scholarly journals The Association of Brain-Derived Neurotrophic Factor with Long-Term Potentiation

2021 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Zahra Salimi ◽  
Farshad Moradpour ◽  
Zahra Rashidi ◽  
Fatemeh Zarei ◽  
Mohammad Rasool Khazaei ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Neurotrophic Factor ◽  
Synapse Formation ◽  
Long Term Potentiation ◽  
Brain Derived Neurotrophic Factor ◽  
Synaptic Efficacy ◽  
Term Potentiation ◽  
The Central Nervous System

: Long-term potentiation (LTP) is one of the most important topics in neuroscience. It refers to a long-lasting increase in synaptic efficacy and is considered as a molecular and cellular mechanism of learning and memory. Neurotrophins play essential roles in different processes in the central nervous system (CNS), such as synaptogenesis, survival of specific populations of neurons, and neuroplasticity. Some evidence suggests that neurotrophins also participate in the synaptic plasticity related to learning and memory formation. Brain-derived neurotrophic factor (BDNF) is an important neurotrophic factor that is extensively expressed in the hippocampus and cerebral cortex, where it promotes neuroprotection, increases synaptogenesis and neurotransmission, and mediates synapse formation and synaptic plasticity. In this review, we first focused on the research investigating the effects of BDNF on synaptic plasticity and LTP induction and then reviewed the neuronal signaling molecules employed by BDNF to promote its effects on these processes.

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.

Calpains: Master Regulators of Synaptic Plasticity

2016 ◽  
Vol 23 (3) ◽  
pp. 221-231 ◽  
Author(s):  
Victor Briz ◽  
Michel Baudry
Keyword(s):  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Long Term Potentiation ◽  
Cytoskeletal Proteins ◽  
Local Protein Synthesis ◽  
Term Potentiation ◽  
Calpain 2 ◽  
The Brain ◽  
Local Protein

Although calpain was proposed to participate in synaptic plasticity and learning and memory more than 30 years ago, the mechanisms underlying its activation and the roles of different substrates have remained elusive. Recent findings have provided evidence that the two major calpain isoforms in the brain, calpain-1 and calpain-2, play opposite functions in synaptic plasticity. In particular, while calpain-1 activation is the initial trigger for certain forms of synaptic plasticity, that is, long-term potentiation, calpain-2 activation restricts the extent of plasticity. Moreover, while calpain-1 rapidly cleaves regulatory and cytoskeletal proteins, calpain-2-mediated stimulation of local protein synthesis reestablishes protein homeostasis. These findings have important implications for our understanding of learning and memory and disorders associated with impairment in these processes.

scholarly journals Mechanisms of high-intensity sound exposure on inhibiting hippocampal long-term potentiation: role of brain-derived neurotrophic factor

2019 ◽  
Author(s):  
Júnia L. de Deus ◽  
Mateus R. Amorim ◽  
Aline B. Ribeiro ◽  
Procópio C. G. Barcellos-Filho ◽  
César C. Ceballos ◽  
...  
Keyword(s):  
Emotional Disorders ◽  
Neurotrophic Factor ◽  
High Intensity ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Brain Derived Neurotrophic Factor ◽  
Sound Stimulation ◽  
Sound Exposure ◽  
Term Potentiation

AbstractExposure to humans and experimental animals to loud noises produce cognitive and emotional disorders and recent studies have shown that hippocampal neuronal function is affected by auditory stimulation or deprivation. We have found previously that in the hippocampus of rats exposed to high-intensity sound (110 dB) for one-minute the Schaffer-CA1 long-term potentiation (LTP) is strongly inhibited. Here we investigated possible mechanisms involved in this effect. We found, using c-fos expression, that exposure to 110 dB sound-activated neurons in the CA1 and CA3 hippocampal region. Using electrophysiological recordings in hippocampal slices, we found that both GABAergic and glutamatergic neurotransmission were unaffected by high-intensity sound stimulation. However, hippocampal brain-derived neurotrophic factor (BDNF), which is involved in promoting hippocampal synaptic plasticity, presented decreased levels in sound-stimulated animals. Perfusion of slices with BDNF revert the inhibition of LTP after a single sound stimulus in comparison to sham-stimulated rats. Furthermore, the perfusion with LM 22A4, a TrkB receptor agonist also rescued LTP from sound-stimulated animals. Our results strongly suggest that the exposure to high-intensity sound inhibits the BDNF production in the hippocampus, which could be a possible mechanism of the inhibition of LTP by high-intensity sound exposure.

scholarly journals Endocannabinoid dynamics gate spike-timing dependent depression and potentiation

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Yihui Cui ◽  
Ilya Prokin ◽  
Hao Xu ◽  
Bruno Delord ◽  
Stephane Genet ◽  
...  
Keyword(s):  
Mathematical Modeling ◽  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Long Term Potentiation ◽  
Cellular Mechanism ◽  
Spike Timing ◽  
Long Term Depression ◽  
Term Potentiation ◽  
Short And Long Term

Synaptic plasticity is a cardinal cellular mechanism for learning and memory. The endocannabinoid (eCB) system has emerged as a pivotal pathway for synaptic plasticity because of its widely characterized ability to depress synaptic transmission on short- and long-term scales. Recent reports indicate that eCBs also mediate potentiation of the synapse. However, it is not known how eCB signaling may support bidirectionality. Here, we combined electrophysiology experiments with mathematical modeling to question the mechanisms of eCB bidirectionality in spike-timing dependent plasticity (STDP) at corticostriatal synapses. We demonstrate that STDP outcome is controlled by eCB levels and dynamics: prolonged and moderate levels of eCB lead to eCB-mediated long-term depression (eCB-tLTD) while short and large eCB transients produce eCB-mediated long-term potentiation (eCB-tLTP). Moreover, we show that eCB-tLTD requires active calcineurin whereas eCB-tLTP necessitates the activity of presynaptic PKA. Therefore, just like glutamate or GABA, eCB form a bidirectional system to encode learning and memory.

Sign in / Sign up

Export Citation Format

Share Document