Modulation of the Neuronal Activity and Neurotransmitter Release by 5-HT1A and 5-HT1B/1D Receptors

2008 ◽  
pp. 365-401
Author(s):  
Pau Celada ◽  
Albert Adell ◽  
Francesc Artigas
Keyword(s):  
Neuronal Activity ◽  
Neurotransmitter Release

scholarly journals Doc2b Ca2+-binding site mutants act as a gain of function at rest and loss of function during neuronal activity

2019 ◽  
Author(s):  
Quentin Bourgeois-Jaarsma ◽  
Matthijs Verhage ◽  
Alexander J. Groffen
Keyword(s):  
Binding Site ◽  
Neuronal Activity ◽  
Neurotransmitter Release ◽  
Action Potentials ◽  
Vesicle Fusion ◽  
Primary Neurons ◽  
Loss Of Function ◽  
Short Term ◽  
Gain Of Function ◽  
Activated State

AbstractCommunication between neurons involves presynaptic neurotransmitter release which can be evoked by action potentials or occur spontaneously as a result of stochastic vesicle fusion. The Ca2+-binding double C2 proteins Doc2a and –b regulate both spontaneous and asynchronous evoked release, but the mechanism remains unclear. Here, we compared wildtype Doc2b with two Ca2+ binding site mutants named DN and 6A, respectively considered gain-and loss-of function mutants and carrying the substitutions D218,220N or D163,218,220,303,357,359A. We found that both mutants bound phospholipids at low free Ca2+ concentrations and were membrane-associated in neurons at rest, mimicking a Ca2+ activated state. Their overexpression in hippocampal primary neurons culture had similar effects on spontaneous and evoked release, inducing higher mEPSC frequencies and increased short-term depression. Together, these data suggest that the DN and 6A mutants both act as gain-of-function mutants at resting conditions but as loss-of-function during neuronal activity.

scholarly journals Neuronal activity determines distinct gliotransmitter release from a single astrocyte

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Ana Covelo ◽  
Alfonso Araque
Keyword(s):  
Neuronal Activity ◽  
Brain Function ◽  
Neurotransmitter Release ◽  
Dynamic Properties ◽  
Firing Frequency ◽  
Synaptic Activity ◽  
Synaptic Regulation ◽  
Synaptic Modulation ◽  
Hippocampal Synapses ◽  
Hippocampal Astrocytes

Accumulating evidence indicates that astrocytes are actively involved in brain function by regulating synaptic activity and plasticity. Different gliotransmitters, such as glutamate, ATP, GABA or D-serine, released form astrocytes have been shown to induce different forms of synaptic regulation. However, whether a single astrocyte may release different gliotransmitters is unknown. Here we show that mouse hippocampal astrocytes activated by endogenous (neuron-released endocannabinoids or GABA) or exogenous (single astrocyte Ca2+ uncaging) stimuli modulate putative single CA3-CA1 hippocampal synapses. The astrocyte-mediated synaptic modulation was biphasic and consisted of an initial glutamate-mediated potentiation followed by a purinergic-mediated depression of neurotransmitter release. The temporal dynamic properties of this biphasic synaptic regulation depended on the firing frequency and duration of the neuronal activity that stimulated astrocytes. Present results indicate that single astrocytes can decode neuronal activity and, in response, release distinct gliotransmitters to differentially regulate neurotransmission at putative single synapses.

scholarly journals FMRP sustains presynaptic function via control of activity-dependent bulk endocytosis

2020 ◽  
Author(s):  
Katherine Bonnycastle ◽  
Peter C. Kind ◽  
Michael A. Cousin
Keyword(s):  
Mental Retardation ◽  
Fragile X Syndrome ◽  
Neuronal Activity ◽  
Neurotransmitter Release ◽  
Fragile X ◽  
High Frequency Stimulation ◽  
Neuronal Cultures ◽  
Fragile X Mental Retardation ◽  
Mental Retardation Protein ◽  
Activity Dependent

ABSTRACTSynaptic vesicle (SV) recycling is essential for the maintenance of neurotransmission, with a number of neurodevelopmental disorders linked to defects in this process. Fragile X syndrome (FXS) results from a loss of fragile X mental retardation protein (FMRP) encoded by the FMR1 gene. FMRP is an established translation repressor, however it also has translation-independent presynaptic roles, including regulation of the trafficking and function of specific ion channels. Since defects in SV recycling are exacerbated during intense neuronal activity, we investigated whether these events were disproportionately affected by the absence of FMRP. We revealed that primary neuronal cultures from a Fmr1 knockout rat model display a specific defect in activity-dependent bulk endocytosis (ADBE). ADBE is dominant during intense neuronal activity, and this defect resulted in an inability of Fmr1 knockout neurons to sustain SV recycling during trains of high frequency stimulation. Using a molecular replacement strategy, we revealed that a human FMRP interaction mutant failed to correct ADBE dysfunction in knockout neurons. Therefore, FMRP performs a key role in sustaining neurotransmitter release via selective control of the endocytosis mode, ADBE.SIGNIFICANCE STATEMENTLoss of fragile X mental retardation protein (FMRP) results in fragile X syndrome (FXS), however whether its loss has a direct role in neurotransmitter release remains a matter of debate. We demonstrate that neurons lacking FMRP display a specific defect in a mechanism that sustains neurotransmitter release during intense neuronal firing, called activity-dependent bulk endocytosis (ADBE). This discovery provides key insights into mechanisms of brain communication that occur due to loss of FMRP function. Importantly it also reveals ADBE as a potential therapeutic target to correct the circuit hyperexcitabilty observed in FXS.

scholarly journals Activity-dependent nucleation of dynamic microtubules at presynaptic boutons is required for neurotransmission

2019 ◽  
Author(s):  
Xiaoyi Qu ◽  
Atul Kumar ◽  
Heike Blockus ◽  
Clarissa Waites ◽  
Francesca Bartolini
Keyword(s):  
Synaptic Vesicle ◽  
Neuronal Activity ◽  
Neurotransmitter Release ◽  
Hippocampal Neurons ◽  
De Novo ◽  
List Type ◽  
Neuronal Function ◽  
Presynaptic Boutons ◽  
Rate Limiting ◽  
Activity Dependent

SUMMARYControl of microtubule (MT) dynamics is critical for neuronal function. Whether MT nucleation is regulated at presynaptic boutons and influences overall presynaptic activity remains unknown. By visualizing MT dynamics at individual excitatory en passant boutons in axons of hippocampal neurons we found that MTs preferentially grow from presynaptic boutons as a result of γ-tubulin and augmin-dependent nucleation. MT nucleation at boutons is promoted by neuronal activity, functionally coupled to synaptic vesicle (SV) transport, and required for neurotransmission. Hence, en passant boutons act as hotspots for activity-dependent MT nucleation, which is required for neurotransmission by providing the tracks for a rate-limiting supply of SVs to sites of neurotransmitter release.HighlightsExcitatory boutons are hotspots for neuronal activity-induced γ-tubulin dependent MT nucleationThe augmin complex is required for the correct polarity of presynaptic de novo nucleated MTsPresynaptic MT nucleation promotes SV motility and exocytosis at sites of releaseIn BriefOur results demonstrate that excitatory en passant boutons are hotspots for neuronal activity-induced γ-tubulin- and augmin-dependent oriented MT nucleation, and that the resulting presynaptic de novo nucleated MTs promote inter-bouton SV motility which is rate-limiting for neurotransmitter release.

Molecular analysis of neurotransmitter release

1998 ◽  
Vol 33 ◽  
pp. 29-41 ◽  
Author(s):  
Giampietro Schiavo ◽  
Gudrun Stenbeck
Keyword(s):  
Molecular Analysis ◽  
Neurotransmitter Release

C-Fos and Fos-Related Antigens as Markers for Neuronal Activity: Perspectives From Neuroendocrine Systems

1993 ◽  
Author(s):  
Gloria E. Hoffman ◽  
◽  
Wen-Sen Lee ◽  
M. Susan Smith ◽  
Rula Abbud ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Neuroendocrine Systems

Neuronal activity in thalamus and the big hemispheres in rabbits during the slow sleep

2004 ◽  
Author(s):  
A. A. Burikov ◽  
N. V. Svetlova ◽  
O. N. Chichinadze ◽  
O. I. Chuguev
Keyword(s):  
Neuronal Activity ◽  
Slow Sleep

Pretreatment Neuronal Activity Predicts Response to CBT for Depression

2006 ◽  
Author(s):  
G. J. Siegle ◽  
C. S. Carter ◽  
M. E. Thase
Keyword(s):  
Neuronal Activity

SPECT-Befunde bei Hemiparkinson-Syndrom mit 99mTc-HMPAO

1989 ◽  
Vol 28 (03) ◽  
pp. 92-94 ◽  
Author(s):  
C. Neumann ◽  
H. Baas ◽  
R. Hefner ◽  
G. Hör
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Neuronal Activity ◽  
Tracer Uptake ◽  
The Body ◽  
99Mtc Hmpao ◽  
Do So

The symptoms of Parkinson’s disease often begin on one side of the body and continue to do so as the disease progresses. First SPECT results in 4 patients with hemiparkinsonism using 99mTc-HMPAO as perfusion marker are reported. Three patients exhibited reduced tracer uptake in the contralateral basal ganglia One patient who was under therapy for 1 year, showed a different perfusion pattern with reduced uptake in both basal ganglia. These results might indicate reduced perfusion secondary to reduced striatal neuronal activity.

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