Related Experiment Video
Updated: Sep 30, 2026

GABA-activated Single-channel and Tonic Currents in Rat Brain Slices
Published on: July 17, 2011
Synaptic Activation of GABAA Receptors Causes a Depolarizing Potential Under Physiological Conditions in Rat
1Montreal Neurological Institute and Department of Neurology and Neurosurgery, McGill University, 3801 University Street, Montreal, QC, Canada H3A 2B4.
Abstract:
Intracellular recordings with K-acetate-filled microelectrodes were performed in slices of the adult rat hippocampus maintained in vitro at 35 - 36 degrees C to analyse the potentials associated with the orthodromic inhibitory sequence generated by CA1 pyramidal cells. In 43 of 72 cells, stimuli that were delivered in the stratum radiatum induced (i) an initial excitatory postsynaptic potential (EPSP), (ii) an early, hyperpolarizing inhibitory postsynaptic potential (IPSP) (peak latency from the stimulus artefact 20 ms), (iii) an intermediate depolarizing component (peak latency=60 - 120 ms; duration=60 - 150 ms, and (iv) a late, long-lasting hyperpolarizing IPSP (peak latency=120 - 160 ms, duration >400 ms). In the remaining cells the orthodromic inhibitory response lacked the intermediate depolarization. The depolarizing component was selectively blocked by local applications of bicuculline or picrotoxin on the apical dendrites of pyramidal cells. This pharmacological procedure induced an increase in the amplitude of the EPSP that was capable of triggering 2 - 3 action potentials, but no reduction of the recurrent IPSP which is caused by GABAA receptors located close to the soma. The amplitude and duration of the depolarizing component was enhanced by lowering the temperature in the tissue chamber to 29 - 31 degrees C or by application of the GABA uptake blocker nipecotic acid, further indicating that the depolarizing component represented an active phenomenon mediated through GABA. Application of the Cl- pump blocker furosemide reduced and eventually blocked the early IPSP and the depolarizing component. These data demonstrate that under physiological conditions rat hippocampal pyramidal cells generate a depolarization that is presumably caused by an outwardly directed Cl- movement due to the activation of GABAA receptors located on the apical dendrites. This novel mechanism might modulate hippocampal excitability in both physiological and pathophysiological conditions.
More Related Videos
07:16Methods for the Discovery of Novel Compounds Modulating a Gamma-Aminobutyric Acid Receptor Type A Neurotransmission
Published on: August 16, 2018
07:51Inhibitory Synapse Formation in a Co-culture Model Incorporating GABAergic Medium Spiny Neurons and HEK293 Cells Stably Expressing GABAA Receptors
Published on: November 14, 2014
Related Concept Videos
Excitatory and Inhibitory Effects of Neurotransmitters
Integration of Synaptic Events
Ligand-Gated Ion Channel Receptor: Gating Mechanism
Antiepileptic Drugs: GABAergic Pathway Potentiators
The key GABA pathway potentiators used in epilepsy management are as follows.
Benzodiazepines are a well-known class of drugs used for their...
G-Protein Gated Ion Channels
Sensory organs,...
Chemical Synapses
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...