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Lecture

Synaptic Plasticity: Forms and Mechanisms

In course

NX-450: Computational neurosciences: biophysics

The course introduces students to a synthesis of modern neuroscience and state-of-the-art data management, modelling and computing technologies with a focus on the biophysical level. ...

Description

This lecture explores various forms of synaptic plasticity, including short-term and long-term enhancement and depression. It delves into the mechanisms behind synaptic plasticity, such as NMDAR and AMPAR involvement, and the importance of calcium in inducing and maintaining plastic changes. The lecture also discusses experimental protocols used to study plasticity, like high and low-frequency stimulations, and spike-timing-dependent plasticity. Different computational models, including rate-based and voltage-based models, are presented to explain synaptic plasticity phenomena. The lecture concludes by highlighting the significance of calcium-based models in understanding the complex dynamics of synaptic plasticity.

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Instructors (2)

Felix Schürmann

Felix Schürmann is co-director of the Blue Brain Project and involved in several research challenges of the European Human Brain Project. He studied physics at the University of Heidelberg, Germany, supported by the German National Academic Foundation. Later, as a Fulbright Scholar, he obtained his Master's degree (M.S.) in Physics from the State University of New York, Buffalo, USA, under the supervision of Richard Gonsalves. During these studies, he became curious about the role of different computing substrates and dedicated his master thesis to the simulation of quantum computing. He studied for his Ph.D. at the University of Heidelberg, Germany, under the supervision of Karlheinz Meier. For his thesis he co-designed an efficient implementation of a neural network in hardware.

Armando Romani

Official source

Ontological neighbourhood

Biology

Cell biology: Neurotransmission

Related concepts (32)

Synaptic plasticity

In neuroscience, synaptic plasticity is the ability of synapses to strengthen or weaken over time, in response to increases or decreases in their activity. Since memories are postulated to be represented by vastly interconnected neural circuits in the brain, synaptic plasticity is one of the important neurochemical foundations of learning and memory (see Hebbian theory). Plastic change often results from the alteration of the number of neurotransmitter receptors located on a synapse.

Spike-timing-dependent plasticity

Spike-timing-dependent plasticity (STDP) is a biological process that adjusts the strength of connections between neurons in the brain. The process adjusts the connection strengths based on the relative timing of a particular neuron's output and input action potentials (or spikes). The STDP process partially explains the activity-dependent development of nervous systems, especially with regard to long-term potentiation and long-term depression.

Long-term depression

In neurophysiology, long-term depression (LTD) is an activity-dependent reduction in the efficacy of neuronal synapses lasting hours or longer following a long patterned stimulus. LTD occurs in many areas of the CNS with varying mechanisms depending upon brain region and developmental progress. As the opposing process to long-term potentiation (LTP), LTD is one of several processes that serves to selectively weaken specific synapses in order to make constructive use of synaptic strengthening caused by LTP.

Neuroplasticity

Neuroplasticity, also known as neural plasticity, or brain plasticity, is the ability of neural networks in the brain to change through growth and reorganization. It is when the brain is rewired to function in some way that differs from how it previously functioned. These changes range from individual neuron pathways making new connections, to systematic adjustments like cortical remapping. Examples of neuroplasticity include circuit and network changes that result from learning a new ability, information acquisition, environmental influences, practice, and psychological stress.

AMPA receptor

The α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (also known as AMPA receptor, AMPAR, or quisqualate receptor) is an ionotropic transmembrane receptor for glutamate (iGluR) that mediates fast synaptic transmission in the central nervous system (CNS). It has been traditionally classified as a non-NMDA-type receptor, along with the kainate receptor. Its name is derived from its ability to be activated by the artificial glutamate analog AMPA.

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Understanding Synaptic Transmission

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Synaptic plasticity: mechanisms and functions MOOC: Cellular Mechanisms of Brain Function

Explores the cellular mechanisms of synaptic plasticity, including LTP, LTD, and STDP.

Introduction to synaptic plasticity MOOC: Simulating a hippocampus micro-circuit

Covers synaptic plasticity, types of synapses, Hebb's postulate, LTP, LTD, and network oscillations in the hippocampus.

Synaptic transmission: Structure and Mechanisms MOOC: Simulation Neurocience

Explores the structure and function of synapses, including neurotransmitter diversity and the role of AMPA and NMDA receptors.

Classification of Plasticity: Short-term vs. Long-term Changes MOOC: Neuronal Dynamics 2- Computational Neuroscience: Neuronal Dynamics of Cognition