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Neuroscience. 2017 Jun 14;353:87-97. doi: 10.1016/j.neuroscience.2017.04.011. Epub 2017 Apr 19.

Chronic nicotine attenuates behavioral and synaptic plasticity impairments in a streptozotocin model of Alzheimer's disease.

Author information

1
Department of Neuroscience and Behavioral Sciences, Ribeirão Preto Medical School, University of São Paulo (USP), Ribeirão Preto, Brazil. Electronic address: ime_br@yahoo.com.
2
Department of Neuroscience and Behavioral Sciences, Ribeirão Preto Medical School, University of São Paulo (USP), Ribeirão Preto, Brazil.
3
Department of Neuroscience and Behavioral Sciences, Ribeirão Preto Medical School, University of São Paulo (USP), Ribeirão Preto, Brazil; Ernst Strüngmann Institut (ESI) for Neuroscience in Cooperation with Max Planck Society, Frankfurt 60528, Germany.
4
Brain Institute, Federal University of Rio Grande do Norte (UFRN), Natal, Brazil.

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 early-stage Alzheimer's disease and mild cognitive impairments.

KEYWORDS:

Alzheimer’s disease; long-term potentiation; nicotine; recognition memory; streptozotocin; synaptic plasticity

[Indexed for MEDLINE]

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