Related Experiment Video
Updated: Jun 28, 2025

05:01
Inducing Long-Term Plasticity of Intrinsic Neuronal Excitability in Neurons of the Dorsal Lateral Geniculate Nucleus
Published on: September 20, 2024
373
Axo-axonic synaptic input drives homeostatic plasticity by tuning the axon initial segment structurally and
Biorxiv : the Preprint Server for Biology
|April 25, 2024
Summary
Homeostatic plasticity in the brain relies on the axon initial segment (AIS). Specific GABAergic inputs from chandelier cells, but not basket cells, tune the AIS in cortical neurons, impacting neuronal excitability and social behavior.
Area of Science:
- Neuroscience
- Cellular Neuroscience
- Synaptic Plasticity
Background:
- Functional brain network stability is maintained by homeostatic plasticity, restoring equilibrium after perturbations.
- The axon initial segment (AIS) of projection neurons (PyNs) dynamically adjusts to control neuronal firing properties.
- The role of direct synaptic input to the AIS in homeostatic plasticity is not well understood.
Purpose of the Study:
- To investigate whether direct synaptic input to the AIS of cortical PyNs can induce homeostatic plasticity.
- To determine if specific types of GABAergic inputs differentially affect AIS plasticity.
Main Methods:
- Examined the effects of altered GABAergic synaptic input from chandelier cells (ChCs) and parvalbumin-positive basket cells on cortical PyNs.
- Assessed changes in AIS morphology, voltage-gated sodium channel expression, and neuronal excitability.
- Correlated AIS tuning timing with social behavior recovery in response to ChC synaptic transmission alterations.
Main Results:
- Changes in GABAergic input from ChCs, but not basket cells, were sufficient to induce AIS homeostatic tuning within 1-2 weeks.
- AIS tuning manifested as alterations in morphology, sodium channel expression, and PyN excitability.
- The timing of AIS tuning in prefrontal cortex PyNs coincided with the recovery of social behavior deficits caused by modified ChC synaptic transmission.
Conclusions:
- Homeostatic plasticity of the AIS in postsynaptic PyNs can be driven by specific GABAergic inputs, particularly from ChCs.
- This AIS tuning mechanism may counteract neuronal dysfunction arising from imbalanced ChC presynaptic input.
- AIS plasticity represents a critical homeostatic mechanism in response to network state changes.
Related Concept Videos
Neuroplasticity
338
Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.
338
The Role of Ion Channels in Neuronal Computation
3.2K
A postsynaptic neuron usually receives numerous impulses from several other presynaptic neurons. The axon hillock of the postsynaptic neuron integrates all these signals and determines the likelihood of firing an action potential.
Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron. However, multiple presynaptic inputs must often create EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential....
Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron. However, multiple presynaptic inputs must often create EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential....
3.2K
Integration of Synaptic Events
1.5K
Synaptic integration mainly includes the summation of graded potentials. Graded potentials, regardless of their type, cause subtle alterations in membrane voltage, resulting in either depolarization or hyperpolarization. These incremental changes, when combined or summed, can propel the neuron toward its threshold. Consider, for example, a membrane experiencing a +15 mV shift, causing it to depolarize from -70 mV to -55 mV. In this scenario, graded potentials govern the membrane's ability to...
1.5K
Neurons: The Axon
3.4K
Axons are long, cytoplasmic processes of nerve cells capable of propagating electrical impulses known as action potentials. The cytoplasm or axoplasm of an axon contains neurofibrils, neurotubules, small vesicles, lysosomes, mitochondria, and various enzymes, all encased within the axolemma, the plasma membrane of the axon.
The axon attaches to the cell body at a cone-shaped elevation called the axon hillock. The initial part of the axon, closest to the hillock, is known as the initial segment....
The axon attaches to the cell body at a cone-shaped elevation called the axon hillock. The initial part of the axon, closest to the hillock, is known as the initial segment....
3.4K
Long-term Potentiation
2.8K
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...
Hebbian LTP
LTP can occur when...
2.8K
Excitatory and Inhibitory Effects of Neurotransmitters
9.9K
When an action potential reaches the presynaptic axon terminal, it releases neurotransmitters from the neuron into the synaptic cleft at a chemical synapse. The released neurotransmitter can be excitatory or inhibitory. The critical criteria commonly used to determine whether a molecule is a neurotransmitter at a chemical synapse are the molecule's presence in the presynaptic neuron. Second, its release is in response to strong presynaptic depolarization. And lastly, the presence of...
9.9K

