Key result
Patients with schizophrenia or schizoaffective disorder showed a 24% increase in KCNH2-3.1 mRNA expression in small neurons of layer IV in the dorsolateral prefrontal cortex compared to healthy controls.
Case-Control (n=74)
Blinded to diagnosis
No
Absolute Event Rate: 8.4% vs 6.8%
p-value: p=<0.002
KCNH2-3.1 mRNA expression is increased in putative interneurons in the dorsolateral prefrontal cortex of patients with schizophrenia, potentially contributing to altered neuronal firing.
Hypothesis-generating for KCNH2-3.1 in schizophrenia cortical pathology; leaves open causal role and therapeutic potential.
Background and Objectives: Abnormalities in neuronal firing, controlled and organised by a series of voltage-gated ion channels, may contribute to the pathogenesis of schizophrenia. KCNH2, encoding the voltage-gated potassium channel Kv11.1, has been identified as a potential risk gene for schizophrenia. Single nucleotide polymorphisms (SNPs) in the second intron promote the expression of a brain-specific isoform, KCNH2-3.1, which exhibits altered gating kinetics and results in less adaptation of firing rate in response to prolonged stimulation. To determine the pathophysiological consequence of these altered gating properties, we need to know in which cells KCNH2-3.1 is expressed and how this is affected by genotype and/or diagnosis.
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Heide et al. (2015) conducted a case-control in Schizophrenia and schizoaffective disorder (n=74). Schizophrenia/schizoaffective diagnosis vs. Healthy controls was evaluated on KCNH2-3.1 mRNA expression (silver grains per cell) in small neurons of layer IV in the dorsolateral prefrontal cortex (p=<0.002). Patients with schizophrenia or schizoaffective disorder showed a 24% increase in KCNH2-3.1 mRNA expression in small neurons of layer IV in the dorsolateral prefrontal cortex compared to healthy controls.
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