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

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.

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...

Psychological and Sociocultural Causes of Schizophrenia

Psychological and Sociocultural Causes of Schizophrenia

Schizophrenia, a complex psychiatric disorder, has been historically misunderstood. Early psychological theories attributed its origins to childhood trauma and unresponsive parenting. However, contemporary research largely rejects these notions, favoring the vulnerability-stress hypothesis. This model proposes that individuals with a genetic predisposition to schizophrenia may develop the disorder following exposure to significant environmental stressors. Notably, studies on high-risk...

Parkinson Disease ll: Pathophysiology

Parkinson Disease ll: Pathophysiology

Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...

You might also read

Related Articles

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

Sort by

Same author

Nose-to-brain delivery of lithium via a sprayable in situ-forming hydrogel composed of chelating starch nanoparticles.

Journal of controlled release : official journal of the Controlled Release Society·2024

Same author

In situ-gelling hydrophobized starch nanoparticle-based nanoparticle network hydrogels for the effective delivery of intranasal olanzapine to treat brain disorders.

International journal of biological macromolecules·2024

Same author

Therapeutic effects of TP5, a Cdk5/p25 inhibitor, in <i>in vitro</i> and <i>in vivo</i> models of Parkinson's disease.

Current research in neurobiology·2022

Same author

Decreased Expression of Cerebral Dopamine Neurotrophic Factor in Platelets of Probable Alzheimer Patients.

Alzheimer disease and associated disorders·2022

Same author

Using the Intranasal Route to Administer Drugs to Treat Neurological and Psychiatric Illnesses: Rationale, Successes, and Future Needs.

CNS drugs·2022

Same author

Ketamine-induced neurotoxicity is mediated through endoplasmic reticulum stress in vitro in STHdh<sup>Q7/Q7</sup> cells.

Neurotoxicology·2022

Search research articles

Related Experiment Video

Updated: Jun 24, 2026

Contextual and Cued Fear Conditioning Test Using a Video Analyzing System in Mice

Contextual and Cued Fear Conditioning Test Using a Video Analyzing System in Mice

Published on: March 1, 2014

Behavioral abnormalities in synapsin II knockout mice implicate a causal factor in schizophrenia.

Bailee A Dyck¹, Kevin J Skoblenick, Jessica M Castellano

¹Department of Psychiatry and Behavioral Neurosciences, McMaster University, Hamilton, Ontario, Canada.

Synapse (New York, N.Y.)

|April 11, 2009

Summary

Synapsin II knockout mice exhibit schizophrenia-like behaviors, including impaired prepulse inhibition and social deficits. These findings suggest synapsin II plays a causal role in schizophrenia pathophysiology.

More Related Videos

Dynamic Clamp Methods to Investigate Impaired Neuronal Excitability Associated with Autism

Dynamic Clamp Methods to Investigate Impaired Neuronal Excitability Associated with Autism

Published on: October 17, 2025

Assessment of Social Interaction Behaviors

Assessment of Social Interaction Behaviors

Published on: February 25, 2011

Related Experiment Videos

Last Updated: Jun 24, 2026

Contextual and Cued Fear Conditioning Test Using a Video Analyzing System in Mice

Contextual and Cued Fear Conditioning Test Using a Video Analyzing System in Mice

Published on: March 1, 2014

Dynamic Clamp Methods to Investigate Impaired Neuronal Excitability Associated with Autism

Dynamic Clamp Methods to Investigate Impaired Neuronal Excitability Associated with Autism

Published on: October 17, 2025

Assessment of Social Interaction Behaviors

Assessment of Social Interaction Behaviors

Published on: February 25, 2011

Area of Science:

Neuroscience
Psychiatry
Genetics

Background:

Reduced synapsin II expression is observed in schizophrenia patients.
Antipsychotic treatment increases synapsin II levels, suggesting its involvement in the disease.

Purpose of the Study:

To investigate the causal role of synapsin II in schizophrenia.
To determine if synapsin II knockout mice display schizophrenia-related behavioral abnormalities.

Main Methods:

Generated synapsin II knockout mice.
Assessed behavioral endophenotypes: prepulse inhibition (PPI), acoustic startle habituation, social behavior, and locomotor activity.
Confirmed gene knockout via immunoblotting.

Main Results:

Synapsin II knockout mice showed significant deficits in PPI and acoustic startle habituation.
Knockout mice displayed reduced social behavior and increased locomotor activity compared to controls.
Complete absence of synapsin II protein was confirmed in knockout brains.

Conclusions:

Synapsin II knockout mice exhibit behavioral deficits mirroring preclinical models of schizophrenia.
These findings support a potential causal role for synapsin II dysfunction in schizophrenia.
Synapsin II may be a key factor in the pathophysiology of schizophrenia.