Related Experiment Video
Updated: Feb 15, 2026

Recording and Modulation of Epileptiform Activity in Rodent Brain Slices Coupled to Microelectrode Arrays
Published on: May 15, 2018
BAD and KATP channels regulate neuron excitability and epileptiform activity
Juan Ramón Martínez-François1, María Carmen Fernández-Agüera2, Nidhi Nathwani1
1Department of Neurobiology, Harvard Medical School, Boston, United States.
Altering BAD (BCL-2 agonist of cell death) impacts brain metabolism and enhances seizure resistance. This protection is linked to ATP-sensitive potassium (KATP) channels, particularly in dentate granule neurons.
Area of Science:
- Neuroscience
- Cellular Metabolism
- Epilepsy Research
Background:
- Brain metabolism significantly impacts neuronal excitability.
- The protein BAD (BCL-2 agonist of cell death) plays a role in cellular metabolism.
- Genetic alterations in BAD are associated with altered brain metabolism and seizure resistance.
Purpose of the Study:
- To investigate the effect of BAD manipulation on KATP channel activity and neuronal excitability.
- To determine the role of neuronal KATP channels in the anticonvulsant effects of BAD.
- To elucidate the cell-autonomous function of BAD in regulating neuronal excitability.
Main Methods:
- Utilized acute brain slices for electrophysiological studies.
- Investigated BAD's effect on KATP channel activity and dentate granule neuron (DGN) excitability.
- Imaged calcium activity during picrotoxin-induced epileptiform activity in entorhinal-hippocampal slices.
Main Results:
- BAD manipulation directly affected DGN excitability in a cell-autonomous manner.
- BAD knockout reduced picrotoxin-induced epileptiform activity.
- The anticonvulsant effect of BAD knockout was abolished by KATP channel knockout or inhibition.
Conclusions:
- BAD influences neuronal excitability through cell-autonomous effects on KATP channels.
- Increased KATP channel activity downstream of BAD reinforces a 'dentate gate' function, conferring seizure protection.
- Targeted manipulation of BAD in DGNs is sufficient to confer an antiseizure effect in brain slices.
More Related Videos
10:19Induction of an Isoelectric Brain State to Investigate the Impact of Endogenous Synaptic Activity on Neuronal Excitability In Vivo
Published on: March 31, 2016
08:32External Excitation of Neurons Using Electric and Magnetic Fields in One- and Two-dimensional Cultures
Published on: May 7, 2017
Related Concept Videos
Antiepileptic Drugs: Potassium Channel Activators
Ezogabine has gained approval as an adjunctive treatment...
The Role of Ion Channels in Neuronal Computation
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....
Enteric Nervous System: Regulation of GI Motor Activity
During periods of fasting, the ENS initiates the migrating myoelectric complex, a...
GPCRs Regulate Adenylyl Cylase Activity
GTPases and their Regulation
Large G-proteins,...
Ion Channels
Ion channels are specialized integral membrane proteins on the plasma membrane that allow...