Is the Basolateral Amygdala Complex Involved in Mediating Propofol-induced Amnesia? Alkire et al. (page 708)

Alkire et al.  designed an experiment to test whether the basolateral amygdala complex (BLAC) is a brain site involved with mediation of propofol-induced amnesia. The team assigned 85 male Sprague-Dawley rats to one of two surgery groups: sham-operated controls or those to receive bilateral N -methyl-d-aspartate lesions of the BLAC. The rats were then allowed 6 or 7 days of recovery time before beginning inhibitory avoidance training.

On the training day, either 25 mg/kg propofol or saline was administered to the rats 5 min before the training procedure began. The training apparatus featured a light-safe compartment and a dark-shock compartment. Rats instinctively favor a dark environment. When the animals stepped into the dark compartment with all four paws, they received a foot shock (0.4 mA) until they escaped back to the light compartment. The door to the dark compartment was left open; learning was considered to have occurred when animals avoided the dark side for more than 60 consecutive seconds. Memory retention was tested 24 h after the training session. No shock was delivered during the memory testing, but longer latencies to cross into the dark side of the apparatus were considered to be indicative of better retention of training. At the end of the experiments, the rats were killed, and their brains were removed for histologic categorization of the BLAC lesions.

Rats in the sham-operated group that were given saline injections had a median memory latency of 300 s, whereas sham-propofol rats had significant amnesia, with a median latency of only 63 s. Rats with BLAC lesions showed robust memory latency despite administration of propofol: those in the saline group had a median memory latency of 300 s, and those in the propofol-injected group had a median memory latency of 323 s. In these experiments, discrete BLAC lesions blocked the amnestic effect of propofol, suggesting that the BLAC is a key brain site mediating anesthetic-induced amnesia. The results may help explain the clinical phenomenon of intraoperative recall and the enhanced retention of negative emotional material, and they point out the need to understand anesthetic-induced amnesia more fully.