Cortical and hippocampal EEG power spectra in animal models of schizophrenia produced with methamphetamine, cocaine, and phencyclidine

Abstract

Cortical and hippocampal EEGs in animal models of schizophrenia were compared to those obtained with psychotomimetics or antipsychotic agents by utilizing power spectral analysis. Models of positive schizophrenic symptoms were created with methamphetamine (MAP) and cocaine, and a model of both negative and positive symptoms was created with PCP. MAP caused a prolonged decrease in the cortical EEG power spectra, cocaine caused a marked decrease for a short time, and PCP produced no significant changes. In the hippocampal spectra, MAP induced a marked increase in the T2(6.0-7.9 Hz)/ T1(4.0-5.9 Hz) ratio, PCP caused a decrease of this ratio after an initial increase, and cocaine produced no significant change. (An increase in the T2/T1 ratio represents a shift of theta waves to higher frequencies.) Since apomorphine (a DA agonist) and MK-801 (an NMDA antagonist) caused the T2/T1 ratio to increase, positive schizophrenic symptoms caused by MAP may be related to the DA and NMDA systems. 3-PPP (a sigma agonist) caused biphasic changes similar to those induced by PCP. Haloperidol and chlorpromazine caused a decrease of the T2/T1 ratio. These results indicate that cortical and hippocampal EEG power spectra (especially the hippocampal T2/T1 ratio) can be used to characterize both qualitatively and quantitatively models of schizophrenia.

NMDA antagonists recreate signal-to-noise ratio and timing perturbations present in schizophrenia

“…This method has been previously established in clinical studies of schizophrenia and autism and to examine power changes in those disorders. To evaluate the state of SNR in this model, baseline, evoked and total power were examined in high and low frequency ranges to determine if these two well established pharmacological models cause perturbations in the noise or stimulus-related signal similar to those found in schizophrenia (Behrendt, 2003; Behrendt and Young, 2004; Brenner et al, 2009; Canive et al, 1998; Dierks et al, 1995; Doheny et al, 2000; Ford et al, 2008; Fujisawa et al, 2004; Gaspar et al, 2009; Hall et al; Hall et al, 2009; Hong et al, 2004; Jensen and Lisman, 1996; Kessler and Kling, 1991; Kirino and Inoue, 1999; Kissler et al, 2000; Koukkou et al, 2000; Krause et al, 2003; Krishnan et al, 2009; Kwon et al, 1999; Leicht et al; Lifshitz et al, 1987; Light et al, 2006; Reinhart et al; Schellenberg and Schwarz, 1993; Spencer et al, 2004; Teale et al, 2008; Yamamoto, 1997). Additionally, inter-trial coherence, a measure for determining the trial to trial response consistency, was examined was analyzed in low and high frequency regions to determine whether or not a loss of response consistency is associated with changes in power.…”

Activation of D2 autoreceptors alters cocaine-induced locomotion and slows down local field oscillations in the rat ventral tegmental area

“…According to it, theta oscillations control the timing of activity across neuronal populations in different brain areas playing a key role in the integration of sensory information with motor output (Bland and Oddie, 2001;Buzsaki and Draguhn, 2004;Hasselmo et al, 2002;Seidenbecher et al, 2003;Siapas et al, 2005). Even small shifts in the theta frequency might change the patterns of neural activity across the brain, leading to significant alterations in the emotional state and behavior (Dzirasa et al, 2009;Yamamoto, 1997Yamamoto, , 1998. Thus, we believe that our electrophysiological results underlie the behavioral alteration that we observed, and may give some insight into mechanisms of locomotor regulation.…”

Isolation of a novel potassium channel gene hSKCa3 containing a polymorphic CAG repeat: a candidate for schizophrenia and bipolar disorder?

“…While toxic and therapeutic drug responses have both implicated NMDA-receptor hypofunction in these diseases, linkage studies have eliminated many glutamate-receptor and dopamine receptor genes as plausible disease candidates. [20][21][22][23][24][25][26] SKCa channels hyperpolarize the membrane potential, 21 and thereby inactivate NMDA-receptors. Hyperactive hSKCa3 channels would therefore be expected to induce NMDA receptor hypo-function and might thereby enhance disease susceptibility.…”