The Neuromolecular Brain

Neuro ◽  
2013 ◽  
Author(s):  
Nikolas Rose ◽  
Joelle M. Abi-Rached
Keyword(s):  
Gene Expression ◽  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Time Scales ◽  
Molecular Level ◽  
Human Life ◽  
Neuronal Circuits ◽  
Molecular Processes ◽  
Nerve Development ◽  
The Brain

This chapter examines the neuromolecular and plastic brain. Ideas about plasticity and the openness of brains to environment influences, from initial evidence about nerve development, through the recognition that synaptic plasticity was the very basis of learning and memory, to evidence about the influence of environment on gene expression and the persistence throughout life of the capacity to make new neurons—all this made the neuromolecular brain seem exquisitely open to its milieu, with changes at the molecular level occurring throughout the course of a human life and thus shaping the growth, organization, and regeneration of neurons and neuronal circuits at time scales from the millisecond to the decade. This was an opportunity to explore the myriad ways in which the milieu got “under the skin,” implying an openness of these molecular processes of the brain to biography, sociality, and culture, and hence perhaps even to history and politics.

scholarly journals The brain-tumor related protein podoplanin regulates synaptic plasticity and hippocampus-dependent learning and memory

2016 ◽  
Vol 48 (8) ◽  
pp. 652-668 ◽  
Author(s):  
Ana Cicvaric ◽  
Jiaye Yang ◽  
Sigurd Krieger ◽  
Deeba Khan ◽  
Eun-Jung Kim ◽  
...  
Keyword(s):  
Brain Tumor ◽  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Related Protein ◽  
Dependent Learning ◽  
The Brain

scholarly journals Synaptic Plasticity and its Modulation by Alcohol

2020 ◽  
Vol 6 (1) ◽  
pp. 103-111 ◽  
Author(s):  
Yosef Avchalumov ◽  
Chitra D. Mandyam
Keyword(s):  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Dorsal Striatum ◽  
Long Term Potentiation ◽  
Brain Regions ◽  
Public Health Issue ◽  
Cellular Mechanisms ◽  
Brain Disorder ◽  
The Brain

Alcohol is one of the oldest pharmacological agents used for its sedative/hypnotic effects, and alcohol abuse and alcohol use disorder (AUD) continues to be major public health issue. AUD is strongly indicated to be a brain disorder, and the molecular and cellular mechanism/s by which alcohol produces its effects in the brain are only now beginning to be understood. In the brain, synaptic plasticity or strengthening or weakening of synapses, can be enhanced or reduced by a variety of stimulation paradigms. Synaptic plasticity is thought to be responsible for important processes involved in the cellular mechanisms of learning and memory. Long-term potentiation (LTP) is a form of synaptic plasticity, and occurs via N-methyl-D-aspartate type glutamate receptor (NMDAR or GluN) dependent and independent mechanisms. In particular, NMDARs are a major target of alcohol, and are implicated in different types of learning and memory. Therefore, understanding the effect of alcohol on synaptic plasticity and transmission mediated by glutamatergic signaling is becoming important, and this will help us understand the significant contribution of the glutamatergic system in AUD. In the first part of this review, we will briefly discuss the mechanisms underlying long term synaptic plasticity in the dorsal striatum, neocortex and the hippocampus. In the second part we will discuss how alcohol (ethanol, EtOH) can modulate long term synaptic plasticity in these three brain regions, mainly from neurophysiological and electrophysiological studies. Taken together, understanding the mechanism(s) underlying alcohol induced changes in brain function may lead to the development of more effective therapeutic agents to reduce AUDs.

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 Insights into Neonatal Oral Feeding through the Salivary Transcriptome

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Jill L. Maron
Keyword(s):  
Gene Expression ◽  
Pathway Analysis ◽  
Molecular Level ◽  
Molecular Techniques ◽  
Oral Feeding ◽  
Potential Candidate ◽  
Biological Processes ◽  
Feeding Skills ◽  
Physiological Pathways ◽  
Nerve Development

Background. The development of safe and effective oral feeding skills in the newborn is complex and may be associated with significant morbidities. Our understanding of neonatal oral feeding maturation at the molecular level is limited, providing an opportunity to utilize emerging molecular techniques to accurately assess neonatal oral feeding skills.Objective. To identify key regulatory genes in neonatal saliva involved in successful oral feeding.Methods. Previously, our laboratory identified 9,286 genes in saliva that statistically significantly altered their gene expression as premature newborns gained advanced oral feeding skills. In this report, genes previously identified underwent an updated and targeted pathway analysis with Ingenuity Pathway Analysis (IPA) to identify potential candidate genes involved in successful oral feeding. Genes were considered if they were in the five most significantly up- and down-regulated physiological pathways and were associated with the keywords “feeding”, “digestion” and “development”.Results. There were 2,186 genes that met criteria. Pathways associated with feeding behavior, cranial nerve development, and the development of the nervous, skeletal, and muscular systems were highlighted.Discussion. These data provide important insights into the biological processes involved in oral feeding in the newborn at a molecular level and identify novel pathways associated with successful oral feeding.

scholarly journals Molekulare Kontrolle der Stabilität und Plastizität von Synapsen

BIOspektrum ◽  
2021 ◽  
Vol 27 (6) ◽  
pp. 588-590
Author(s):  
Zeeshan Mushtaq ◽  
Jan Pielage
Keyword(s):  
Nervous System ◽  
Synaptic Plasticity ◽  
Neurodegenerative Diseases ◽  
Information Flow ◽  
Molecular Mechanisms ◽  
Synaptic Connectivity ◽  
Genetic Mutations ◽  
Neuronal Circuits ◽  
The Brain

AbstractThe precise regulation of synaptic connectivity is essential for the processing of information in the brain. Any aberrant loss of synaptic connectivity due to genetic mutations will disrupt information flow in the nervous system and may represent the underlying cause of psychiatric or neurodegenerative diseases. Therefore, identification of the molecular mechanisms controlling synaptic plasticity and maintenance is essential for our understanding of neuronal circuits in development and disease.

scholarly journals Competition for synaptic building blocks shapes synaptic plasticity

2017 ◽  
Author(s):  
Jochen Triesch ◽  
Anh Duong Vo ◽  
Anne-Sophie Hafner
Keyword(s):  
Mathematical Model ◽  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Time Scales ◽  
Building Blocks ◽  
Neurotransmitter Receptors ◽  
Rapid Exchange ◽  
Heterosynaptic Plasticity ◽  
Spontaneous Fluctuations ◽  
Receptor Pool

AbstractChanges in the efficacies of synapses are thought to be the neurobiological basis of learning and memory. The efficacy of a synapse depends on its current number of neurotransmitter receptors. Recent experiments have shown that these receptors are highly dynamic, moving back and forth between synapses on time scales of seconds and minutes. This suggests spontaneous fluctuations in synaptic efficacies and a competition of nearby synapses for available receptors. Here we propose a mathematical model of this competition of synapses for neurotransmitter receptors from a local dendritic pool. Using minimal assumptions, the model produces a fast multiplicative scaling behavior of synapses. Furthermore, the model explains a transient form of heterosynaptic plasticity and predicts that its amount is inversely related to the size of the local receptor pool. Overall, our model reveals logistical tradeoffs during the induction of synaptic plasticity due to the rapid exchange of neurotransmitter receptors between synapses.

Postnatal exposure to poly (I:C) impairs learning and memory through changes in synaptic plasticity gene expression in developing rat brain

2018 ◽  
Vol 155 ◽  
pp. 379-389 ◽  
Author(s):  
Meghraj Singh Baghel ◽  
Brijendra Singh ◽  
Yogesh Kumar Dhuriya ◽  
Rajendra Kumar Shukla ◽  
Nisha Patro ◽  
...  
Keyword(s):  
Gene Expression ◽  
Synaptic Plasticity ◽  
Rat Brain ◽  
Learning And Memory ◽  
Poly I:C ◽  
Postnatal Exposure ◽  
Developing Rat

Memory formation: its molecular and cell biology

1995 ◽  
Vol 3 (3) ◽  
pp. 243-256 ◽  
Author(s):  
Steven P. R. Rose
Keyword(s):  
Gene Expression ◽  
Cell Adhesion ◽  
Cell Adhesion Molecules ◽  
Cell Biology ◽  
Small Region ◽  
Memory Formation ◽  
Synaptic Connectivity ◽  
Molecular Processes ◽  
Synaptic Changes ◽  
The Brain

Memories are stored in the brain in the form of changes in synaptic connectivity brought about through a cascade of molecular processes. Transient synaptic changes result in alterations in gene expression and, ultimately, the synthesis of a family of cell adhesion molecules which are responsible for holding the synapse in a new configuration. However, memory remains a dynamic property of the brain system as a whole, rather than ‘residing’ in any particular small region.

Cellular and molecular neuroscience of alcoholism

1997 ◽  
Vol 77 (1) ◽  
pp. 1-20 ◽  
Author(s):  
I. Diamond ◽  
A. S. Gordon
Keyword(s):  
Gene Expression ◽  
Signal Transduction ◽  
Molecular Level ◽  
Cellular Functions ◽  
Short Term ◽  
Medical Disorders ◽  
Molecular Neuroscience ◽  
Long Term Changes ◽  
The Brain

Recent advances in neuroscience have made it possible to investigate the pathophysiology of alcoholism at a cellular and molecular level. Evidence indicates that ethanol affects hormone- and neurotransmitter-activated signal transduction, leading to short-term changes in regulation of cellular functions and long-term changes in gene expression. Such changes in the brain probably underlie many of the acute and chronic neurological events in alcoholism. In addition, genetic vulnerability also plays a role in alcoholism and, perhaps, in alcoholic medical disorders.

scholarly journals Competition for synaptic building blocks shapes synaptic plasticity

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Jochen Triesch ◽  
Anh Duong Vo ◽  
Anne-Sophie Hafner
Keyword(s):  
Mathematical Model ◽  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Time Scales ◽  
Building Blocks ◽  
Neurotransmitter Receptors ◽  
Rapid Exchange ◽  
Heterosynaptic Plasticity ◽  
Spontaneous Fluctuations ◽  
Receptor Pool

Changes in the efficacies of synapses are thought to be the neurobiological basis of learning and memory. The efficacy of a synapse depends on its current number of neurotransmitter receptors. Recent experiments have shown that these receptors are highly dynamic, moving back and forth between synapses on time scales of seconds and minutes. This suggests spontaneous fluctuations in synaptic efficacies and a competition of nearby synapses for available receptors. Here we propose a mathematical model of this competition of synapses for neurotransmitter receptors from a local dendritic pool. Using minimal assumptions, the model produces a fast multiplicative scaling behavior of synapses. Furthermore, the model explains a transient form of heterosynaptic plasticity and predicts that its amount is inversely related to the size of the local receptor pool. Overall, our model reveals logistical tradeoffs during the induction of synaptic plasticity due to the rapid exchange of neurotransmitter receptors between synapses.

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