• I M Esteves, C Lopes-Aguiar, M T Rossignoli, R N Ruggiero, A C S Broggini, L S Bueno-Junior, L Kandratavicius, M R Monteiro, R N Romcy-Pereira, and J P Leite.
• Department of Neuroscience and Behavioral Sciences, Ribeirão Preto Medical School, University of São Paulo (USP), Ribeirão Preto, Brazil. Electronic address: ime_br@yahoo.com.
• Neuroscience. 2017 Jun 14; 353: 87-97.

AbstractBrain 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 early-stage Alzheimer's disease and mild cognitive impairments.Copyright © 2017 IBRO. Published by Elsevier Ltd. All rights reserved.

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