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Title: Chronic nicotine attenuates behavioral and synaptic plasticity impairments in a Streptozotocin model of Alzheimer’s disease
Authors: Esteves, I. M.
Lopes-Aguiar, C.
Ruggiero, R. N.
Broggini, A. C. S.
Bueno-Junior, L. S.
Kandratavicius, L.
Monteiro, M. R.
Romcy-Pereira, R. N.
Leite, J. P.
Keywords: Alzheimer’s disease;streptozotocin;nicotine;recognition memory;synaptic plasticity;long-term potentiation
Issue Date: 2017
Portuguese Abstract: Brain glucose metabolism is altered in sporadic Alzheimer’s disease (sAD), whose pathologies are reproduced in rodents by intracerebroventricular (icv) infusion of streptozotocin (STZ) in subdiabetogenic doses. The icv- STZ model also culminates in central cholinergic dysfunctions, which in turn are known to underlie both the sAD cognitive decline, and synaptic plasticity impairments. Considering the cognitive-enhancing potential of chronic nicotine (Nic), we investigated whether it attenuates icv- STZ-induced impairments in recognition memory and synaptic plasticity in a cognition-relevant substrate: the hippocampal CA1-medial prefrontal cortex (mPFC) pathway. Rats treated with icv-STZ were submitted to a chronic Nic regime, and were evaluated for recognition memory. We then examined long-term potentiation (LTP), paired-pulse facilitation (PPF) under urethane anesthesia, and brains were also evaluated for hippocampus-mPFC cell density. We found that Nic treatment prevents icv-STZ-induced disruptions in recognition memory and LTP. STZ did not precipitate neuronal death, while Nic alone was associated with higher neuronal density in CA1 when compared to vehicle-injected animals. Through combining behavioral, neurophysiological, and neuropathological observations into the Nic-STZ interplay, our study reinforces that cholinergic treatments are of clinical importance against earlystage Alzheimer’s disease and mild cognitive impairments
ISSN: 0306-4522
Appears in Collections:ICe - Artigos publicados em periódicos

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