Rationale: Contextual control over drug relapse depends on the successful reconsolidation and retention of context-response-cocaine associations in long-term memory stores. The basolateral amygdala (BLA) plays a critical role in cocaine memory reconsolidation and subsequent drug context-induced cocaine-seeking behavior; however, less is known about the cellular mechanisms of this phenomenon.
Objectives: The present study evaluated the hypothesis that protein kinase A (PKA) and calcium/calmodulin-dependent protein kinase II (CaMKII) activation in the BLA is necessary for the reconsolidation of context-response-cocaine memories that promote subsequent drug context-induced cocaine-seeking behavior.
Methods: Rats were trained to lever-press for cocaine infusions in a distinct context, followed by extinction training in a different context. Rats were then briefly re-exposed to the previously cocaine-paired context or an unpaired context in order to reactivate cocaine-related contextual memories and initiate their reconsolidation or to provide a similar behavioral experience without explicit cocaine-related memory reactivation, respectively. Immediately after this session, rats received bilateral microinfusions of vehicle, the PKA inhibitor, Rp-adenosine 3',5'-cyclic monophosphorothioate triethylammonium salt (Rp-cAMPS), or the CaMKII inhibitor, KN-93, into the BLA or the posterior caudate putamen (anatomical control region). Rats were then tested for cocaine-seeking behavior (responses on the previously cocaine-paired lever) in the cocaine-paired context and the extinction context.
Results: Intra-BLA infusion of Rp-cAMPS, but not KN-93, following cocaine memory reconsolidation impaired subsequent cocaine-seeking behavior in a dose-dependent, site-specific, and memory reactivation-dependent fashion.
Conclusions: PKA, but not CaMKII, activation in the BLA is critical for cocaine memory re-stabilization processes that facilitate subsequent drug context-induced instrumental cocaine-seeking behavior.
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http://dx.doi.org/10.1007/s00213-013-3203-9 | DOI Listing |
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Pediatric Rheumatology Department, Faculty of Medicine, Cairo University, Cairo, Egypt.
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Department of Histology and Embryology, Faculty of Medicine, Masaryk University, Brno, Czech Republic.
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Department of Genetics & Biotechnology, Graduate School of Biotechnology, College of Life Sciences, Kyung Hee University, Youngin, 17104, Republic of Korea.
Abnormal melanin synthesis within melanocytes can result in pigmentary skin disorders. Although pigmentation alterations associated with inflammation are frequently observed, the precise reason for this clinical observation is still unknown. More specifically, although many cytokines are known to be critical for inflammatory skin processes, it is unclear how they affect epidermal melanocyte function.
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Department of Physiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
We have recently shown that fluoxetine (FX) suppressed polyinosinic-polycytidylic acid-induced inflammatory response and endothelin release in human epidermal keratinocytes, via the indirect inhibition of the phosphoinositide 3-kinase (PI3K)-pathway. Because PI3K-signaling is a positive regulator of the proliferation, in the current, highly focused follow-up study, we assessed the effects of FX (14 µM) on the proliferation and differentiation of human epidermal keratinocytes. We found that FX exerted anti-proliferative actions in 2D cultures (HaCaT and primary human epidermal keratinocytes [NHEKs]; 48- and 72-h; CyQUANT-assay) as well as in 3D reconstructed epidermal equivalents (48-h; Ki-67 immunohistochemistry).
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