Fig. 1. Representative electroencephalogram recordings for CS (A , C , E , G ) and CD (B , D , F , H ) at baseline (A , B ) as well as at various, comparable time points: within 15 min of the start of cocaine (C , D ), within 15 min of the start of saline (E ) or dexmedetomidine (F ), and at the onset of generalized seizure activity (G , H ). Each electroencephalogram tracing is from a rat that received the infusion of cocaine (1.25 mg · kg−1· min−1) followed 15 min later by the coinfusion of either dexmedetomidine (CD, n = 8) or saline (CS, n = 8). The infusion of dexmedetomidine produced significant electroencephalogram slowing in the presence of cocaine (F ). Cocaine typically produced burst epileptiform activity that corresponded to generalized seizure activity in the rats (G , H ).

Fig. 1. Representative electroencephalogram recordings for CS (A , C , E , G ) and CD (B , D , F , H ) at baseline (A , B ) as well as at various, comparable time points: within 15 min of the start of cocaine (C , D ), within 15 min of the start of saline (E ) or dexmedetomidine (F ), and at the onset of generalized seizure activity (G , H ). Each electroencephalogram tracing is from a rat that received the infusion of cocaine (1.25 mg · kg−1· min−1) followed 15 min later by the coinfusion of either dexmedetomidine (CD, n = 8) or saline (CS, n = 8). The infusion of dexmedetomidine produced significant electroencephalogram slowing in the presence of cocaine (F ). Cocaine typically produced burst epileptiform activity that corresponded to generalized seizure activity in the rats (G , H ).

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