scholarly journals Brain is modulated by neuronal plasticity during postnatal development

2021 ◽  
Vol 71 (1) ◽  
Author(s):  
Masoumeh Kourosh-Arami ◽  
Nasrin Hosseini ◽  
Alireza Komaki
Keyword(s):  
Activity Patterns ◽  
Long Term Potentiation ◽  
Inhibitory Synapses ◽  
Neural Systems ◽  
Neural Structure ◽  
Term Potentiation ◽  
Study Results ◽  
Development Processes ◽  
Adaptation Processes

AbstractNeuroplasticity is referred to the ability of the nervous system to change its structure or functions as a result of former stimuli. It is a plausible mechanism underlying a dynamic brain through adaptation processes of neural structure and activity patterns. Nevertheless, it is still unclear how the plastic neural systems achieve and maintain their equilibrium. Additionally, the alterations of balanced brain dynamics under different plasticity rules have not been explored either. Therefore, the present article primarily aims to review recent research studies regarding homosynaptic and heterosynaptic neuroplasticity characterized by the manipulation of excitatory and inhibitory synaptic inputs. Moreover, it attempts to understand different mechanisms related to the main forms of synaptic plasticity at the excitatory and inhibitory synapses during the brain development processes. Hence, this study comprised surveying those articles published since 1988 and available through PubMed, Google Scholar and science direct databases on a keyword-based search paradigm. All in all, the study results presented extensive and corroborative pieces of evidence for the main types of plasticity, including the long-term potentiation (LTP) and long-term depression (LTD) of the excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs).

Novel Scenes Improve Recollection and Recall of Words

2008 ◽  
Vol 20 (7) ◽  
pp. 1250-1265 ◽  
Author(s):  
Daniela B. Fenker ◽  
Julietta U. Frey ◽  
Hartmut Schuetze ◽  
Dorothee Heipertz ◽  
Hans-Jochen Heinze ◽  
...  
Keyword(s):  
Specific Activity ◽  
Activity Patterns ◽  
Long Term Potentiation ◽  
Contextual Memory ◽  
Memory Enhancement ◽  
Term Potentiation ◽  
Outdoor Scenes ◽  
Indoor And Outdoor ◽  
Hippocampus Dependent Memory

Exploring a novel environment can facilitate subsequent hippocampal long-term potentiation in animals. We report a related behavioral enhancement in humans. In two separate experiments, recollection and free recall, both measures of hippocampus-dependent memory formation, were enhanced for words studied after a 5-min exposure to unrelated novel as opposed to familiar images depicting indoor and outdoor scenes. With functional magnetic resonance imaging, the enhancement was predicted by specific activity patterns observed during novelty exposure in parahippocampal and dorsal prefrontal cortices, regions which are known to be linked to attentional orienting to novel stimuli and perceptual processing of scenes. Novelty was also associated with activation of the substantia nigra/ventral tegmental area of the midbrain and the hippocampus, but these activations did not correlate with contextual memory enhancement. These findings indicate remarkable parallels between contextual memory enhancement in humans and existing evidence regarding contextually enhanced hippocampal plasticity in animals. They provide specific behavioral clues to enhancing hippocampus-dependent memory in humans.

scholarly journals Poststress Block of Kappa Opioid Receptors Rescues Long-Term Potentiation of Inhibitory Synapses and Prevents Reinstatement of Cocaine Seeking

2014 ◽  
Vol 76 (10) ◽  
pp. 785-793 ◽  
Author(s):  
Abigail M. Polter ◽  
Rachel A. Bishop ◽  
Lisa A. Briand ◽  
Nicholas M. Graziane ◽  
R. Christopher Pierce ◽  
...  
Keyword(s):  
Opioid Receptors ◽  
Long Term Potentiation ◽  
Inhibitory Synapses ◽  
Kappa Opioid Receptors ◽  
Kappa Opioid ◽  
Term Potentiation ◽  
Cocaine Seeking

scholarly journals A physiological role for GABAA receptor desensitization – induction of long-term potentiation at inhibitory synapses

2020 ◽  
Author(s):  
Martin Field ◽  
Philip Thomas ◽  
Trevor G Smart
Keyword(s):  
Physiological Role ◽  
Long Term Potentiation ◽  
Inhibitory Synapses ◽  
Structural Basis ◽  
Inhibitory Neurotransmission ◽  
Term Potentiation ◽  
Physiological Relevance ◽  
Kinetic Effects ◽  
Physiological Impact

AbstractGABAA receptors (GABAARs) are pentameric ligand-gated ion channels distributed throughout the brain where they mediate synaptic and tonic inhibition. Following activation, these receptors undergo desensitization which involves entry into long-lived agonist-bound closed states. Although the kinetic effects of this state are recognised and its structural basis has been uncovered, the physiological impact of desensitization on inhibitory neurotransmission remains unknown. Here we describe an enduring new form of long-term potentiation at inhibitory synapses that elevates synaptic current amplitude for 24 hrs following desensitization of GABAARs in response to prolonged agonist exposure or allosteric modulation. Using receptor mutants and allosteric modulators we demonstrate that desensitization of GABAARs facilitates their phosphorylation by PKC, which increases the number of receptors at inhibitory synapses. These observations provide a new physiological relevance to the desensitized state of GABAARs, acting as a signal to regulate the efficacy of inhibitory synapses during prolonged periods of inhibitory neurotransmission.

scholarly journals Intracellular calcium stores mediate a synapse-specific form of metaplasticity at hippocampal dendritic spines

2018 ◽  
Author(s):  
Gaurang Mahajan ◽  
Suhita Nadkarni
Keyword(s):  
Dendritic Spines ◽  
Activity Patterns ◽  
Long Term Potentiation ◽  
Multiple Time Scales ◽  
Calcium Stores ◽  
Multiple Time ◽  
Additional Layer ◽  
Term Potentiation ◽  
Activity Dependent

ABSTRACTLong-term plasticity mediated by NMDA receptors supports input-specific, Hebbian forms of learning at excitatory CA3-CA1 connections in the hippocampus. An additional layer of stabilizing mechanisms that act globally as well as locally over multiple time scales may be in place to ensure that plasticity occurs in a constrained manner. Here, we investigate the potential role of calcium (Ca2+) stores associated with the endoplasmic reticulum (ER) in the local regulation of plasticity dynamics at individual CA1 synapses. Our study is spurred by (1) the curious observation that ER is sparsely distributed in dendritic spines, but over-represented in large spines that are likely to have undergone activity-dependent strengthening, and (2) evidence suggesting that ER motility within synapses can be rapid, and accompany activity-regulated spine remodeling. Based on a physiologically realistic computational model for ER-bearing CA1 spines, we characterize the contribution of IP3-sensitive Ca2+ stores to spine Ca2+ dynamics during activity patterns mimicking the induction of long-term potentiation (LTP) and depression (LTD). Our results suggest graded modulation of the NMDA receptor-dependent plasticity profile by ER, which selectively enhances LTD induction. We propose that spine ER can locally tune Ca2+-based plasticity on an as-needed basis, providing a braking mechanism to mitigate runaway strengthening at potentiated synapses. Our model suggests that the presence of ER in the CA1 spine may promote re-use of synapses with saturated strengths.

Presynaptic Activity and Ca2+ Entry Are Required for the Maintenance of NMDA Receptor–Independent LTP at Visual Cortical Excitatory Synapses

2004 ◽  
Vol 92 (2) ◽  
pp. 1077-1087 ◽  
Author(s):  
Hong Nian Liu ◽  
Tohru Kurotani ◽  
Ming Ren ◽  
Kazumasa Yamada ◽  
Yumiko Yoshimura ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Long Term Potentiation ◽  
Inhibitory Synapses ◽  
Excitatory Synapses ◽  
Test Stimulation ◽  
Term Potentiation ◽  
Pharmacological Blockade ◽  
Visual Cortical ◽  
P Type

We have shown that some neural activity is required for the maintenance of long-term potentiation (LTP) at visual cortical inhibitory synapses. We tested whether this was also the case in N-methyl-d-aspartate (NMDA) receptor–independent LTP of excitatory connections in layer 2/3 cells of developing rat visual cortex. This LTP occurred after 2-Hz stimulation was applied for 15 min and always persisted for several hours while test stimulation was continued at 0.1 Hz. When test stimulation was stopped for 1 h after LTP induction, only one-third of the LTP instances disappeared, but most did disappear under a pharmacological suppression of spontaneous firing, indicating that LTP maintenance requires either evoked or spontaneous activities. LTP was totally abolished by a temporary blockade of action potentials with lidocaine or the removal of extracellular Ca2+ after LTP induction, but it persisted under a voltage clamp of postsynaptic cells or after a temporary blockade of postsynaptic activity with the glutamate receptor antagonist kynurenate, suggesting that LTP maintenance requires presynaptic, but not postsynaptic, firing and Ca2+ entry. More than one-half of the LTP instances were abolished after a pharmacological blockade of P-type Ca2+ channels, whereas it persisted after either L-type or Ni2+-sensitive Ca2+ channel blockades. These results show that the maintenance of NMDA receptor–independent excitatory LTP requires presynaptic firing and Ca2+ channel activation as inhibitory LTP, although the necessary level of firing and Ca2+ entry seems lower for the former than the latter and the Ca2+ channel types involved are only partly the same.

2-Deoxyglucose–Induced Long-Term Potentiation of Monosynaptic IPSPs in CA1 Hippocampal Neurons

2000 ◽  
Vol 83 (2) ◽  
pp. 879-887 ◽  
Author(s):  
Krešimir Krnjević ◽  
Yong-Tao Zhao
Keyword(s):  
Hippocampal Neurons ◽  
Long Term Potentiation ◽  
Inhibitory Synapses ◽  
Current Clamp ◽  
Glutamate Antagonists ◽  
Postsynaptic Potentials ◽  
Postsynaptic Currents ◽  
Inhibitory Postsynaptic Potentials ◽  
Term Potentiation

In previous experiments on excitatory synaptic transmission in CA1, temporary (10–20 min) replacement of glucose with 10 mM 2-deoxyglucose (2-DG) consistently caused a marked and very sustained potentiation (2-DG LTP). To find out whether 2-DG has a similar effect on inhibitory synapses, we recorded pharmacologically isolated mononosynaptic inhibitory postsynaptic potentials (IPSPs; under current clamp) and inhibitory postsynaptic currents (IPSCs; under voltage clamp); 2-DG was applied both in the presence and the absence of antagonists of N-methyl-d-aspartate (NMDA). In spite of sharply varied results (some neurons showing large potentiation, lasting for >1 h, and many little or none), overall there was a significant and similar potentiation of IPSP conductance, both for the early (at ≈30 ms) and later (at ≈140 ms) components of IPSPs or IPSCs: by 35.1 ± 10.25% (mean ± SE; for n = 24, P = 0.0023) and 36.5 ± 16.3% (for n = 19, P = 0.038), respectively. The similar potentiation of the early and late IPSP points to a presynaptic mechanism of LTP. Overall, the LTP was statistically significant only when 2-DG was applied in the absence of glutamate antagonists. Tetanic stimulations (in presence or absence of glutamate antagonists) only depressed IPSPs (by half). In conclusion, although smaller and more variable, 2-DG–induced LTP of inhibitory synapses appears to be broadly similar to the 2-DG–induced LTP of excitatory postsynaptic potentials previously observed in CA1.

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