Timing and location of nicotinic activity enhances or depresses hippocampal synaptic plasticity.

摘要: 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 acetylcholine receptors. Properly timed activity at pyramidal neurons boosted induction long-term potentiation presynaptic postsynaptic pathways. On other hand, interneurons inhibited nearby thereby prevented or diminished potentiation. The modulation was dependent location timing activity. Loss these contribute to cognitive deficits experienced during Alzheimer's diseases, which associated with a loss cholinergic projections decrease number