neurotoxicity and mechanisms of induced hyperexcitability

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clidine (time) and the interactions between these factors.In this analysis, the time effect was a repeated-measuresfactor. The baseline and the drug-induced locomotor activitywere part of the data set analysed. In the prepulse inhibitionexperiments, the factors were group and habituation(four blocks of ten startle responses) or group and prepulse(five different prepulse intensities), where habituation andprepulse were repeated-measures factors. After calculatingANOVAs for all of the surgery groups, subsequent pairwiseANOVAs were performed where needed. A ‘p-value’of p
with the other rats. After a saline injection, the locomotoractivity levels were very low, and there was no significantdifference between the lesioned group and thesham-operated group (Figure 2).The effects of the microinjection of 5,7-DHT on thestartle response, habituation and prepulse inhibitionThe startle amplitude in the pulse-alone trials and thehabituation of the rats were not different between the mP-FC-lesioned rats compared to the sham-operated controls(Figure 3). An ANOVA revealed that there was no significantmain effect of group or of the habituation x group interaction.Figure 4 appeared to suggest that the mPFC-lesionedrats showed an increase in prepulse inhibition at PP2 andPP4 compared to the sham-operated controls; however, anANOVA indicated that there was no significant main effectof group or of the prepulse x group interaction.DISCUSSIONThe behavioural assessment of rats with serotonergiclesions of the mPFC, using the locomotor hyperactivity andprepulse inhibition paradigms, revealed that there were nodifferences between the lesioned and control groups. Thepresent findings suggest that normal regulation of locomotoractivity and prepulse inhibition is independent of serotoninrelease from terminals in the mPFC.Figure 3Effect of sham surgery (n=10) or 5,7-DHT lesions of the mPFC (n=9) onstartle amplitude, startle habituation and prepulse inhibition. The top panelillustrates the basal startle reactivity and the startle habituation. The dataare expressed as mean startle amplitudes ± SEM for each of the four blocksof ten 115 dB pulses. The bottom panel illustrates the prepulse inhibition ofthe acoustic startle response. The prepulse inhibition is expressed as the %inhibition ± SEM at different prepulse intensities. There were no significantdifferences between the groups as indicated by ANOVA.The effects of the microinjection of 5,7-DHT onamphetamine- and phencyclidine-induced locomotorhyperactivityThe locomotor hyperactivity caused by treatmentwith amphetamine or phencyclidine was not significantlydifferent between sham-operated rats and mP-FC-lesioned rats (Figure 2). After treatment with eitheramphetamine or phencyclidine, there was an expectedmain effect of time (F 2,34=10.4, p
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