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

Highlights • STZ-icv induced dysfunction in CA1-mPFC plasticity and recognition memory. • Nicotine was effective to prevent prefrontal LTP and memory deficits induced by. • STZ-icv. • Modulation of nicotinic receptor might be an alternative approach for AD treatment.

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Bibliographische Detailangaben
Veröffentlicht in:	Neuroscience 2017-06, Vol.353, p.87-97
Hauptverfasser:	IM, Esteves, C, Lopes-Aguiar, MT, Rossignoli, RN, Ruggiero, ACS, Broggini, LS, Bueno-Junior, L, Kandratavicius, MR, Monteiro, RN, Romcy-Pereira, JP, Leite
Format:	Artikel
Sprache:	eng
Schlagworte:	Alzheimer Disease - chemically induced Alzheimer Disease - physiopathology Alzheimer Disease - psychology Alzheimer’s disease Animals CA1 Region, Hippocampal - drug effects CA1 Region, Hippocampal - physiology Cell Count Disease Models, Animal Locomotion - drug effects long-term potentiation Long-Term Potentiation - drug effects Male Neurology Neurons - drug effects nicotine Nicotine - administration & dosage Prefrontal Cortex - drug effects Prefrontal Cortex - physiology Rats, Wistar Recognition (Psychology) - drug effects Recognition (Psychology) - physiology recognition memory Streptozocin streptozotocin synaptic plasticity Synaptic Potentials - drug effects
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Beschreibung
Zusammenfassung:	Highlights • STZ-icv induced dysfunction in CA1-mPFC plasticity and recognition memory. • Nicotine was effective to prevent prefrontal LTP and memory deficits induced by. • STZ-icv. • Modulation of nicotinic receptor might be an alternative approach for AD treatment.
ISSN:	0306-4522 1873-7544
DOI:	10.1016/j.neuroscience.2017.04.011