scholarly journals Fine-tuning synaptic plasticity by modulation of CaV2.1 channels with Ca2+ sensor proteins

2012 ◽  
Vol 109 (42) ◽  
pp. 17069-17074 ◽  
Author(s):  
K. Leal ◽  
S. Mochida ◽  
T. Scheuer ◽  
W. A. Catterall
Keyword(s):  
Synaptic Plasticity ◽  
Fine Tuning ◽  
Sensor Proteins

Neuronal calcium sensors and synaptic plasticity

2009 ◽  
Vol 37 (6) ◽  
pp. 1359-1363 ◽  
Author(s):  
Mascia Amici ◽  
Andrew Doherty ◽  
Jihoon Jo ◽  
David Jane ◽  
Kwangwook Cho ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Long Term Potentiation ◽  
Signalling Pathways ◽  
Calcium Sensor ◽  
Calcium Sensors ◽  
Term Potentiation ◽  
Neuronal Calcium Sensor Protein ◽  
The Central Nervous System ◽  
Sensor Proteins

Calcium entry plays a major role in the induction of several forms of synaptic plasticity in different areas of the central nervous system. The spatiotemporal aspects of these calcium signals can determine the type of synaptic plasticity induced, e.g. LTP (long-term potentiation) or LTD (long-term depression). A vast amount of research has been conducted to identify the molecular and cellular signalling pathways underlying LTP and LTD, but many components remain to be identified. Calcium sensor proteins are thought to play an essential role in regulating the initial part of synaptic plasticity signalling pathways. However, there is still a significant gap in knowledge, and it is only recently that evidence for the importance of members of the NCS (neuronal calcium sensor) protein family has started to emerge. The present minireview aims to bring together evidence supporting a role for NCS proteins in plasticity, focusing on emerging roles of NCS-1 and hippocalcin.

scholarly journals Regulation of Presynaptic CaV2.1 Channels by Ca2+ Sensor Proteins Mediates Short-Term Synaptic Plasticity

Neuron ◽  
2008 ◽  
Vol 57 (2) ◽  
pp. 210-216 ◽  
Author(s):  
Sumiko Mochida ◽  
Alexandra P. Few ◽  
Todd Scheuer ◽  
William A. Catterall
Keyword(s):  
Synaptic Plasticity ◽  
Short Term ◽  
Sensor Proteins

scholarly journals Fine Tuning of Synaptic Plasticity and Filtering by GABA Released from Hippocampal Autaptic Granule Cells

2015 ◽  
Vol 26 (3) ◽  
pp. 1149-1167 ◽  
Author(s):  
Pierluigi Valente ◽  
Marta Orlando ◽  
Andrea Raimondi ◽  
Fabio Benfenati ◽  
Pietro Baldelli
Keyword(s):  
Synaptic Plasticity ◽  
Granule Cells ◽  
Fine Tuning

scholarly journals Hebbian plasticity requires compensatory processes on multiple timescales

2017 ◽  
Vol 372 (1715) ◽  
pp. 20160259 ◽  
Author(s):  
Friedemann Zenke ◽  
Wulfram Gerstner
Keyword(s):  
Synaptic Plasticity ◽  
Experimental Research ◽  
Neural Circuits ◽  
Homeostatic Plasticity ◽  
Fine Tuning ◽  
Control Mechanisms ◽  
Network Stability ◽  
Multiple Timescales ◽  
Hebbian Plasticity ◽  
Compensatory Process

We review a body of theoretical and experimental research on Hebbian and homeostatic plasticity, starting from a puzzling observation: while homeostasis of synapses found in experiments is a slow compensatory process, most mathematical models of synaptic plasticity use rapid compensatory processes (RCPs). Even worse, with the slow homeostatic plasticity reported in experiments, simulations of existing plasticity models cannot maintain network stability unless further control mechanisms are implemented. To solve this paradox, we suggest that in addition to slow forms of homeostatic plasticity there are RCPs which stabilize synaptic plasticity on short timescales. These rapid processes may include heterosynaptic depression triggered by episodes of high postsynaptic firing rate. While slower forms of homeostatic plasticity are not sufficient to stabilize Hebbian plasticity, they are important for fine-tuning neural circuits. Taken together we suggest that learning and memory rely on an intricate interplay of diverse plasticity mechanisms on different timescales which jointly ensure stability and plasticity of neural circuits. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.

scholarly journals Neuromodulation of Hippocampal-Prefrontal Cortical Synaptic Plasticity and Functional Connectivity: Implications for Neuropsychiatric Disorders

2021 ◽  
Vol 15 ◽  
Author(s):  
Rafael Naime Ruggiero ◽  
Matheus Teixeira Rossignoli ◽  
Danilo Benette Marques ◽  
Bruno Monteiro de Sousa ◽  
Rodrigo Neves Romcy-Pereira ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Functional Connectivity ◽  
Neuropsychiatric Symptoms ◽  
Neuropsychiatric Disorders ◽  
Long Term Potentiation ◽  
Mental Illnesses ◽  
Fine Tuning ◽  
Comprehensive Overview ◽  
Neurophysiological Studies

The hippocampus-prefrontal cortex (HPC-PFC) pathway plays a fundamental role in executive and emotional functions. Neurophysiological studies have begun to unveil the dynamics of HPC-PFC interaction in both immediate demands and long-term adaptations. Disruptions in HPC-PFC functional connectivity can contribute to neuropsychiatric symptoms observed in mental illnesses and neurological conditions, such as schizophrenia, depression, anxiety disorders, and Alzheimer’s disease. Given the role in functional and dysfunctional physiology, it is crucial to understand the mechanisms that modulate the dynamics of HPC-PFC communication. Two of the main mechanisms that regulate HPC-PFC interactions are synaptic plasticity and modulatory neurotransmission. Synaptic plasticity can be investigated inducing long-term potentiation or long-term depression, while spontaneous functional connectivity can be inferred by statistical dependencies between the local field potentials of both regions. In turn, several neurotransmitters, such as acetylcholine, dopamine, serotonin, noradrenaline, and endocannabinoids, can regulate the fine-tuning of HPC-PFC connectivity. Despite experimental evidence, the effects of neuromodulation on HPC-PFC neuronal dynamics from cellular to behavioral levels are not fully understood. The current literature lacks a review that focuses on the main neurotransmitter interactions with HPC-PFC activity. Here we reviewed studies showing the effects of the main neurotransmitter systems in long- and short-term HPC-PFC synaptic plasticity. We also looked for the neuromodulatory effects on HPC-PFC oscillatory coordination. Finally, we review the implications of HPC-PFC disruption in synaptic plasticity and functional connectivity on cognition and neuropsychiatric disorders. The comprehensive overview of these impairments could help better understand the role of neuromodulation in HPC-PFC communication and generate insights into the etiology and physiopathology of clinical conditions.

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