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Protein synthesis in dorsal hippocampus supports the drug tolerance induced by prior elevated plus-maze experience.
Neuroscience. 2011 Apr 14; 179:179-87.N

Abstract

Tolerance to the anxiolytic-like effect of drugs may develop because of a memory derived from prior experience in certain apparatuses such as the elevated plus-maze (EPM). Activity in basolateral amygdala was shown to be required for consolidating this knowledge. The dorsal hippocampus (DH) is also implicated in long-term memory consolidation, a process relying on new protein synthesis. It is unknown, however, whether the DH protein synthesis disruption would prevent the phenomenon rendering animals unresponsive to benzodiazepines in the EPM retest. To address this, we bilaterally infused the protein synthesis inhibitor anisomycin (ANI) into the rat DH 0, 3 or 6 h after, or 15 min before, the EPM test. DH infusion of ANI (80 μg) around the time of EPM testing preserved the anxiolysis of the midazolam (MDZ; 0.5 mg/kg, i.p.) in rats retested in the EPM 24 h later, suggesting that information consolidated by DH protein synthesis impacts on the subsequent animal's responsiveness to this drug. To examine whether impaired memory acquisition could also contribute to the prevention of MDZ tolerance seen in EPM-experienced animals infused with ANI before testing, the EPM retest was performed 3 h after testing to coincide with the temporal window in which short-term memory remains, for the reason that this process does not require protein synthesis for its formation. The pretest DH anisomycin infusion's ability to prevent the MDZ tolerance on retesting was now missing. This result confirms a specific action of the ANI on memory consolidation. We also found that rats express further avoidance to open-arms in the EPM retest. However, neither pretest nor posttest DH ANI infusion interfered with this pattern of results exhibited by EPM-experienced rats.

Authors+Show Affiliations

Departamento de Farmacologia, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Florianópolis, Santa Catarina, 88040-900, Brazil.No affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

21284953

Citation

Gazarini, L, et al. "Protein Synthesis in Dorsal Hippocampus Supports the Drug Tolerance Induced By Prior Elevated Plus-maze Experience." Neuroscience, vol. 179, 2011, pp. 179-87.
Gazarini L, Stern CA, Bertoglio LJ. Protein synthesis in dorsal hippocampus supports the drug tolerance induced by prior elevated plus-maze experience. Neuroscience. 2011;179:179-87.
Gazarini, L., Stern, C. A., & Bertoglio, L. J. (2011). Protein synthesis in dorsal hippocampus supports the drug tolerance induced by prior elevated plus-maze experience. Neuroscience, 179, 179-87. https://doi.org/10.1016/j.neuroscience.2011.01.057
Gazarini L, Stern CA, Bertoglio LJ. Protein Synthesis in Dorsal Hippocampus Supports the Drug Tolerance Induced By Prior Elevated Plus-maze Experience. Neuroscience. 2011 Apr 14;179:179-87. PubMed PMID: 21284953.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Protein synthesis in dorsal hippocampus supports the drug tolerance induced by prior elevated plus-maze experience. AU - Gazarini,L, AU - Stern,C A J, AU - Bertoglio,L J, Y1 - 2011/02/01/ PY - 2010/12/07/received PY - 2011/01/07/revised PY - 2011/01/25/accepted PY - 2011/2/3/entrez PY - 2011/2/3/pubmed PY - 2011/7/14/medline SP - 179 EP - 87 JF - Neuroscience JO - Neuroscience VL - 179 N2 - Tolerance to the anxiolytic-like effect of drugs may develop because of a memory derived from prior experience in certain apparatuses such as the elevated plus-maze (EPM). Activity in basolateral amygdala was shown to be required for consolidating this knowledge. The dorsal hippocampus (DH) is also implicated in long-term memory consolidation, a process relying on new protein synthesis. It is unknown, however, whether the DH protein synthesis disruption would prevent the phenomenon rendering animals unresponsive to benzodiazepines in the EPM retest. To address this, we bilaterally infused the protein synthesis inhibitor anisomycin (ANI) into the rat DH 0, 3 or 6 h after, or 15 min before, the EPM test. DH infusion of ANI (80 μg) around the time of EPM testing preserved the anxiolysis of the midazolam (MDZ; 0.5 mg/kg, i.p.) in rats retested in the EPM 24 h later, suggesting that information consolidated by DH protein synthesis impacts on the subsequent animal's responsiveness to this drug. To examine whether impaired memory acquisition could also contribute to the prevention of MDZ tolerance seen in EPM-experienced animals infused with ANI before testing, the EPM retest was performed 3 h after testing to coincide with the temporal window in which short-term memory remains, for the reason that this process does not require protein synthesis for its formation. The pretest DH anisomycin infusion's ability to prevent the MDZ tolerance on retesting was now missing. This result confirms a specific action of the ANI on memory consolidation. We also found that rats express further avoidance to open-arms in the EPM retest. However, neither pretest nor posttest DH ANI infusion interfered with this pattern of results exhibited by EPM-experienced rats. SN - 1873-7544 UR - https://www.unboundmedicine.com/medline/citation/21284953/Protein_synthesis_in_dorsal_hippocampus_supports_the_drug_tolerance_induced_by_prior_elevated_plus_maze_experience_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306-4522(11)00109-6 DB - PRIME DP - Unbound Medicine ER -