GABA(B) receptor modulation of feedforward inhibition through hippocampal neurogliaform cells
| Autor: | Christopher J. Price, Marco Capogna, Ricardo Scott, Dmitri A. Rusakov |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2008 |
| Předmět: |
Baclofen
Action Potentials Action Potentials/drug effects Hippocampus Synaptic Transmission GABA Antagonists Propanolamines Neural Pathways gamma-Aminobutyric Acid/metabolism gamma-Aminobutyric Acid Propanolamines/pharmacology GABAA receptor General Neuroscience Pyramidal Cells medicine.anatomical_structure GABA Antagonists/pharmacology Receptors GABA-A/drug effects Receptors GABA-B/drug effects Calcium Signaling/drug effects Excitatory postsynaptic potential Hippocampus/cytology Inhibitory Postsynaptic Potentials/drug effects Pyramidal cell Neuroglia medicine.drug Phosphinic Acids/pharmacology Calcium/metabolism Interneuron Synaptic Transmission/drug effects GABAB receptor Neurotransmission Biology Baclofen/pharmacology Neural Inhibition/drug effects gamma-Aminobutyric acid Article Organ Culture Techniques Interneurons medicine Animals Calcium Signaling Pyramidal Cells/drug effects GABA Agonists GABA Agonists/pharmacology Interneurons/cytology Neural Inhibition Neuroglia/drug effects GABA receptor antagonist Receptors GABA-A Phosphinic Acids Rats Inhibitory Postsynaptic Potentials Receptors GABA-B nervous system Neural Pathways/cytology Calcium Neuroscience |
| Zdroj: | Price, C J, Scott, R, Rusakov, D A & Capogna, M 2008, ' GABA(B) receptor modulation of feedforward inhibition through hippocampal neurogliaform cells ', The Journal of neuroscience : the official journal of the Society for Neuroscience, vol. 28, no. 27, pp. 6974-82 . https://doi.org/10.1523/JNEUROSCI.4673-07.2008 |
| ISSN: | 1529-2401 0270-6474 |
| DOI: | 10.1523/JNEUROSCI.4673-07.2008 |
| Popis: | Feedforward inhibition of neurons is a fundamental component of information flow control in the brain. We studied the roles played by neurogliaform cells (NGFCs) of stratum lacunosum moleculare of the hippocampus in providing feedforward inhibition to CA1 pyramidal cells. We recorded from synaptically coupled pairs of anatomically identified NGFCs and CA1 pyramidal cells and found that, strikingly, a single presynaptic action potential evoked a biphasic unitary IPSC (uIPSC), consisting of two distinct components mediated by GABA A and GABA B receptors. A GABA B receptor-mediated unitary response has not previously been observed in hippocampal excitatory neurons. The decay of the GABA A receptor-mediated response was slow (time constant = 50 ms), and was tightly regulated by presynaptic GABA B receptors. Surprisingly, the GABA B receptor ligands baclofen and (2 S )-3-{[(1 S )-1-(3,4-dichlorophenyl)ethyl]amino-2-hydroxypropyl}(phenylmethyl)phosphinic acid (CGP55845), while affecting the NGFC-mediated uIPSCs, had no effect on action potential-evoked presynaptic Ca 2+ signals monitored in individual axonal boutons of NGFCs with two-photon microscopy. In contrast, baclofen clearly depressed presynaptic Ca 2+ transients in non-NGF interneurons. Changes in extracellular Ca 2+ concentration that mimicked the effects of baclofen or CGP55845 on uIPSCs significantly altered presynaptic Ca 2+ transients. Electrophysiological data suggest that GABA B receptors expressed by NGFCs contribute to the dynamic control of the excitatory input to CA1 pyramidal neurons from the temporoammonic path. The NGFC–CA1 pyramidal cell connection therefore provides a unique and subtle mechanism to shape the integration time domain for signals arriving via a major excitatory input to CA1 pyramidal cells. |
| Databáze: | OpenAIRE |
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