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

Esteves, I.M.; Lopes-Aquiar, C.; Rossignoli, M.; Ruggiero, R.N.; Broggini, A.C.S.; Bueno-Junior, L.S.; Kandratavicius, L.; Monteiro, M.R.; Romcy-Pereira, R.N.; Leite, J.P.

doi:10.1016/j.neuroscience.2017.04.011

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

Esteves, I., Lopes-Aquiar, C., Rossignoli, M., Ruggiero, R., Broggini, A., Bueno-Junior, L., et al. (2017). Chronic nicotine attenuates behavioral and synaptic plasticity impairments in a streptozotocin model of Alzheimer's disease. Neuroscience. doi:10.1016/j.neuroscience.2017.04.011.

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Datensatz-Permalink: https://hdl.handle.net/11858/00-001M-0000-002E-7FAE-0 Versions-Permalink: https://hdl.handle.net/11858/00-001M-0000-002E-7FAF-E

Genre: Zeitschriftenartikel

Alternativer Titel : Neuroscience

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Urheber:
Esteves, I.M., Autor
Lopes-Aquiar, C., Autor
Rossignoli, M., Autor
Ruggiero, R.N., Autor
Broggini, A.C.S.¹, Autor
Bueno-Junior, L.S., Autor
Kandratavicius, L., Autor
Monteiro, M.R., Autor
Romcy-Pereira, R.N., Autor
Leite, J.P., Autor

Affiliations:
1Ernst Strüngmann Institute (ESI) for Neuroscience in Cooperation with Max Planck Society, Max Planck Society, Deutschordenstr. 46, 60528 Frankfurt, DE, ou_2074314

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Zusammenfassung: 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.