Navegando por Palavras-chave "cholinergic"
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- ItemSomente MetadadadosEffects of the M1 Muscarinic Antagonist Dicyclomine on Emotional Memory Retrieval(Amer Psychological Assoc, 2016) Soares, Juliana Carlota Kramer [UNIFESP]; Perfetto, Juliano Genaro [UNIFESP]; Antonio, Bruno Brito [UNIFESP]; Oliveira, Maria Gabriela Menezes [UNIFESP]Extensive research has shown the involvement of the central cholinergic system in the acquisition and consolidation of tasks involving conditioned fear responses, such as those observed in contextual fear conditioning (CFC), tone fear conditioning (TFC) and inhibitory avoidance (IA). However, there are few data concerning the role of this system in the memory retrieval process. Therefore, the present study aimed to compare the effects of the administration of an M1 antagonist on retrieval during these tasks. For each behavioral procedure, groups of male Wistar rats were trained. Twenty-four hr later, they were treated with different doses of dicyclomine (16, 32, or 64 mg/kg, i.p.) or with saline 30 min before the test session. The results showed that dicyclomine at doses of 16 and 32 mg/kg impaired CFC without interfering with IA performance. Moreover, only 64 mg/kg impaired TFC. These data suggest that M1 muscarinic receptors contribute to memory retrieval in CFC and TFC but are not essential for retrieval in IA.
- ItemSomente MetadadadosEffects of the M1 Muscarinic Antagonist Dicyclomine on Emotional Memory Retrieval(Amer Psychological Assoc, 2016) Soares, Juliana Carlota Kramer [UNIFESP]; Perfetto, Juliano Genaro [UNIFESP]; Antonio, Bruno Brito [UNIFESP]; Oliveira, Maria Gabriela Menezes [UNIFESP]Extensive research has shown the involvement of the central cholinergic system in the acquisition and consolidation of tasks involving conditioned fear responses, such as those observed in contextual fear conditioning (CFC), tone fear conditioning (TFC) and inhibitory avoidance (IA). However, there are few data concerning the role of this system in the memory retrieval process. Therefore, the present study aimed to compare the effects of the administration of an M1 antagonist on retrieval during these tasks. For each behavioral procedure, groups of male Wistar rats were trained. Twenty-four hr later, they were treated with different doses of dicyclomine (16, 32, or 64 mg/kg, i.p.) or with saline 30 min before the test session. The results showed that dicyclomine at doses of 16 and 32 mg/kg impaired CFC without interfering with IA performance. Moreover, only 64 mg/kg impaired TFC. These data suggest that M1 muscarinic receptors contribute to memory retrieval in CFC and TFC but are not essential for retrieval in IA.
- ItemSomente MetadadadosRole of muscarinic M1 receptors in inhibitory avoidance and contextual fear conditioning(Elsevier B.V., 2006-09-01) Kramer Soares, Juliana Carlota; Fornari, Raquel Vecchio; Menezes Oliveira, Maria Gabriela; Universidade Federal de São Paulo (UNIFESP)The objective of the present study was to observe the effects of pre-training or post-training administration of dicyclomine, a M1 muscarinic antagonist, on inhibitory avoidance (IA) and contextual fear conditioning (CFC) and to investigate if the effects observed with the pre-training administration of dicyclomine are state-dependent. for each behavioral procedure (IA and CFC) groups of Wistar male rats were treated with saline or dicyclomine either 30 min before training (pre-training), immediately after training or 30 min before training/30 min before test (pre-training/pre-test). the animals were tested 24 h after training. the acquisition of IA and CFC was impaired by pre-training administration of dicyclomine. the consolidation of both tasks was not affected by dicyclomine given immediately after training. Pre-training/pre-test administration of dicyclomine impaired both tasks, an effect similar to that observed in the group which only received pre-training administration. Pre-test treatment induced dissociation between both tasks, impairing CFC retrieval, without interfering with the animals avoidance response. These results show that the dicyclomine did not affect IA and CFC consolidation, suggesting specific involvement of M1 muscarinic receptor only in acquisition these tasks, and these effects was not state-dependent. However, it is possible that the retrieval of these tasks may be mediated, at least in part, by different neurochemical mechanisms and may be dissociated by dicyclomine. (c) 2006 Elsevier Inc. All rights reserved.
- ItemSomente MetadadadosSpontaneous recurrent seizures and neuropathology in the chronic phase of the pilocarpine and picrotoxin model epilepsy(Forefront Publ Group, 2002-03-01) Hamani, C.; Mello, LEAM; Universidade Federal de São Paulo (UNIFESP)In a recent publication, we have shown a potent interaction between the cholinergic and GABAergic systems in regard to seizure generation and developed the pilocarpine(pilo)/picrotoxin(PTX) model, in which combined injections of these agents have induced status epilepticus (SE) in rats. Here we report on the chronic features of this new animal model of epilepsy. Adult male Wistar rats were systemically injected with solutions containing 750/0.5 mg kg(-1), 75/1.5 mg kg(-1) and 50/2.0 mg kg(-1) (pilo dose/PTX dose). Six epileptic and six control animals were observed for 120-131 days for the occurrence of spontaneous recurrent seizures (SRS). Electroencephalographic, neuropathologic and behavioral analyses were subsequently performed. Following SE, the animals went through a latent period and, subsequently, towards a state of 'chronic' epilepsy, characterized by the emergence of SRS. Animals that received 150/0.5 mg kg(-1) presented a relatively short latent period, partial events as their most common initial seizure manifestations and a considerable subsequent progression towards generalization. the group injected with 75/7.5 mg kg(-1) presented an extensive period during which the majority of the animals exclusively developed partial seizures (50 days). Animals injected with 50/2.0 mg kg(-1) presented an average latent period of over 100 days. Only few animals within this group developed SRS. Our EEG, neuropathological and ictal behavioral findings, in conjunction with the fact that SE was required for the posterior development of SRS, suggest that our model parallels a human TLE condition. Even though diverse TLE models have been described, the pilo/PTX model has as a major feature the intriguing occurrence of disparities among these three groups in the chronic period, although no differences could be observed during SE induction. Future experiments conducted in this sense, might lead to important results in regard to the elucidation of mechanisms of epileptogenesis.
- ItemSomente MetadadadosStatus epilepticus induced by pilocarpine and picrotoxin(Elsevier B.V., 1997-07-01) Hamani, C.; Mello, LEAM; Universidade Federal de São Paulo (UNIFESP)Since its original description over 10 years ago, the pilocarpine model of status epilepticus (SE) has gained considerable attention. Much work has been done with the model in order to characterize the involvement of different brain structures in seizure genesis and spread. Electrophysiological studies of temporal lobe epileptic slices of both human and animal models, have failed to reveal hyperexcitability, unless blockade of GABAergic inhibition is performed. Thus, we have decided to evaluate potential contributions of picrotoxin, a GABA, channel blocker, on pilocarpine-induced SE. Animals injected with three specific dose combinations (pilocarpine dose/picrotoxin dose), 150/0.5, 75/1.5 and 50/2.0 mg/kg, evoked status epilepticus (SE) within 23, 31 and 27 min, respectively. Ictal events and EEG spikes were initially observed either in the amygdala or in the hippocampus, with a later spread to cerebral cortex. Neuropathological analysis, performed 5-7 days after SE, has shown a high degree of cell loss predominantly in the piriform cortex, amygdala, hippocampus, thalamus and substantia nigra. Mortality rates for 150/0.5, 75/1.5 and 50/2.0 mg/kg (pilocarpine dose/picrotoxin dose) were 53, 42 and 51%, respectively. Single injections of 150 mg/kg of pilocarpine or 3 mg/kg of picrotoxin did not evoke any form of sustained epileptic activity. Previous studies in which simultaneous injections of other GABA(A) antagonists (i.e. bicuculline) and pirocarpine were performed, did not show clear evidences of a synergistic action between these two systems. the present study reveals a proconvulsant role for picrotoxin when co-administered with subconvulsant doses of pilocarpine. Possible mechanisms that might account for the interactions between the cholinergic and GABAergic systems in regard to epileptogenesis are discussed. (C) 1997 Elsevier Science B.V.