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Bilateral inhibition of gamma-aminobutyric acid type A receptor function within the basolateral amygdala blocked propofol-induced amnesia and activity-regulated cytoskeletal protein expression inhibition in the hippocampus.
Anesthesiology. 2008 Nov; 109(5):775-81.A

Abstract

BACKGROUND

It has been reported that bilateral lesions of the basolateral amygdala complex (BLA) blocked propofol-induced amnesia of inhibitory avoidance (IA) training. Based on these results, the authors hypothesized that the amnesia effect of propofol was partly due to its impairment of memory formation in the hippocampus through activating the BLA gamma-aminobutyric acid type A receptor function. The authors determined the changes in activity-regulated cytoskeleton-associated protein (Arc) expression to be an indicator of IA memory formation.

METHODS

Male Sprague-Dawley rats received bilateral injection of bicuculline methiodide (10, 50, or 100 pmol/0.5 microl) or saline (0.5 microl) into the BLA. Fifteen minutes later, the rats were intraperitoneally injected with either propofol (25 mg/kg) or saline. After 5 min, the one-trial IA training was conducted. Rats intraperitoneally infused with saline served as controls and only received saline injections into the BLA. Twenty-four hours later, the IA retention latency was tested. Separate groups of rats treated the same way were killed either 30 min after IA training for hippocampal Arc mRNA measurement or after 45 min for protein level quantification.

RESULTS

The largest dose of bicuculline methiodide (100 pmol) not only blocked the propofol-induced amnesia but also reversed the inhibition effect of propofol on Arc protein expression in the hippocampus (P < 0.05). However, the mRNA level of Arc showed no significant changes after propofol and bicuculline methiodide administration.

CONCLUSIONS

The amnesic effect of propofol seems to involve the modulation of Arc protein expression in the hippocampus, occurring through a network interaction with the BLA.

Authors+Show Affiliations

Department of Anesthesiology, Ruijin Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, PR China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18946287

Citation

Ren, Yu, et al. "Bilateral Inhibition of Gamma-aminobutyric Acid Type a Receptor Function Within the Basolateral Amygdala Blocked Propofol-induced Amnesia and Activity-regulated Cytoskeletal Protein Expression Inhibition in the Hippocampus." Anesthesiology, vol. 109, no. 5, 2008, pp. 775-81.
Ren Y, Zhang FJ, Xue QS, et al. Bilateral inhibition of gamma-aminobutyric acid type A receptor function within the basolateral amygdala blocked propofol-induced amnesia and activity-regulated cytoskeletal protein expression inhibition in the hippocampus. Anesthesiology. 2008;109(5):775-81.
Ren, Y., Zhang, F. J., Xue, Q. S., Zhao, X., & Yu, B. W. (2008). Bilateral inhibition of gamma-aminobutyric acid type A receptor function within the basolateral amygdala blocked propofol-induced amnesia and activity-regulated cytoskeletal protein expression inhibition in the hippocampus. Anesthesiology, 109(5), 775-81. https://doi.org/10.1097/ALN.0b013e31818a37c4
Ren Y, et al. Bilateral Inhibition of Gamma-aminobutyric Acid Type a Receptor Function Within the Basolateral Amygdala Blocked Propofol-induced Amnesia and Activity-regulated Cytoskeletal Protein Expression Inhibition in the Hippocampus. Anesthesiology. 2008;109(5):775-81. PubMed PMID: 18946287.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Bilateral inhibition of gamma-aminobutyric acid type A receptor function within the basolateral amygdala blocked propofol-induced amnesia and activity-regulated cytoskeletal protein expression inhibition in the hippocampus. AU - Ren,Yu, AU - Zhang,Fu-Jun, AU - Xue,Qing-Sheng, AU - Zhao,Xin, AU - Yu,Bu-Wei, PY - 2008/10/24/pubmed PY - 2008/11/19/medline PY - 2008/10/24/entrez SP - 775 EP - 81 JF - Anesthesiology JO - Anesthesiology VL - 109 IS - 5 N2 - BACKGROUND: It has been reported that bilateral lesions of the basolateral amygdala complex (BLA) blocked propofol-induced amnesia of inhibitory avoidance (IA) training. Based on these results, the authors hypothesized that the amnesia effect of propofol was partly due to its impairment of memory formation in the hippocampus through activating the BLA gamma-aminobutyric acid type A receptor function. The authors determined the changes in activity-regulated cytoskeleton-associated protein (Arc) expression to be an indicator of IA memory formation. METHODS: Male Sprague-Dawley rats received bilateral injection of bicuculline methiodide (10, 50, or 100 pmol/0.5 microl) or saline (0.5 microl) into the BLA. Fifteen minutes later, the rats were intraperitoneally injected with either propofol (25 mg/kg) or saline. After 5 min, the one-trial IA training was conducted. Rats intraperitoneally infused with saline served as controls and only received saline injections into the BLA. Twenty-four hours later, the IA retention latency was tested. Separate groups of rats treated the same way were killed either 30 min after IA training for hippocampal Arc mRNA measurement or after 45 min for protein level quantification. RESULTS: The largest dose of bicuculline methiodide (100 pmol) not only blocked the propofol-induced amnesia but also reversed the inhibition effect of propofol on Arc protein expression in the hippocampus (P < 0.05). However, the mRNA level of Arc showed no significant changes after propofol and bicuculline methiodide administration. CONCLUSIONS: The amnesic effect of propofol seems to involve the modulation of Arc protein expression in the hippocampus, occurring through a network interaction with the BLA. SN - 1528-1175 UR - https://www.unboundmedicine.com/medline/citation/18946287/Bilateral_inhibition_of_gamma_aminobutyric_acid_type_A_receptor_function_within_the_basolateral_amygdala_blocked_propofol_induced_amnesia_and_activity_regulated_cytoskeletal_protein_expression_inhibition_in_the_hippocampus_ DB - PRIME DP - Unbound Medicine ER -