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Queiroz,C.M.; Tiba,P.A.; Moreira,K.M.; Guidine,P.A.M.; Rezende,G.H.S.; Moraes,M.F.D.; Prado,M.A.M.; Prado,V.F.; Tufik,S.; Mello,L.E.. |
Impaired cholinergic neurotransmission can affect memory formation and influence sleep-wake cycles (SWC). In the present study, we describe the SWC in mice with a deficient vesicular acetylcholine transporter (VAChT) system, previously characterized as presenting reduced acetylcholine release and cognitive and behavioral dysfunctions. Continuous, chronic ECoG and EMG recordings were used to evaluate the SWC pattern during light and dark phases in VAChT knockdown heterozygous (VAChT-KDHET, n=7) and wild-type (WT, n=7) mice. SWC were evaluated for sleep efficiency, total amount and mean duration of slow-wave, intermediate and paradoxical sleep, as well as the number of awakenings from sleep. After recording SWC, contextual fear-conditioning tests were used... |
Tipo: Info:eu-repo/semantics/article |
Palavras-chave: Sleep-wake cycle; Intermediate sleep; Acetylcholine; Contextual fear conditioning; Memory; Neurodegenerative disorders. |
Ano: 2013 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2013001000844 |
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Queiroz,C.M.; Mello,L.E.. |
Intrahippocampal administration of kainic acid (KA) induces synaptic release of neurotrophins, mainly brain-derived neurotrophic factor, which contributes to the acute neuronal excitation produced by the toxin. Two protein tyrosine kinase inhibitors, herbimycin A and K252a, were administered intracerebroventricularly, in a single dose, to attenuate neurotrophin signaling during the acute effects of KA, and their role in epileptogenesis was evaluated in adult, male Wistar rats weighing 250-300 g. The latency for the first Racine stage V seizure was 90 ± 8 min in saline controls (N = 4) which increased to 369 ± 71 and 322 ± 63 min in animals receiving herbimycin A (1.74 nmol, N = 4) and K252a (10 pmol, N = 4), respectively. Behavioral alterations were... |
Tipo: Info:eu-repo/semantics/article |
Palavras-chave: Herbimycin A; K252a; Cell death; EEG; Epilepsy. |
Ano: 2008 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2008000500009 |
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