The Cellular Basis of GABAB-Mediated Interhemispheric Inhibition

The Cellular Basis of GABAB-Mediated Interhemispheric Inhibition

Interhemispheric inhibition is thought to mediate cortical rivalry between the two hemispheres through callosal input. The long-lasting form of this inhibition is believed to operate via γ-aminobutyric acid type B (GABA B ) receptors, but the process is poorly understood at the cellular level. We fo...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 2012-02, Vol.335 (6071), p.989-993
Main Authors: Palmer, Lucy M., Schulz, Jan M., Murphy, Sean C., Ledergerber, Debora, Murayama, Masanori, Larkum, Matthew E.
Format: Article
Language:eng
Subjects:
Behavioral neuroscience
Biological and medical sciences
Cellular biology
Dendrites
Electric potential
Experiment design
Fundamental and applied biological sciences. Psychology
Hemispheres
Histograms
Interneurons
Neurology
Neurons
Neurotransmitters
Receptors
Rodents
Somesthesis and somesthetic pathways (proprioception, exteroception, nociception)
interoception
electrolocation. Sensory receptors
Vertebrates: nervous system and sense organs
Waveforms
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Summary:Interhemispheric inhibition is thought to mediate cortical rivalry between the two hemispheres through callosal input. The long-lasting form of this inhibition is believed to operate via γ-aminobutyric acid type B (GABA B ) receptors, but the process is poorly understood at the cellular level. We found that the firing of layer 5 pyramidal neurons in rat somatosensory cortex due to contralateral sensory stimulation was inhibited for hundreds of milliseconds when paired with ipsilateral stimulation. The inhibition acted directly on apical dendrites via layer 1 interneurons but was silent in the absence of pyramidal cell firing, relying on metabotropic inhibition of active dendritic currents recruited during neuronal activity. The results not only reveal the microcircuitry underlying interhemispheric inhibition but also demonstrate the importance of active dendritic properties for cortical output.
ISSN:0036-8075
1095-9203