Chronic nicotine attenuates behavioral and synaptic plasticity impairments in a Streptozotocin model of Alzheimer’s disease
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 tur...
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Principais autores: | , , , , , , , , |
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Formato: | article |
Idioma: | eng |
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Endereço do item: | https://repositorio.ufrn.br/jspui/handle/123456789/23358 |
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Resumo: | 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 |
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