scholarly journals TRPM7 is critical for short-term synaptic depression by regulating synaptic vesicle endocytosis

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Zhong-Jiao Jiang ◽  
Wenping Li ◽  
Li-Hua Yao ◽  
Badeia Saed ◽  
Yan Rao ◽  
...  
Keyword(s):  
Nervous System ◽  
Synaptic Vesicle ◽  
Neuronal Death ◽  
Physiological Role ◽  
Neuroendocrine Cells ◽  
Short Term ◽  
Widespread Distribution ◽  
Short Term Plasticity ◽  
Inhibitory Synaptic Transmission

TRPM7 contributes to a variety of physiological and pathological processes in many tissues and cells. With a widespread distribution in the nervous system, TRPM7 is involved in animal behaviors and neuronal death induced by ischemia. However, the physiological role of TRPM7 in CNS neuron remains unclear. Here, we identify endocytic defects in neuroendocrine cells and neurons from TRPM7 knockout (KO) mice, indicating a role of TRPM7 in synaptic vesicle endocytosis. Our experiments further pinpoint the importance of TRPM7 as an ion channel in synaptic vesicle endocytosis. Ca2+ imaging detects a defect in presynaptic Ca2+ dynamics in TRPM7 KO neuron, suggesting an importance of Ca2+ influx via TRPM7 in synaptic vesicle endocytosis. Moreover, the short-term depression is enhanced in both excitatory and inhibitory synaptic transmission from TRPM7 KO mice. Taken together, our data suggests that Ca2+ influx via TRPM7 may be critical for short-term plasticity of synaptic strength by regulating synaptic vesicle endocytosis in neurons.

scholarly journals TRPM7 is critical for short-term synaptic depression by regulating synaptic vesicle endocytosis

2021 ◽  
Author(s):  
Zhong-Jiao Jiang ◽  
Wenping Li ◽  
Li-Hua Yao ◽  
Brian S. Grewe ◽  
Andrea McGinley ◽  
...  
Keyword(s):  
Nervous System ◽  
Synaptic Vesicle ◽  
Neuronal Death ◽  
Physiological Role ◽  
Neuroendocrine Cells ◽  
Short Term ◽  
Widespread Distribution ◽  
Short Term Plasticity ◽  
Inhibitory Synaptic Transmission

AbstractTRPM7 contributes to a variety of physiological and pathological processes in many tissues and cells. With a widespread distribution in the nervous system, TRPM7 is involved in animal behaviors and neuronal death induced by ischemia. However, the physiological role of TRPM7 in CNS neuron remains unclear. Here, we identify endocytic defects in neuroendocrine cells and neurons from TRPM7 knockout (KO) mice, indicating a role of TRPM7 in synaptic vesicle endocytosis. Our experiments further pinpoint the importance of TRPM7 as an ion channel in synaptic vesicle endocytosis. Ca2+ imaging detects a defect in presynaptic Ca2+ dynamics in TRPM7 KO neuron, suggesting an importance of Ca2+ influx via TRPM7 in synaptic vesicle endocytosis. Moreover, the short-term depression is enhanced in both excitatory and inhibitory synaptic transmission from TRPM7 KO mice. Taking together, our data suggests that Ca2+ influx via TRPM7 may be critical for short-term plasticity of synaptic strength by regulating synaptic vesicle endocytosis in neurons.

Synapsin Regulates Basal Synaptic Strength, Synaptic Depression, and Serotonin-Induced Facilitation of Sensorimotor Synapses in Aplysia

2007 ◽  
Vol 98 (6) ◽  
pp. 3568-3580 ◽  
Author(s):  
Diasinou Fioravante ◽  
Rong-Yu Liu ◽  
Anne K. Netek ◽  
Leonard J. Cleary ◽  
John H. Byrne
Keyword(s):  
Synaptic Plasticity ◽  
Synaptic Vesicle ◽  
Transmitter Release ◽  
Computational Analysis ◽  
Spontaneous Recovery ◽  
Synaptic Strength ◽  
Short Term ◽  
Homosynaptic Depression ◽  
Heterosynaptic Plasticity

Synapsin is a synaptic vesicle-associated protein implicated in the regulation of vesicle trafficking and transmitter release, but its role in heterosynaptic plasticity remains elusive. Moreover, contradictory results have obscured the contribution of synapsin to homosynaptic plasticity. We previously reported that the neuromodulator serotonin (5-HT) led to the phosphorylation and redistribution of Aplysia synapsin, suggesting that synapsin may be a good candidate for the regulation of vesicle mobilization underlying the short-term synaptic plasticity induced by 5-HT. This study examined the role of synapsin in homosynaptic and heterosynaptic plasticity. Overexpression of synapsin reduced basal transmission and enhanced homosynaptic depression. Although synapsin did not affect spontaneous recovery from depression, it potentiated 5-HT–induced dedepression. Computational analysis showed that the effects of synapsin on plasticity could be adequately simulated by altering the rate of Ca2+-dependent vesicle mobilization, supporting the involvement of synapsin not only in homosynaptic but also in heterosynaptic forms of plasticity by regulating vesicle mobilization.

Muscarinic presynaptic modulation in GABAergic pallidal synapses of the rat

2015 ◽  
Vol 113 (3) ◽  
pp. 796-807 ◽  
Author(s):  
Ricardo Hernández-Martínez ◽  
José J. Aceves ◽  
Pavel E. Rueda-Orozco ◽  
Teresa Hernández-Flores ◽  
Omar Hernández-González ◽  
...  
Keyword(s):  
Receptor Agonist ◽  
Projection Neurons ◽  
Quantal Content ◽  
Short Term ◽  
Paired Pulse ◽  
Short Term Plasticity ◽  
Striatal Projection Neurons ◽  
Muscarinic Cholinergic ◽  
Muscarinic Modulation

The external globus pallidus (GPe) is central for basal ganglia processing. It expresses muscarinic cholinergic receptors and receives cholinergic afferents from the pedunculopontine nuclei (PPN) and other regions. The role of these receptors and afferents is unknown. Muscarinic M1-type receptors are expressed by synapses from striatal projection neurons (SPNs). Because axons from SPNs project to the GPe, one hypothesis is that striatopallidal GABAergic terminals may be modulated by M1 receptors. Alternatively, some M1 receptors may be postsynaptic in some pallidal neurons. Evidence of muscarinic modulation in any of these elements would suggest that cholinergic afferents from the PPN, or other sources, could modulate the function of the GPe. In this study, we show this evidence using striatopallidal slice preparations: after field stimulation in the striatum, the cholinergic muscarinic receptor agonist muscarine significantly reduced the amplitude of inhibitory postsynaptic currents (IPSCs) from synapses that exhibited short-term synaptic facilitation. This inhibition was associated with significant increases in paired-pulse facilitation, and quantal content was proportional to IPSC amplitude. These actions were blocked by atropine, pirenzepine, and mamba toxin-7, suggesting that receptors involved were M1. In addition, we found that some pallidal neurons have functional postsynaptic M1 receptors. Moreover, some evoked IPSCs exhibited short-term depression and a different kind of modulation: they were indirectly modulated by muscarine via the activation of presynaptic cannabinoid CB1 receptors. Thus pallidal synapses presenting distinct forms of short-term plasticity were modulated differently.

scholarly journals 1M0900 The role of Ca^ concentration for short term plasticity (augmentation, potentiation)

2002 ◽  
Vol 42 (supplement2) ◽  
pp. S73
Author(s):  
H. Yamamoto ◽  
M. Murase ◽  
N. Suzuki
Keyword(s):  
Short Term ◽  
Short Term Plasticity

scholarly journals Store-Operated Calcium Channels in Physiological and Pathological States of the Nervous System

2020 ◽  
Vol 14 ◽  
Author(s):  
Isis Zhang ◽  
Huijuan Hu
Keyword(s):  
Nervous System ◽  
Calcium Channels ◽  
Neurological Disorders ◽  
Neurological Diseases ◽  
Physiological Role ◽  
The Body ◽  
Store Operated Calcium Entry ◽  
Important Pathway ◽  
Molecular Components

Store-operated calcium channels (SOCs) are widely expressed in excitatory and non-excitatory cells where they mediate significant store-operated calcium entry (SOCE), an important pathway for calcium signaling throughout the body. While the activity of SOCs has been well studied in non-excitable cells, attention has turned to their role in neurons and glia in recent years. In particular, the role of SOCs in the nervous system has been extensively investigated, with links to their dysregulation found in a wide variety of neurological diseases from Alzheimer’s disease (AD) to pain. In this review, we provide an overview of their molecular components, expression, and physiological role in the nervous system and describe how the dysregulation of those roles could potentially lead to various neurological disorders. Although further studies are still needed to understand how SOCs are activated under physiological conditions and how they are linked to pathological states, growing evidence indicates that SOCs are important players in neurological disorders and could be potential new targets for therapies. While the role of SOCE in the nervous system continues to be multifaceted and controversial, the study of SOCs provides a potentially fruitful avenue into better understanding the nervous system and its pathologies.

Leptin response to short-term fasting in sympathectomized men: role of the SNS

2003 ◽  
Vol 284 (3) ◽  
pp. E634-E640 ◽  
Author(s):  
Justin Y. Jeon ◽  
Vicki J. Harber ◽  
Robert D. Steadward
Keyword(s):  
Body Mass Index ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Short Term ◽  
Cord Injury ◽  
Before And After ◽  
Sympathetic Nervous ◽  
Plasma Leptin

We studied plasma leptin levels in six people with high-lesion spinal cord injury [SCI; body mass index (BMI) 25.9 ± 1.5 kg/m2, age 37 ± 3.0 yr] and six able-bodied (AB) controls (BMI 29.1 ± 1.9 kg/m2, age 35 ± 3.5 yr) before and after 12, 24, and 36 h of fasting. The plasma leptin levels significantly decreased during 36 h fasting by 48.8 ± 4.5% (pre: 11.3 ± 2.3, post: 6.2 ± 1.5 ng/ml) and 38.6 ± 7.9% (pre: 7.6 ± 5.0, post: 4.2 ± 1.0 ng/ml) in SCI and AB, respectively. Plasma leptin started to decrease at 24 h of fasting in the SCI group, whereas plasma leptin started to decrease at 12 h of fasting in the AB group. The current study demonstrated that plasma leptin decreased with fasting in both SCI and AB groups, with the leptin decrease being delayed in the SCI group. The delayed leptin response to fasting in the SCI group may be because of increased fat mass (%body fat, SCI: 33.8 ± 3.0, AB: 24.1 ± 2.9) and sympathetic nervous system dysfunction.

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