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Inducing Long-Term Plasticity of Intrinsic Neuronal Excitability in Neurons of the Dorsal Lateral Geniculate Nucleus
Published on: September 20, 2024
Cholinergic induction of input-specific late-phase LTP via localized Ca2+ release in the visual cortex
Kwang-Hyun Cho1, Hyun-Jong Jang, Yang-Hyeok Jo
1Department of Physiology, College of Medicine, The Catholic University of Korea, Seoul 137-701, South Korea.
Summary
Cholinergic activation regulates synaptic plasticity by controlling calcium (Ca2+) release from internal stores. This mechanism dictates whether muscarinic long-term potentiation (LTPm) or long-term depression (LTDm) occurs, impacting learning and memory.
Area of Science:
- Neuroscience
- Cellular and Molecular Biology
- Neurophysiology
Background:
- Acetylcholine (ACh) is vital for learning, memory, and sensory processing, modulating synaptic plasticity like long-term potentiation (LTP) and long-term depression (LTD).
- Intracellular calcium ions (Ca2+) are key regulators of LTP/LTD, but the precise influence of ACh on Ca2+ dynamics remains unclear.
- Understanding ACh's role in Ca2+ signaling is crucial for elucidating the cellular mechanisms of learning and memory.
Purpose of the Study:
- To investigate the impact of acetylcholine on dendritic Ca2+ dynamics during synaptic stimulation.
- To determine the role of these Ca2+ dynamics in inducing muscarinic LTP (LTPm) and muscarinic LTD (LTDm) in rat visual cortex neurons.
- To explore the spatial and molecular requirements for ACh-mediated synaptic plasticity.
Main Methods:
- Electrophysiological recordings in layer 2/3 pyramidal neurons of the rat visual cortex.
- Synaptic stimulation and muscarinic receptor activation to evoke Ca2+ transients.
- Pharmacological manipulation using D(-)-2-amino-5-phosphopentanoic acid and heparin to block Ca2+ release and plasticity.
- Confocal microscopy to visualize localized Ca2+ dynamics.
Main Results:
- Muscarinic stimulation induced NMDA receptor-dependent Ca2+ transients and subsequent Ca2+ release from IP3-sensitive stores.
- This secondary Ca2+ release was localized and essential for inducing LTPm, while its absence led to LTDm.
- LTPm was protein synthesis-dependent and restricted to specific dendritic compartments, unlike LTDm.
- Blockade of Ca2+ release prevented LTPm induction.
Conclusions:
- Cholinergic activation precisely controls synaptic plasticity by modulating localized dendritic Ca2+ release.
- The presence or absence of IP3-dependent Ca2+ release determines whether LTPm or LTDm is induced, highlighting a critical switch mechanism.
- This study reveals a compartment-specific, ACh-driven pathway for late-phase LTP, crucial for cognitive functions.
Related Concept Videos
01:35Long-term Potentiation
Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
01:25Long-term Potentiation
Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Hebbian LTP
LTP can occur when presynaptic neurons...
Hebbian LTP
LTP can occur when presynaptic neurons...
01:24Vision
Vision is the result of light being detected and transduced into neural signals by the retina of the eye. This information is then further analyzed and interpreted by the brain. First, light enters the front of the eye and is focused by the cornea and lens onto the retina—a thin sheet of neural tissue lining the back of the eye. Because of refraction through the convex lens of the eye, images are projected onto the retina upside-down and reversed.