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Partial hippocampal kindling increases GABAB receptor-mediated postsynaptic currents in CA1 pyramidal cells
1Department of Physiology and Pharmacology, University of Western Ontario, London, Ont, Canada N6A 5C1.
Epilepsy Research
|January 7, 2004
Summary
Partial hippocampal kindling enhances GABAB receptor-mediated inhibitory postsynaptic currents (GABAB-IPSCs) in CA1 neurons. This suggests kindling alters inhibitory neurotransmission through multiple presynaptic mechanisms.
Area of Science:
- Neuroscience
- Neurophysiology
Background:
- Previous studies indicated partial hippocampal kindling reduces presynaptic GABAB receptor efficacy.
- GABAB receptors modulate neurotransmitter release at GABAergic and glutamatergic terminals.
Purpose of the Study:
- To investigate the effect of partial hippocampal kindling on GABAB receptor-mediated inhibitory postsynaptic currents (GABAB-IPSCs) in CA1 pyramidal neurons.
- To elucidate the presynaptic mechanisms underlying changes in GABABergic inhibition following kindling.
Main Methods:
- Whole-cell recordings were performed in hippocampal slices from kindled and control Long-Evans rats.
- GABAB-IPSCs were measured using specific stimulation protocols and pharmacological agents.
- GABA uptake blockade and GABAB receptor activation were used to assess presynaptic function.
Main Results:
- Peak GABAB-IPSCs were significantly larger in kindled rats compared to controls.
- Outward currents induced by nipecotic acid (GABA uptake blocker) were greater in kindled rats.
- Baclofen (GABAB receptor agonist)-induced currents showed no significant difference between groups.
Conclusions:
- Partial hippocampal kindling increases GABAB-IPSCs in CA1 pyramidal cells.
- These increases are mediated by multiple presynaptic mechanisms, including altered GABA uptake.
- Findings suggest a complex modulation of GABABergic inhibition following kindling.