Neuromodulatory control of localized dendritic spiking in critical period cortex
| Autor: | Joshua T. Trachtenberg, Courtney E. Yaeger, Dario L. Ringach |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Male genetic structures Vision Action Potentials Mice 0302 clinical medicine Cortex (anatomy) Neural Pathways Visual Cortex Pediatric Basal forebrain Vision Binocular Multidisciplinary Neuronal Plasticity Pyramidal Cells medicine.anatomical_structure Parvalbumins Critical Period Female Pyramidal cell Somatostatin General Science & Technology 1.1 Normal biological development and functioning Sensory system Biology Article 03 medical and health sciences Underpinning research Interneurons medicine Biological neural network Animals Calcium Signaling Eye Disease and Disorders of Vision Ocular Physiological Phenomena Critical Period Psychological Neurosciences Neural Inhibition Dendrites Binocular Acetylcholine Optogenetics 030104 developmental biology Visual cortex Receptive field Cholinergic Psychological Neuroscience 030217 neurology & neurosurgery |
| Zdroj: | Nature Nature, vol 567, iss 7746 |
| ISSN: | 1476-4687 0028-0836 |
| Popis: | Sensory experience in early postnatal life, during so-called critical periods, restructures neural circuitry to enhance information processing. It is unclear why the cortex is susceptible to sensory instruction in early life and why this susceptibility wanes with age. Here, we define a developmentally-restricted engagement of inhibitory circuitry that shapes localized dendritic activity and is needed for vision to drive the emergence of binocular visual responses in mouse primary visual cortex. We find that at the peak of the critical period for binocular plasticity, acetylcholine released from the basal forebrain during periods of heightened arousal directly excites somatostatin-expressing (SST) interneurons. Their inhibition of pyramidal cell dendrites and of fast-spiking, parvalbumin-expressing (PV) interneurons enhances branch-specific dendritic responses and somatic spike rates within pyramidal cells. By adulthood, this cholinergic sensitivity is lost, and compartmentalized dendritic responses are absent but can be re-instated by optogenetic activation of SST cells. Conversely, suppressing SST cell activity during the critical period prevents the normal development of binocular receptive fields by impairing the maturation of ipsilateral eye inputs. This transient cholinergic modulation of SST cells, therefore, appears to orchestrate two features of neural plasticity – somatic disinhibition and compartmentalized dendritic spiking. Loss of this modulation may contribute to critical period closure. |
| Databáze: | OpenAIRE |
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