Pathological mechanism

Data

Name Nicotine enhances depressive actions of Abeta on LTP in rat CA1 region in vivo

Description

Hypothesis Nicotinic Receptor Hypothesis Show Other

Extracelular pathological element beta Amyloid Show Other

Intracelular pathological element

Pathological action Inhibits Show Other

Process

Process action

Transmitter(s)

Receptor(s) Nicotinic Show Other Cholinergic Receptors Show Other

Channel(s)

Pharmacological Agent

Pharmacological Action

Brain region Hippocampus CA1 Show Other

Neuron

Cell model Oocyte Show Other

Cellular compartment

PubMed ID 12611941

Citation Nicotine enhances the depressive actions of A beta 1-40 on long-term potentiation in the rat hippocampal CA1 region in vivo. Show Other

AlzWeb

Notes Hippocampal long-term potentiation (LTP) is a form of synaptic plasticity used as a cellular model of memory. Beta amyloid (A beta) is involved in Alzheimer's disease (AD), a neurode-generative disorder leading to cognitive deficits. Nicotine is also claimed to act as a cognitive enhancer. A beta is known to bind with high affinity to the alpha 7-nicotinic acetylcholine receptor (nAChR). ... (Experiments) demonstrate that nicotine enhances the deficit in LTP produced by A beta 1-40. This then suggests that nicotine may exacerbate the depressive actions of A beta on synaptic plasticity in AD. (Freir DB, Herron CE 2003)

Pathology Alzheimer Show Other

Stage Early Show Other

Question

Claim