scholarly journals Optical quantal analysis of synaptic transmission in wild-type and rab3-mutant Drosophila motor axons

2011 ◽  
Vol 14 (4) ◽  
pp. 519-526 ◽  
Author(s):  
Einat S Peled ◽  
Ehud Y Isacoff
Keyword(s):  
Synaptic Transmission ◽  
Motor Axons ◽  
Wild Type ◽  
Quantal Analysis

scholarly journals The splicing regulator PTBP2 controls a program of embryonic splicing required for neuronal maturation

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Qin Li ◽  
Sika Zheng ◽  
Areum Han ◽  
Chia-Ho Lin ◽  
Peter Stoilov ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Neurite Growth ◽  
Protein Isoforms ◽  
Neuronal Maturation ◽  
Wild Type ◽  
Mouse Cortex ◽  
Final Maturation ◽  
Splicing Regulator ◽  
Mutant Cells ◽  
Normal Cortex

We show that the splicing regulator PTBP2 controls a genetic program essential for neuronal maturation. Depletion of PTBP2 in developing mouse cortex leads to degeneration of these tissues over the first three postnatal weeks, a time when the normal cortex expands and develops mature circuits. Cultured Ptbp2−/− neurons exhibit the same initial viability as wild type, with proper neurite outgrowth and marker expression. However, these mutant cells subsequently fail to mature and die after a week in culture. Transcriptome-wide analyses identify many exons that share a pattern of mis-regulation in the mutant brains, where isoforms normally found in adults are precociously expressed in the developing embryo. These transcripts encode proteins affecting neurite growth, pre- and post-synaptic assembly, and synaptic transmission. Our results define a new genetic regulatory program, where PTBP2 acts to temporarily repress expression of adult protein isoforms until the final maturation of the neuron.

Delayed Synaptic Transmission in Drosophila cacophonynull Embryos

2008 ◽  
Vol 100 (5) ◽  
pp. 2833-2842 ◽  
Author(s):  
Jiamei Hou ◽  
Takuya Tamura ◽  
Yoshiaki Kidokoro
Keyword(s):  
Neuromuscular Junction ◽  
Synaptic Transmission ◽  
Nerve Stimulation ◽  
Wild Type ◽  
Synaptic Currents ◽  
Voltage Gated ◽  
Delayed Release ◽  
Spider Toxin ◽  
High K

Ca2+ influx through the Drosophila N-type Ca2+ channel, encoded by cacophony ( cac), triggers fast synaptic transmission. We now ask whether the cac Ca2+ channel is the Ca2+ channel solely dedicated for fast synaptic transmission. Because the cac null mutation is lethal, we used cac null embryos to address this question. At the neuromuscular junction in HL3 solution, no fast synchronous synaptic transmission was detected on nerve stimulation. When the wild-type cac gene was introduced in the cac null background, fast synaptic transmission recovered. However, even in cac null embryos, nerve stimulation infrequently induced delayed synaptic events in the minority of cells in 1.5 mM [Ca2+]e and in the majority of cells in 5 mM [Ca2+]e. The number of delayed quantal events per stimulus was greater in 5 mM [Ca2+]e than in 1.5 mM. Thus the delayed release is [Ca2+]e dependent. Plectreurys toxin II (PLTXII) (10 nM; a spider toxin analog) depressed the frequency of delayed events, suggesting that voltage-gated Ca2+ channels, other than cac Ca2+ channels, are contributing to them. However, delayed events were not affected by 50 μM La3+. The frequency of miniature synaptic currents in cac null embryos was ∼1/2 of control, whereas in high K+ solutions, it was ∼1/135. The hypertonicity response was ∼1/10 of control. These findings indicate that the number of release-ready vesicles is smaller in cac null embryos. Taken together, the cac Ca2+ channel is indispensable for fast synaptic transmission in normal conditions, and another type of Ca2+ channel, the non- cac, PLTXII-sensitive Ca2+ channel, is contributing to delayed release in cacnull embryos.

Quantal analysis of synaptic transmission in hippocampus

1988 ◽  
Vol 7 ◽  
pp. S78
Author(s):  
Chosaburo Yamamoto ◽  
Satsuki Sawada ◽  
Kazuo Koshiya
Keyword(s):  
Synaptic Transmission ◽  
Quantal Analysis

scholarly journals Glial response to hypoxia in trachealess mutants induces synapse remodeling

2019 ◽  
Author(s):  
Pei-Yi Chen ◽  
Yi-Wei Tsai ◽  
Angela Giangrande ◽  
Cheng-Ting Chien
Keyword(s):  
Synaptic Transmission ◽  
Neuromuscular Junctions ◽  
Hypoxia Inducible Factor ◽  
Wild Type ◽  
Animal Cells ◽  
Hypoxia Response ◽  
Synaptic Remodeling ◽  
Environmental Perturbations ◽  
Synaptic Structure ◽  
And Function

AbstractSynaptic structure and activity are sensitive to environmental alterations. Modulation of synaptic morphology and function is often induced by signals from glia. However, the process by which glia mediate synaptic responses to environmental perturbations such as hypoxia remains unknown. Here, we report that, in the Drosophila trachealess (trh) mutant, smaller synaptic boutons form clusters named bunch boutons appear at larval neuromuscular junctions (NMJs), which is induced by the reduction of internal oxygen levels due to defective tracheal branches. Thus, the bunch bouton phenotype in the trh mutant is suppressed by hyperoxia, and recapitulated in wild-type larvae raised under hypoxia. We further show that hypoxia-inducible factor (HIF)-1α/Similar (Sima) is critical in mediating hypoxia-induced bunch bouton formation. Sima upregulates the level of the Wnt/Wingless (Wg) signal in glia, leading to reorganized microtubule structures within presynaptic sites. Finally, hypoxia-induced bunch boutons maintain normal synaptic transmission at the NMJs, which is crucial for coordinated larval locomotion.Author summaryOxygen is essential for animals to maintain their life such as growth, metabolism, responsiveness, and movement. It is therefore important to understand how animal cells trigger hypoxia response and adapt to hypoxia thereafter. Both mammalian vascular and insect tracheal branches are induced to enhance the oxygen delivery. However, the study of hypoxia response in the nervous system remains limited. In this study, we assess the morphology of Drosophila neuromuscular junctions (NMJs), a model system to study development and function of synapses, in two hypoxia conditions, one with raising wild-type larvae in hypoxia, and the other in the trachealess (trh) mutant in which the trachea is defective, causing insufficient oxygen supply. Interestingly, glia, normally wrapping the axons of NMJs, invade into synapse and trigger Wg signals to reconstitute the synaptic structure under hypoxia. This synaptic remodeling maintains the synaptic transmission of synapse, which associate the locomotor behavior of larvae.

scholarly journals Neuronal NT-3 Is not Required For Synaptic Transmission or Long-Term Potentiation in Area CA1 of the Adult Rat Hippocampus

1999 ◽  
Vol 6 (3) ◽  
pp. 267-275 ◽  
Author(s):  
Long Ma ◽  
Gerald Reis ◽  
Luis F. Parada ◽  
Erin M. Schuman
Keyword(s):  
Synaptic Transmission ◽  
Hippocampal Slices ◽  
Field Potential ◽  
Early Death ◽  
Long Term Potentiation ◽  
Wild Type ◽  
Adult Rat ◽  
Term Potentiation ◽  
Knockout Animals

Neurotrophic factors, including BDNF and NT-3, have been implicated in the regulation of synaptic transmission and plasticity. Previous attempts to analyze synaptic transmission and plasticity in mice lacking the NT-3 gene have been hampered by the early death of the NT-3 homozygous knockout animals. We have bypassed this problem by examining synaptic transmission in mice in which the NT-3 gene is deleted in neurons later in development, by crossing animals expressing the CRE recombinase driven by the synapsin I promoter to animals in which the NT-3 gene is floxed. We conducted blind field potential recordings at the Schaffer collateral–CA1 synapse in hippocampal slices from homozygous knockout and wild-type mice. We examined the following indices of synaptic transmission: (1) input-output relationship; (2) paired-pulse facilitation; (3) post-tetanic potentiation; and (4) long-term potentiation: induced by two different protocols: (a) two trains of 100-Hz stimulation and (b) theta burst stimulation. We found no difference between the knockout and wild-type mice in any of the above measurements. These results suggest that neuronal NT-3 does not play an essential role in normal synaptic transmission and some forms of plasticity in the mouse hippocampus.

scholarly journals A critical residue in the α1M2–M3 linker regulating mammalian GABAA receptor pore gating by diazepam

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Joseph W Nors ◽  
Shipra Gupta ◽  
Marcel P Goldschen-Ohm
Keyword(s):  
Ion Channels ◽  
Synaptic Transmission ◽  
Molecular Mechanism ◽  
Psychotropic Drugs ◽  
Wild Type ◽  
Critical Residue ◽  
Positive Modulator ◽  
Pore Opening ◽  
Important Residue

Benzodiazepines (BZDs) are a class of widely prescribed psychotropic drugs that modulate activity of GABAA receptors (GABAARs), neurotransmitter-gated ion channels critical for synaptic transmission. However, the physical basis of this modulation is poorly understood. We explore the role of an important gating domain, the α1M2–M3 linker, in linkage between the BZD site and pore gate. To probe energetics of this coupling without complication from bound agonist, we use a gain of function mutant (α1L9'Tβ2γ2L) directly activated by BZDs. We identify a specific residue whose mutation (α1V279A) more than doubles the energetic contribution of the BZD positive modulator diazepam (DZ) to pore opening and also enhances DZ potentiation of GABA-evoked currents in a wild-type background. In contrast, other linker mutations have little effect on DZ efficiency, but generally impair unliganded pore opening. Our observations reveal an important residue regulating BZD-pore linkage, thereby shedding new light on the molecular mechanism of these drugs.

scholarly journals Pre- and postsynaptic modulations of hypoglossal motoneurons by α-adrenoceptor activation in wild-type and Mecp2−/Y mice

2013 ◽  
Vol 305 (10) ◽  
pp. C1080-C1090 ◽  
Author(s):  
Xiao-Tao Jin ◽  
Ningren Cui ◽  
Weiwei Zhong ◽  
Xin Jin ◽  
Zhongying Wu ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Upper Airway ◽  
Membrane Properties ◽  
Compensatory Mechanism ◽  
Tongue Movement ◽  
Wild Type ◽  
Airway Patency ◽  
Hypoglossal Motoneurons ◽  
Therapeutical Modalities ◽  
Intrinsic Membrane Properties

Hypoglossal motoneurons (HNs) control tongue movement and play a role in maintenance of upper airway patency. Defects in these neurons may contribute to the development of sleep apnea and other cranial motor disorders including Rett syndrome (RTT). HNs are modulated by norepinephrine (NE) through α-adrenoceptors. Although postsynaptic mechanisms are known to play a role in this effect, how NE modulates the synaptic transmissions of HNs remains poorly understood. More importantly, the NE system is defective in RTT, while how the defect affects HNs is unknown. Believing that information of NE modulation of HNs may help the understanding of RTT and the design of new therapeutical interventions to motor defects in the disease, we performed these studies in which glycinergic inhibitory postsynaptic currents and intrinsic membrane properties were examined in wild-type and Mecp2 −/Y mice, a mouse of model of RTT. We found that activation of α1-adrenoceptor facilitated glycinergic synaptic transmission and excited HNs. These effects were mediated by both pre- and postsynaptic mechanisms. The latter effect involved an inhibition of barium-sensitive G protein-dependent K+ currents. The pre- and postsynaptic modulations of the HNs by α1-adrenoceptors were not only retained in Mecp2-null mice but also markedly enhanced, which appears to be a compensatory mechanism for the deficiencies in NE and GABAergic synaptic transmission. The existence of the endogenous compensatory mechanism is an encouraging finding, as it may allow therapeutical modalities to alleviate motoneuronal defects in RTT.

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