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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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Schizophrenia, a severe psychiatric disorder, arises from a complex interplay of biological factors, including genetic predisposition, structural brain abnormalities, neurotransmitter dysregulation, and developmental irregularities. These factors collectively contribute to the onset and progression of the disorder, which typically manifests in late adolescence or early adulthood.
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The Synapse02:47

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Neurons communicate with one another by passing on their electrical signals to other neurons. A synapse is the location where two neurons meet to exchange signals. At the synapse, the neuron that sends the signal is called the presynaptic cell, while the neuron that receives the message is called the postsynaptic cell. Note that most neurons can be both presynaptic and postsynaptic, as they both transmit and receive information.
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Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
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Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
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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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Standardized Data Acquisition for Neuromelanin-Sensitive Magnetic Resonance Imaging of the Substantia Nigra
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The synapse in schizophrenia.

Andrew J Pocklington1, Michael O'Donovan, Michael J Owen

  • 1MRC Centre for Neuropsychiatric Genetics and Genomics, Institute of Psychological Medicine and Clinical Neurosciences, Cardiff University School of Medicine, Hadyn Ellis Building, Maindy Road, Cathays, Cardiff, CF24 4HQ, UK.

The European Journal of Neuroscience
|April 10, 2014
PubMed
Summary
This summary is machine-generated.

Genetic studies reveal synaptic dysfunction in schizophrenia. Disruption of glutamatergic signaling pathways regulating synaptic plasticity contributes to schizophrenia

Keywords:
proteomicspsychiatric geneticssynaptic plasticity

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Area of Science:

  • Neuroscience
  • Psychiatry
  • Genetics

Background:

  • Synaptic dysfunction has been implicated in schizophrenia for decades.
  • Recent advances in understanding the genetic basis of schizophrenia have provided new evidence.
  • The complex macromolecular structure of the synapse is increasingly understood.

Purpose of the Study:

  • To outline the current understanding of schizophrenia's genetic architecture.
  • To examine the evidence supporting synaptic involvement in schizophrenia.
  • To explore the role of glutamatergic signaling in schizophrenia.

Main Methods:

  • Review of recent genetic studies on schizophrenia.
  • Analysis of research on synaptic structure and function.
  • Examination of evidence linking synaptic plasticity to schizophrenia.

Main Results:

  • Convincing evidence for synaptic dysfunction in schizophrenia has emerged.
  • Genetic studies are leveraging advances in synaptic biology.
  • Disruption of glutamatergic signaling pathways is a key factor.

Conclusions:

  • A strong case exists for synaptic dysfunction in schizophrenia.
  • Glutamatergic signaling pathways regulating synaptic plasticity are implicated in schizophrenia's etiology.
  • Further research into synaptic mechanisms is crucial for understanding schizophrenia.