Related Experiment Video
Updated: Jul 19, 2026
10:36
Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons
Published on: November 6, 2017
Volume changes in neurons: hyperexcitability and neuronal death.
Herminia Pasantes-Morales1, Karina Tuz
1Department of Biophysics, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico.
Contributions to Nephrology
|October 27, 2006
Summary
Hyponatremia, or low sodium levels, can trigger seizures by affecting brain cell volume and excitability. Understanding these cell volume changes is key to preventing neuronal damage in conditions like epilepsy.
Area of Science:
- Neuroscience
- Cell Physiology
- Pathophysiology
Background:
- Hyponatremia is linked to increased seizure susceptibility.
- Hypotonicity in vitro increases neuronal hyperexcitability and epileptiform activity.
- Neuronal volume regulation is crucial for maintaining brain function.
Purpose of the Study:
- To explore the mechanisms by which hyponatremia affects neuronal excitability and cell volume.
- To elucidate the roles of ion channels and osmolytes in neuronal swelling and shrinkage.
- To understand the link between cell volume changes and neuronal death pathways.
Main Methods:
- In vitro electrophysiology to study neuronal excitability.
- Analysis of ion and osmolyte transport mechanisms.
- Investigation of cell volume regulation in response to osmotic stress.
Main Results:
- Hypotonicity increases excitatory postsynaptic potentials via synaptic and non-synaptic mechanisms.
- Neuronal swelling in necrosis involves Na+, Cl-, and water influx, exacerbated by excitotoxicity.
- Apoptotic neuronal death features apoptotic volume decrease, involving K+ and Cl- efflux through specific channels.
Conclusions:
- Cell volume regulation is a critical determinant of neuronal excitability and survival.
- Dysregulation of ion and osmolyte transport contributes to hyponatremia-induced seizures and neuronal death.
- Targeting ion channels and osmolytes may offer therapeutic strategies for hyponatremia-related neurological disorders.
Related Concept Videos
01:29Excitatory and Inhibitory Effects of Neurotransmitters
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 specific...
01:14Action Potential
Neurons communicate by firing action potentials—the electrochemical signal that is propagated along the axon. The signal results in the release of neurotransmitters at axon terminals, thereby transmitting information to the nervous system. An action potential is a specific "all-or-none" change in membrane potential that results in a rapid spike in voltage.
Membrane potential in neurons
Neurons typically have a resting membrane potential of about -70 millivolts (mV). When they receive...
Membrane potential in neurons
Neurons typically have a resting membrane potential of about -70 millivolts (mV). When they receive...
01:14Action Potential
Neurons communicate by firing action potentials—the electrochemical signal that is propagated along the axon. The signal results in the release of neurotransmitters at axon terminals, thereby transmitting information to the nervous system. An action potential is a specific "all-or-none" change in membrane potential that results in a rapid spike in voltage.
Membrane potential in neurons
Neurons typically have a resting membrane potential of about -70 millivolts (mV). When they receive...
Membrane potential in neurons
Neurons typically have a resting membrane potential of about -70 millivolts (mV). When they receive...
01:19The Role of Ion Channels in Neuronal Computation
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.
01:16Cellular Injury IV: Necrosis
Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
01:41Action Potentials
Overview