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

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The chandelier neuron in schizophrenia.

David A Lewis¹

¹Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. lewisda@upmc.edu

Developmental Neurobiology

|December 15, 2010

Summary

Schizophrenia alters GABA neurotransmission markers in the brain's dorsolateral prefrontal cortex (DLPFC). Specifically, GABA transporter 1 (GAT1) and GABA(A) receptor α2 subunit changes suggest disrupted chandelier neuron-pyramidal neuron connections.

Area of Science:

Neuroscience
Psychiatry
Cell Biology

Background:

Schizophrenia is associated with altered neurotransmission in the dorsolateral prefrontal cortex (DLPFC).
Chandelier neurons form critical inhibitory synapses onto the axon initial segment (AIS) of pyramidal neurons, regulating neuronal output.

Purpose of the Study:

To investigate alterations in GABAergic markers and synaptic components of chandelier neuron-pyramidal neuron connections in the DLPFC of individuals with schizophrenia.
To explore the developmental implications of these alterations in the context of schizophrenia pathogenesis.

Main Methods:

Immunohistochemical analysis of GABAergic markers (GAT1, GABA(A) receptor α2 subunit) and AIS-associated proteins (ankyrin-G) in human DLPFC tissue.
Examination of alterations in specific cortical layers (2-3) and pyramidal neuron subtypes.

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Automated Sholl Analysis of Digitized Neuronal Morphology at Multiple Scales

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Main Results:

Decreased GAT1 immunoreactivity in presynaptic chandelier terminals.
Increased GABA(A) receptor α2 subunit and altered ankyrin-G in postsynaptic AIS of pyramidal neurons, particularly in superficial layers.
These molecular changes exhibit distinct developmental trajectories.

Conclusions:

Aberrant GABAergic signaling and synaptic organization in chandelier neuron-pyramidal neuron circuits may contribute to cortical dysfunction in schizophrenia.
Disturbances in the developmental trajectories of these synaptic components are implicated in schizophrenia pathogenesis.
Novel findings suggest excitatory inputs from neocortical chandelier neurons offer new insights into schizophrenia pathophysiology.