, TRPM1 could be activated by local application of capsaicin; in null cells, it did not. These results suggest that the TRPM1 channel in mGluR6-null rod bipolar cells is inactive. To explore the reason for this lack of activity, we tested if mGluR6 deletion affected expression of cascade components. Immunostaining for G protein subunit candidates Gαo, Gβ3, and Gγ13 showed no significant changes in their expression or distribution. Immunostaining for TRPM1 in the dendritic tips was greatly reduced, but the channel was still present in the soma and primary dendrites of mGluR6-null bipolar cells, where a certain fraction of TRPM1 appears to localize to the plasma membrane. Consequently, the lack of TRPM1 activity in the null retina is unlikely to be due to failure of the channels to localize to the plasma membrane. We speculate that, to be constitutively active, TRPM1 channels in ON bipolar cells have to be in a complex, or perhaps require an unidentified factor.

scholarly journals Autoantibody against transient receptor potential M1 cation channels of retinal ON bipolar cells in paraneoplastic vitelliform retinopathy

2012 ◽  
Vol 12 (1) ◽  
Author(s):  
Yujuan Wang ◽  
Mones S Abu-Asab ◽  
Wei Li ◽  
Mary E Aronow ◽  
Arun D Singh ◽  
...  
Keyword(s):  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Bipolar Cells ◽  
Cation Channels ◽  
Transient Receptor
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