ausblenden:
Schlagwörter:
Alzheimer Disease/chemically induced/*physiopathology/*psychology
Animals
CA1 Region, Hippocampal/*drug effects/physiology
Cell Count
Disease Models, Animal
Locomotion/drug effects
Long-Term Potentiation/*drug effects
Male
Neurons/drug effects
Nicotine/*administration & dosage
Prefrontal Cortex/*drug effects/physiology
Rats, Wistar
Recognition (Psychology)/*drug effects/physiology
Streptozocin
Synaptic Potentials/drug effects
*Alzheimer's disease
*long-term potentiation
*nicotine
*recognition memory
*streptozotocin
*synaptic plasticity
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.
