Journal
NEURON
Volume 31, Issue 1, Pages 131-141Publisher
CELL PRESS
DOI: 10.1016/S0896-6273(01)00332-4
Keywords
-
Categories
Funding
- NIDA NIH HHS [DA12661, DA09411] Funding Source: Medline
- NINDS NIH HHS [NS21229] Funding Source: Medline
Ask authors/readers for more resources
This study reveals mechanisms in the mouse hippocampus that may underlie nicotinic influences on attention, memory, and cognition. Induction of synaptic plasticity, arising via generally accepted mechanisms, is modulated by nicotinic acetylcholine receptors. Properly timed nicotinic activity at pyramidal neurons boosted the induction of long-term potentiation via presynaptic and postsynaptic pathways. On the other hand, nicotinic activity on interneurons inhibited nearby pyramidal neurons and thereby prevented or diminished the induction of synaptic potentiation. The synaptic modulation was dependent on the location and timing of the nicotinic activity. Loss of these synaptic mechanisms may contribute to the cognitive deficits experienced during Alzheimer's diseases, which is associated with a loss of cholinergic projections and with a decrease in the number of nicotinic receptors.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available