Navegando por Autor "Nicolelis, M. A. L."
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Apresentado em Evento Experience-dependent reactivation of the calcium signal transduction pathway in the rat hippocampus during sleep(2009-10-20) Pereira, C. M.; Cota, V. R.; Santos, S.; Dias, G.; Souza, A. C.; Ribeiro, Sidarta Tollendal Gomes; Nicolelis, M. A. L.Sleep-dependent plastic changes play a key role in the consolidation of newly acquired memories. Two distinct and successive phases of sleep, slow wave sleep (SWS), and rapid eye movement (REM) sleep can be recognized in mammals. Both phases have been implicated in the sensorimotor processing of daytime events, but the molecular mechanisms involved remain poorly understood. Brain expression of the plasticity-associated immediate-early gene (IEG) zif-268 is upregulated during REM sleep in the cerebral cortex and hippocampus of animals exposed to rich sensorimotor experience in the preceding waking period (Learn Mem. 6; 500, 1999). Zif-268 integrates a major calcium signal transduction pathway which includes Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) and mitogen activated protein kinase (MAPK). CaMKII autophosphorylation of T286 is of special importance because it makes the enzyme active in the absence of Ca(2+), providing a biochemical memory that is critical for plasticity. MAPK, an integral component of cellular signaling during mitotic cell differentiation, has been implicated in hippocampal long-term potentiation (LTP) and learning and memory in behaving animals. Our goal here is to investigate the phosphorylation levels of CaMKII and MAPK during sleep in rats exposed to a new rich environment in the preceding waking period. Intracranial local field potentials (LFPs) recorded in the cortex and hippocampus were used to characterize the wake-sleep cycle (J. Neurosci. 24; 11137, 2004). The phosphorylation levels of CaMKII and MAPK were assessed using specific antibodies for western blots and immunohistochemistry. Our preliminary data (WK n=3, SWS n=5 and REM n=3)) indicate that the MAPK pathway was reactivated in the hippocampus after a few minutes of SWS. Interestingly, for reasons still unknown, MAPK phosphorylation decreased to WK level after a single episode of REM sleep. Our results also showed CaMKII reactivation during REM sleep in the hippocampus of rats previously exposed to novel objects in the preceding WK period. Controls unexposed to novel experience did not show kinase reactivation during sleep. Our results support the notion that sleep harbors experience-dependent mechanisms of synaptic upscaling (Learn Mem. 6; 500, 1999, J. Neurosci. 22; 10914, 2002, J. Neurochem. 95; 418, 2005, Science, 313; 1775, 2006, FINS 1; 43, 2007, Neuron 61; 454, 2009).Artigo Role of neuronal reverberation during slow wave sleep in the consolidation of recently acquired memory traces(2009-10-19) Cota, V.R.; Pereira, C.; Souza, A. C.; Nicolelis, M. A. L.; Ribeiro, Sidarta Tollendal GomesEvidence exists to state that the main sleep states, slow wave (SWS) and rapid eye movement (REM) periods perform two complementary roles for post-novelty memory consolidation: respectively neuronal reverberation for short-term recall (PLoS Bio., 2:0126, 2004); and synaptic plasticity for long-term storage (Learn. Mem. 6: 500, 1999). Moreover, memory traces gradually migrate from hippocampus (HP) to primary somatosensory cortex (SI) through consecutive waves of neuronal reverberation during SWS (Frontiers Neurosci., 1:43, 2007). Our goal is to test this hypothesis by assessing the importance of sleep reverberatory phenomena in memory consolidation. Adult male Long Evans rats (n = 3) received implants of electrode array (32 microwires) in SI for multi-site single-unit and local field potential (LFP) recordings; and a bilateral cannula in HP for local neuronal inhibition through muscimol micro-injection (0.5 μl; 1 mg/ml; 0.25 μl/min). Novel tactile stimulation was provided by a 20 minutes exposure to four objects at the end of the first third of a 12 hours recording session. Muscimol was injected after animals reached a criterion of 30 minutes of SWS in the post- exposure period, as assessed by an online state map algorithm (Frontiers Neurosci., 1:43, 2007). Memory consolidation was assessed by comparing exploration times of animals re-exposed to two familiar plus two new objects over several post-novelty days. Firing rates strongly increased during object exploration and remained elevated afterwards during waking. SI single-unit activity during SWS showed even greater Post/Pre differences in firing rates, displaying periodic waves of reverberation yet to be understood. Muscimol application in the hippocampus completely abolished cortical reverberation a few minutes after micro-injection. Hippocampal deactivation by muscimol induced an electrographic rhythm characterized by greater power in the delta band as revealed by LFP recordings. This rhythm was distinctly separated from the SWS spectral cluster in the state map. Importantly, the time spent in exploration of the new objects was not significantly different from the time spent exploring familiar objects, indicating impairment in the learning of object identities. The results suggest that inhibition of HP neuronal activity 1) impaired SI neuronal reverberation during SWS (possibly by altering slow wave stereotypical brain rhythm) and 2) led to decreased memory consolidation for familiar objects.