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Related Concept Videos

Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders01:27

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Schizophrenia is a neurodevelopmental disorder whose origins are rooted in complex genetic components. Despite our burgeoning understanding, the pathophysiology of this disorder remains incompletely deciphered.
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When an action potential reaches the presynaptic axon terminal, it releases neurotransmitters from the neuron into the synaptic cleft at a chemical synapse. The released neurotransmitter can be excitatory or inhibitory. The critical criteria commonly used to determine whether a molecule is a neurotransmitter at a chemical synapse are the molecule's presence in the presynaptic neuron. Second, its release is in response to strong presynaptic depolarization. And lastly, the presence of...
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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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Synaptic plasticity in schizophrenia pathophysiology.

Kexuan Zhang1,2, Panlin Liao1,3, Jin Wen1,3

  • 1Hunan Key Laboratory of Molecular Precision Medicine, Department of Critical Care Medicine, Xiangya Hospital, Central South University, Changsha 410008, Hunan, PR China.

IBRO Neuroscience Reports
|January 2, 2023
PubMed
Summary
This summary is machine-generated.

Schizophrenia pathogenesis involves disrupted synaptic plasticity. Understanding how genetic and environmental factors affect synaptic function offers new insights into this complex brain disorder.

Keywords:
Neuropsychiatric diseaseNeurotransmissionSchizophreniaSynaptic plasticity

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Area of Science:

  • Neuroscience
  • Psychiatry
  • Genetics

Background:

  • Schizophrenia is a severe neuropsychiatric disorder characterized by psychosis and cognitive deficits.
  • While genetic and environmental factors are implicated, its etiology and pathology remain unclear.
  • Synaptopathology and dysregulated synaptic plasticity are emerging as key mechanisms in schizophrenia.

Purpose of the Study:

  • To review the molecular and cellular mechanisms of synaptic plasticity.
  • To examine the influence of schizophrenia-risk factors on synaptic plasticity and animal behavior.

Main Methods:

  • Literature review of molecular and cellular mechanisms of synaptic plasticity.
  • Analysis of functional regulations of schizophrenia-risk factors on synaptic plasticity and behavior.
  • Integration of findings from genome-wide association studies.

Main Results:

  • Synaptic plasticity is crucial for brain function, learning, memory, and behavior relevant to psychiatric diseases.
  • Schizophrenia-risk genes and environmental factors can alter synaptic transmission and plasticity.
  • Multiple forms of synaptic plasticity are affected in schizophrenia.

Conclusions:

  • Dysregulated synaptic plasticity is a prominent biological mechanism in schizophrenia.
  • Further research into disease-risk genes' role in synaptic plasticity is vital for understanding schizophrenia.
  • Clarifying these mechanisms can advance knowledge of both schizophrenia pathology and synaptic plasticity.