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neurotoxicity and mechanisms of induced hyperexcitability

neurotoxicity and mechanisms of induced hyperexcitability

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with the other rats. After a saline injection, the locomotoractivity levels were very low, <strong>and</strong> there was no significantdifference between the lesioned group <strong>and</strong> thesham-operated group (Figure 2).The effects <strong>of</strong> the microinjection <strong>of</strong> 5,7-DHT on thestartle response, habituation <strong>and</strong> prepulse inhibitionThe startle amplitude in the pulse-alone trials <strong>and</strong> thehabituation <strong>of</strong> 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 <strong>of</strong> group or <strong>of</strong> the habituation x group interaction.Figure 4 appeared to suggest that the mPFC-lesionedrats showed an increase in prepulse inhibition at PP2 <strong>and</strong>PP4 compared to the sham-operated controls; however, anANOVA indicated that there was no significant main effect<strong>of</strong> group or <strong>of</strong> the prepulse x group interaction.DISCUSSIONThe behavioural assessment <strong>of</strong> rats with serotonergiclesions <strong>of</strong> the mPFC, using the locomotor hyperactivity <strong>and</strong>prepulse inhibition paradigms, revealed that there were nodifferences between the lesioned <strong>and</strong> control groups. Thepresent findings suggest that normal regulation <strong>of</strong> locomotoractivity <strong>and</strong> prepulse inhibition is independent <strong>of</strong> serotoninrelease from terminals in the mPFC.Figure 3Effect <strong>of</strong> sham surgery (n=10) or 5,7-DHT lesions <strong>of</strong> the mPFC (n=9) onstartle amplitude, startle habituation <strong>and</strong> prepulse inhibition. The top panelillustrates the basal startle reactivity <strong>and</strong> the startle habituation. The dataare expressed as mean startle amplitudes ± SEM for each <strong>of</strong> the four blocks<strong>of</strong> ten 115 dB pulses. The bottom panel illustrates the prepulse inhibition <strong>of</strong>the 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 <strong>of</strong> the microinjection <strong>of</strong> 5,7-DHT onamphetamine- <strong>and</strong> phencyclidine-<strong>induced</strong> locomotorhyperactivityThe locomotor hyperactivity caused by treatmentwith amphetamine or phencyclidine was not significantlydifferent between sham-operated rats <strong>and</strong> mP-FC-lesioned rats (Figure 2). After treatment with eitheramphetamine or phencyclidine, there was an expectedmain effect <strong>of</strong> time (F 2,34=10.4, p

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