Pérez-Garci, Enrique; Gassmann, Martin; Bettler, Bernhard; Larkum, Matthew E (2006). The GABAB1b isoform mediates long-lasting inhibition of dendritic Ca2+ spikes in layer 5 somatosensory pyramidal neurons. Neuron, 50(4), pp. 603-16. Cambridge, Mass.: Cell Press 10.1016/j.neuron.2006.04.019
Full text not available from this repository.The apical tuft of layer 5 pyramidal neurons is innervated by a large number of inhibitory inputs with unknown functions. Here, we studied the functional consequences and underlying molecular mechanisms of apical inhibition on dendritic spike activity. Extracellular stimulation of layer 1, during blockade of glutamatergic transmission, inhibited the dendritic Ca2+ spike for up to 400 ms. Activation of metabotropic GABAB receptors was responsible for a gradual and long-lasting inhibitory effect, whereas GABAA receptors mediated a short-lasting (approximately 150 ms) inhibition. Our results suggest that the mechanism underlying the GABAB inhibition of Ca2+ spikes involves direct blockade of dendritic Ca2+ channels. By using knockout mice for the two predominant GABAB1 isoforms, GABAB1a and GABAB1b, we showed that postsynaptic inhibition of Ca2+ spikes is mediated by GABAB1b, whereas presynaptic inhibition of GABA release is mediated by GABAB1a. We conclude that the molecular subtypes of GABAB receptors play strategically different physiological roles in neocortical neurons.
Item Type: |
Journal Article (Original Article) |
|---|---|
Division/Institute: |
04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Physiology |
UniBE Contributor: |
Larkum, Matthew |
ISSN: |
0896-6273 |
ISBN: |
16701210 |
Publisher: |
Cell Press |
Language: |
English |
Submitter: |
Factscience Import |
Date Deposited: |
04 Oct 2013 14:45 |
Last Modified: |
05 Dec 2022 14:14 |
Publisher DOI: |
10.1016/j.neuron.2006.04.019 |
PubMed ID: |
16701210 |
Web of Science ID: |
000237875200011 |
URI: |
https://boris.unibe.ch/id/eprint/18510 (FactScience: 682) |
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