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Neurotransmitters are integral to the brain's communication system, enabling neurons to transmit signals across synapses. This chemical exchange underpins various cognitive functions, including memory processes. The role of neurotransmitters in memory is multifaceted, influencing the encoding, consolidation, and retrieval of memories through their action on different neural circuits.
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Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
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Memory is one of the most vital higher mental functions of the brain. Memory is closely related to learning because it enables us to retain information and experiences from our past to use them in our present life. It also helps us to remember facts, events, and skills, such as riding a bike or swimming. There are two types of memory — declarative memory, which involves memorizing facts or events, and procedural memory, which enables us to remember how to do something like writing or...
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Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.
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Long-term Potentiation01:35

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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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High Resolution Quantitative Synaptic Proteome Profiling of Mouse Brain Regions After Auditory Discrimination Learning
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The m6A-epitranscriptome in brain plasticity, learning and memory.

Jocelyn Widagdo1, Justin J-L Wong2, Victor Anggono1

  • 1Clem Jones Centre for Ageing Dementia Research, Queensland Brain Institute, The University of Queensland, Brisbane, Queensland, 4072, Australia.

Seminars in Cell & Developmental Biology
|May 31, 2021
PubMed
Summary
This summary is machine-generated.

N6-methyladenosine (m6A) RNA modification is crucial for brain functions like learning and memory. This review highlights m6A

Keywords:
Cognitive dysfunctionsN(6)-methyladenosineNeurological disordersNeuronal plasticityRNA metabolismRNA modifications

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Author Spotlight: Enhancements in Gene Expression Regulation Research
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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Neuronal plasticity, learning, and memory depend on activity-dependent gene expression and protein translation.
  • Epitranscriptomics, particularly RNA modifications, is revolutionizing the understanding of gene expression regulation.
  • N6-methyladenosine (m6A) is the most abundant reversible mRNA modification in the brain.

Purpose of the Study:

  • To review experimental evidence on the role of m6A signaling in learning and memory.
  • To provide an overview of the molecular mechanisms of m6A in neurons.
  • To discuss the implications of altered m6A signaling in cognitive disorders.

Main Methods:

  • Literature review of experimental studies on m6A.
  • Analysis of molecular mechanisms underlying m6A regulation in neurons.
  • Examination of links between m6A and cognitive disorders.

Main Results:

  • m6A signaling dynamically regulates mRNA processing, impacting neuronal plasticity.
  • Evidence supports m6A's critical role in learning and memory formation.
  • Dysregulation of m6A pathways is associated with various human cognitive impairments.

Conclusions:

  • m6A is a key regulator of nervous system functions, including learning and memory.
  • Understanding m6A mechanisms offers insights into cognitive health and disease.
  • Targeting m6A pathways may hold therapeutic potential for cognitive disorders.