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Integration of Synaptic Events

Integration of Synaptic Events

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...

Action Potential: Phases of Stimulation

Action Potential: Phases of Stimulation

The action potential is a complex electrical event that occurs in excitable cells, such as neurons and muscle cells. It consists of several distinct phases, each with specific characteristics.
Resting Phase:
In this phase, the cell's membrane is at its resting potential, typically around -70 millivolts (mV) for neurons. Inside the cell, there is a higher concentration of potassium ions (K+) and a lower concentration of sodium ions (Na+). Voltage-gated sodium channels are closed, and...

Graded Potential

Graded Potential

Graded potentials are localized fluctuations in the cell membrane's electrical charge, commonly found in the dendrites of neurons. The magnitude of these potential changes depends on the strength of the initiating stimulus. In a membrane at its resting potential, a graded potential signifies a voltage shift either above -70 mV or below -70 mV.
Graded potentials fall into two categories: depolarizing and hyperpolarizing. Depolarizing graded potentials typically occur when sodium (Na+) or...

Propagation of Action Potentials

Propagation of Action Potentials

The propagation of an action potential refers to the process by which a nerve impulse, or "action potential," travels along a neuron.
Neurons (nerve cells) have a resting membrane potential, with a slightly negative charge inside compared to outside. This is maintained by ion channels, such as sodium (Na+) and potassium (K+) channels, which control the flow of ions. When a stimulus, like a touch or a signal from another neuron, triggers the neuron, sodium channels open, allowing sodium ions to...

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Related Experiment Video

Updated: Oct 29, 2025

Combining Imaging and Electrophysiology to Visualize and Record Spreading Depolarizations in Mice

Combining Imaging and Electrophysiology to Visualize and Record Spreading Depolarizations in Mice

Published on: October 4, 2024

Intracranial pressure spikes trigger spreading depolarizations.

Fumiaki Oka^1,2, Homa Sadeghian¹, Mohammad A Yaseen³

¹Neurovascular Research Laboratory, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02129, USA.

Brain : a Journal of Neurology

|July 10, 2021

Summary

Mild, brief intracranial pressure spikes trigger spreading depolarizations (SDs) in brain injury, worsening outcomes. Preventing these spikes may improve recovery by reducing SD occurrence.

Keywords:

cerebral infarction clinical experimental intracranial pressure peri-infarct depolarization

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Generation and On-Demand Initiation of Acute Ictal Activity in Rodent and Human Tissue

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Published on: January 19, 2019

Area of Science:

Neuroscience
Neurology
Critical Care Medicine

Background:

Spreading depolarizations (SDs) are common in brain injury and worsen outcomes.
Triggers for SDs are poorly understood but linked to impaired brain tissue oxygen supply-demand balance.
Intracranial pressure (ICP) elevations are frequent in injured brains.

Purpose of the Study:

To investigate if mild, brief ICP elevations can trigger SDs in ischemic stroke.
To elucidate the hemodynamic and ionic mechanisms underlying ICP-induced SDs.
To correlate ICP spikes with SDs in a clinical patient cohort.

Main Methods:

Mouse model of large hemispheric ischemic stroke.
Laser speckle flowmetry and two-photon pO2 microscopy to assess cerebral perfusion and oxygenation.
Extracellular potassium measurements.
Retrospective analysis of patients with aneurysmal subarachnoid hemorrhage.

Main Results:

Mild ICP elevations (20-30 mmHg) for brief durations (30s-3min) significantly increased SD occurrence (4-fold).
Sustained ICP elevation did not increase SD rate, indicating abrupt change is key.
ICP spikes caused reduced perfusion, increased oxygen extraction, and elevated extracellular potassium in ischemic penumbra.
ICP spikes temporally correlated with SD clusters in stroke patients.

Conclusions:

Even mild and brief ICP spikes can trigger spreading depolarizations in ischemic brain tissue.
These ICP spikes worsen the supply-demand mismatch, leading to ionic shifts that promote SDs.
Preventing ICP spikes may be a therapeutic strategy to reduce SDs and improve brain injury outcomes.