Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders

Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders

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.
Researchers have identified genetic factors that increase susceptibility to schizophrenia, underscoring the intricate interplay between genetics and environment in disease development. At the core of schizophrenia's pathophysiology is excessive dopaminergic neurotransmission within the...

Excitatory and Inhibitory Effects of Neurotransmitters

Excitatory and Inhibitory Effects of Neurotransmitters

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 specific...

Biological Causes of Schizophrenia

Biological Causes of Schizophrenia

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.
Genetic Factors in Schizophrenia
The genetic basis of schizophrenia is strongly supported by family and twin studies.

Neurotransmitters

Neurotransmitters

Neurotransmitters are essential chemical messengers within the nervous system, facilitating the communication between neurons. These chemical messengers, varying in function and effect, are critical for sustaining various aspects of neurological health and emotional well-being.

Chemical Synapses

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...

Chemical Synapses

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Model of the Reticular Formation of the Brainstem Based on Glial-Neuronal Interactions.

Cognitive computation·2015

Same author

Balancing and imbalancing effects of astrocytic receptors in tripartite synapses. Common pathophysiological model of mental disorders and epilepsy.

Medical hypotheses·2015

Same author

Intuition in autistic savantism: a hypothetical model based on glial-neuronal interactions.

Medical hypotheses·2013

Same author

Neuromodulatory systems.

Frontiers in neural circuits·2013

Same author

Ketamine may block NMDA receptors in astrocytes causing a rapid antidepressant effect.

Frontiers in synaptic neuroscience·2012

Same author

Astrocyte mega-domain hypothesis of the autistic savantism.

Medical hypotheses·2012

Same journal

Spatiotemporal bursting in simulated cultures of cortical neurons.

Bio Systems·2026

Same journal

A brief discussion on recent models shedding light on how life emerged.

Bio Systems·2026

Same journal

Memory-based strategy reputation and adaptive learning in spatial evolutionary games: A robust agent-based model for cooperation dynamics.

Bio Systems·2026

Same journal

Coherent Photonic Biofields: Revisiting Fritz-Albert Popp's Hypothesis.

Bio Systems·2026

Same journal

Ruliological Resilience: Pattern Restoration and Robustness in Wolfram Patterns. A Basis for Regeneration, Not Just in Cone Shells?

Bio Systems·2026

Same journal

The quantum-to-classical transducer: A thermodynamic and quantum mechanical framework for the emergence of bioenergetics.

Bio Systems·2026

See all related articles

Search research articles

Related Experiment Video

Updated: Jun 16, 2026

Standardized Data Acquisition for Neuromelanin-Sensitive Magnetic Resonance Imaging of the Substantia Nigra

Standardized Data Acquisition for Neuromelanin-Sensitive Magnetic Resonance Imaging of the Substantia Nigra

Published on: September 8, 2021

Synaptic imbalances in endogenous psychoses.

Bernhard J Mitterauer¹

¹Institute of Forensic Neuropsychiatry and Gotthard Günther Archives, University of Salzburg, Austria. bernhard.mitterauer@sbg.ac.at <bernhard.mitterauer@sbg.ac.at>

|February 24, 2010

Summary

This summary is machine-generated.

Information processing imbalances in tripartite synapses may explain depression, mania, and schizophrenia. This novel model links synaptic balance to the pathophysiology of major psychiatric disorders.

More Related Videos

Developing a Rat Model for Bipolar Disorder

Developing a Rat Model for Bipolar Disorder

Published on: May 2, 2025

Related Experiment Videos

Last Updated: Jun 16, 2026

Standardized Data Acquisition for Neuromelanin-Sensitive Magnetic Resonance Imaging of the Substantia Nigra

Standardized Data Acquisition for Neuromelanin-Sensitive Magnetic Resonance Imaging of the Substantia Nigra

Published on: September 8, 2021

Developing a Rat Model for Bipolar Disorder

Developing a Rat Model for Bipolar Disorder

Published on: May 2, 2025

Area of Science:

Neuroscience
Psychiatry
Systems Biology

Background:

Endogenous psychoses like depression, mania, and schizophrenia have complex pathophysiology.
Tripartite synapses, comprising neuronal and glial components, are crucial for synaptic function.
Existing models do not fully explain the information processing dynamics underlying these disorders.

Purpose of the Study:

To propose a novel model of synaptic information processing based on logical balance.
To explain the pathophysiology of endogenous psychoses by synaptic imbalances in tripartite synapses.

Main Methods:

Applying the principle of logical balance to tripartite synapse structure and function.
Interpreting neuronal components as 'values' and glial components as 'variables'.
Deducing specific synaptic imbalance states (underbalanced, overbalanced, unbalanced) from this model.

Main Results:

Underbalanced tripartite synapses (excess variables) may underlie depression.
Overbalanced tripartite synapses (excess values) may be linked to mania.
Unbalanced tripartite synapses (lack of functional variables) may contribute to schizophrenia.

Conclusions:

Synaptic information processing imbalances in tripartite synapses offer a potential explanation for endogenous psychoses.
This logical balance model provides a framework for understanding the neurobiological basis of depression, mania, and schizophrenia.
The model suggests that alterations in neuronal-glial interactions are central to these psychiatric conditions.