Abstract
To investigate how neuronal activity in the prefrontal cortex changes in an animal model of schizophrenia, we recorded single unit activity in the medial prefrontal cortex of urethane-anesthetized and awake rats following methamphetamine (MA) administration. Systemic MA injection (4 mg/kg, IP) induced inconsistent changes, that is, both enhancement and reduction, in unit discharge rate, with a subset of neurons transiently (30 min) elevating their activities. The direction of firing rate change was poorly predicted by the mean firing rate or the degree of burst firing during the baseline period. Also, simultaneously recorded units showed opposite directions of firing rate change, indicating that recording location is a poor predictor of the direction of firing rate change. These results raise the possibility that systemic MA injection induces random bidirectional changes in prefrontal cortical unit activity, which may underlie some of MA-induced psychotic symptoms.
Highlights
Several lines of evidence indicate the involvement of the prefrontal cortex (PFC) in the pathophysiology of schizophrenia
Our results show that MA injection changes medial PFC (mPFC) unit activity in at least two different stages and in an unpredictable manner
The degree of burst firing was 0.11 ± 0.02 (n = 18) and 0.08 ± 0.02 (n = 14) for rate-elevated and rate-reduced units, respectively, which did not vary significantly either (Wilcoxon rank-sum test, P = .262). These results further indicate that two physiological indices, baseline firing rate and the degree of burst firing, cannot predict the direction of mPFC unit activity change following MA injection
Summary
Several lines of evidence indicate the involvement of the prefrontal cortex (PFC) in the pathophysiology of schizophrenia. Clinical response to clozapine, an atypical antipsychotic drug, was inversely related to prefrontal atrophy [14]. These studies suggest strongly that pathophysiology of schizophrenia involves abnormal PFC neural activity. AMP/MA facilitates the release and blocks the reuptake of dopamine, augments synaptic actions of dopamine [20]. In this respect, AMP/MA model is especially useful for investigating the role of dopamine hyperactivity in schizophrenia. Neural activity in the PFC has not been examined in intact animals following systemic injection of AMP/MA. Our results show that MA injection changes mPFC unit activity in at least two different stages and in an unpredictable manner
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