The afterhyperpolarizing potential following a train of action potentials is suppressed in an acute epilepsy model in the rat Cornu Ammonis 1 area

Abstract In hippocampal Cornu Ammonis 1 (CA1) neurons, a prolonged depolarization evokes a train of action potentials followed by a prominent afterhyperpolarizing potential (AHP), which critically dampens neuronal excitability. Because it is not known whether epileptiform activity alters the AHP and...

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Bibliographic Details
Published in:Neuroscience 2012-01, Vol.201, p.288-296
Main Authors: Kernig, K, Kirschstein, T, Würdemann, T, Rohde, M, Köhling, R
Format: Article
Language:English
Subjects:
2-Amino-5-phosphonovalerate - pharmacology
6-Cyano-7-nitroquinoxaline-2,3-dione - pharmacology
Action Potentials - physiology
afterhyperpolarization
AMPA
Animals
Biological and medical sciences
CA1 Region, Hippocampal - pathology
CNQX
d-AP5
Disease Models, Animal
Drug Interactions
Electric Stimulation
Enzyme Inhibitors - pharmacology
Epilepsy - chemically induced
Epilepsy - pathology
Excitatory Amino Acid Antagonists - pharmacology
Fundamental and applied biological sciences. Psychology
GABA Antagonists - adverse effects
Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy
In Vitro Techniques
Isoquinolines - pharmacology
Male
Medical sciences
Nervous system (semeiology, syndromes)
Neural Inhibition - drug effects
Neural Inhibition - physiology
Neurology
Neurons - physiology
NMDA
Pyridazines - adverse effects
Rats
Rats, Wistar
SR95531
Statistics, Nonparametric
Sulfonamides - pharmacology
Time Factors
Vertebrates: nervous system and sense organs
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Summary:Abstract In hippocampal Cornu Ammonis 1 (CA1) neurons, a prolonged depolarization evokes a train of action potentials followed by a prominent afterhyperpolarizing potential (AHP), which critically dampens neuronal excitability. Because it is not known whether epileptiform activity alters the AHP and whether any alteration of the AHP is independent of inhibition, we acutely induced epileptiform activity by bath application of the GABAA receptor blocker gabazine (5 μM) in the rat hippocampal slice preparation and studied its impact on the AHP using intracellular recordings. Following 10 min of gabazine wash-in, slices started to develop spontaneous epileptiform discharges. This disinhibition was accompanied by a significant shift of the resting membrane potential of CA1 neurons to more depolarized values. Prolonged depolarizations (600 ms) elicited a train of action potentials, the number of which was not different between baseline and gabazine treatment. However, the AHP following the train of action potentials was significantly reduced after 20 min of gabazine treatment. When the induction of epileptiform activity was prevented by co-application of 6-cyano-7-nitroquinoxaline-2,3-dione disodium (CNQX, 10 μM) and d -(−)-2-amino-5-phosphonopentanoic acid ( d -AP5, 50 μM) to block α-amino-3-hydroxy-5-methylisoxazolepropionate (AMPA) and N -methyl- d -aspartate (NMDA) receptors, respectively, the AHP was preserved despite of GABAA receptor inhibition suggesting that the epileptiform activity was required to suppress the AHP. Moreover, the AHP was also preserved when the slices were treated with the protein kinase blockers H-9 (100 μM) and H-89 (1 μM). These results demonstrate that the AHP following a train of action potentials is rapidly suppressed by acutely induced epileptiform activity due to a phosphorylation process—presumably involving protein kinase A.
ISSN:0306-4522
1873-7544
DOI:10.1016/j.neuroscience.2011.11.008