title: Lesions of the basolateral amygdala complex block propofol-induced amnesia for inhibitory avoidance learning in rats.
abstract: BACKGROUND
  As the unitary theory of anesthesia gives way to the "multiple sites, multiple mechanisms" concept, the sites involved in mediating the components of anesthesia must be identified. In the current study, we test the hypothesis that the basolateral amygdala complex (BLAC) is a brain site involved with mediating propofol-induced amnesia.
  
  
  METHODS
  Male Sprague-Dawley rats were divided into two groups, sham-operated control animals and rats given bilateral excitotoxic N-methyl-D-aspartate lesions of the BLAC. For each group, animals were given intraperitoneal saline or propofol (25 mg/kg) 5 min before inhibitory avoidance learning. Rats were given a foot shock (0.4 mA) upon entering the dark side of a two-sided apparatus. Rats could escape additional shock by returning to and staying in the light side. Training ended after shock avoidance for greater than 60 s. Memory was tested at 24 h. Longer latencies to enter the dark side 24 h after training imply better memory.
  
  
  RESULTS
  Sham-saline-treated animals had a robust memory latency (median latency [interquartile range] = 300 [163-567] s). Sham-propofo-treated animals exhibited a significant anterograde amnesia (latency = 63 [14-111] s) (P < 0.05 vs. sham-saline-treated animal). Both the saline-injected and propofol-injected animals with BLAC lesions showed robust memory (latency = 300 [264-485] and 323 [143480] s, respectively). These latencies did not differ from performance in the sham-saline-treated group and were significantly higher than the latency of the sham-propofol-treated group (both P < 0.05).
  
  
  CONCLUSIONS
  Discrete BLAC lesions blocked the amnestic effect of propofol. BLAC activity appears to be a requirement for propofol-induced amnesia. This finding suggests that the BLAC is a key brain site mediating anesthetic-induced amnesia.
authors.affiliation: Department of Anesthesiology, Center for the Neurobiology of Learning and Memory, University of California, Irvine 92868, USA. Malkire@UCI.edu
authors.forename: M T
authors.initials: MT
authors.lastname: Alkire
authors.forename: A
authors.initials: A
authors.lastname: Vazdarjanova
authors.forename: H
authors.initials: H
authors.lastname: Dickinson-Anson
authors.forename: N S
authors.initials: NS
authors.lastname: White
authors.forename: L
authors.initials: L
authors.lastname: Cahill
mesh_terms: D000647:Amnesia / Q000139:chemically induced*; D000679:Amygdala / Q000187:drug effects* / Q000502:physiology; D018686:Anesthetics, Intravenous / Q000494:pharmacology*; D000818:Animals; D001362:Avoidance Learning / Q000187:drug effects*; D008297:Male; D008568:Memory / Q000187:drug effects; D015742:Propofol / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D018686:Anesthetics, Intravenous; D015742:Propofol