For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
13
views
88
references
 Top references
cited by
1
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
1 collections
    0
    shares
      0
      similar
       All similar

          The flagship journal of the Society for Endocrinology. Learn more

      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Thyroid hormone as a temporal switch in mouse development

      review-article
      Author(s): 1 , 1 ,
      Publication date (Electronic):
      Journal: European Thyroid Journal
      Publisher: Bioscientifica Ltd
      Keywords: thyroid hormone, mouse, postnatal development, metamorphosis

      Read this article at

      ScienceOpenPublisherPMC
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Thyroid hormones are known to trigger metamorphosis in an amphibian. This review discusses the hypothesis according to which they act in a similar manner to synchronize the post-natal development of mice, using brain, brown adipose tissue, and heart as examples.

          Related collections

          Most cited references88

          • Record: found
          • Abstract: found
          • Article: not found

          Parvalbumin neurons and gamma rhythms enhance cortical circuit performance.

          Vikaas Sohal, Feng Zhang, Ofer Yizhar … (2009)
          Synchronized oscillations and inhibitory interneurons have important and interconnected roles within cortical microcircuits. In particular, interneurons defined by the fast-spiking phenotype and expression of the calcium-binding protein parvalbumin have been suggested to be involved in gamma (30-80 Hz) oscillations, which are hypothesized to enhance information processing. However, because parvalbumin interneurons cannot be selectively controlled, definitive tests of their functional significance in gamma oscillations, and quantitative assessment of the impact of parvalbumin interneurons and gamma oscillations on cortical circuits, have been lacking despite potentially enormous significance (for example, abnormalities in parvalbumin interneurons may underlie altered gamma-frequency synchronization and cognition in schizophrenia and autism). Here we use a panel of optogenetic technologies in mice to selectively modulate multiple distinct circuit elements in neocortex, alone or in combination. We find that inhibiting parvalbumin interneurons suppresses gamma oscillations in vivo, whereas driving these interneurons (even by means of non-rhythmic principal cell activity) is sufficient to generate emergent gamma-frequency rhythmicity. Moreover, gamma-frequency modulation of excitatory input in turn was found to enhance signal transmission in neocortex by reducing circuit noise and amplifying circuit signals, including inputs to parvalbumin interneurons. As demonstrated here, optogenetics opens the door to a new kind of informational analysis of brain function, permitting quantitative delineation of the functional significance of individual elements in the emergent operation and function of intact neural circuitry.
          Article 0 comments Cited 427 times – based on 0 reviews     Review now
            • Record: found
            • Abstract: found
            • Article: not found

            Driving fast-spiking cells induces gamma rhythm and controls sensory responses.

            Jessica A Cardin, Marie Carlén, Konstantinos Meletis … (2009)
            Cortical gamma oscillations (20-80 Hz) predict increases in focused attention, and failure in gamma regulation is a hallmark of neurological and psychiatric disease. Current theory predicts that gamma oscillations are generated by synchronous activity of fast-spiking inhibitory interneurons, with the resulting rhythmic inhibition producing neural ensemble synchrony by generating a narrow window for effective excitation. We causally tested these hypotheses in barrel cortex in vivo by targeting optogenetic manipulation selectively to fast-spiking interneurons. Here we show that light-driven activation of fast-spiking interneurons at varied frequencies (8-200 Hz) selectively amplifies gamma oscillations. In contrast, pyramidal neuron activation amplifies only lower frequency oscillations, a cell-type-specific double dissociation. We found that the timing of a sensory input relative to a gamma cycle determined the amplitude and precision of evoked responses. Our data directly support the fast-spiking-gamma hypothesis and provide the first causal evidence that distinct network activity states can be induced in vivo by cell-type-specific activation.
            Article 0 comments Cited 425 times – based on 0 reviews     Review now
              • Record: found
              • Abstract: found
              • Article: not found

              Critical period plasticity in local cortical circuits.

              Takao Hensch (2005)
              Neuronal circuits in the brain are shaped by experience during 'critical periods' in early postnatal life. In the primary visual cortex, this activity-dependent development is triggered by the functional maturation of local inhibitory connections and driven by a specific, late-developing subset of interneurons. Ultimately, the structural consolidation of competing sensory inputs is mediated by a proteolytic reorganization of the extracellular matrix that occurs only during the critical period. The reactivation of this process, and subsequent recovery of function in conditions such as amblyopia, can now be studied with realistic circuit models that might generalize across systems.
              Article 0 comments Cited 343 times – based on 0 reviews     Review now
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Eur Thyroid J
                Journal ID (iso-abbrev): Eur Thyroid J
                Journal ID (publisher-id): ETJ
                Title: European Thyroid Journal
                Publisher: Bioscientifica Ltd (Bristol )
                ISSN (Print): 2235-0640
                ISSN (Electronic): 2235-0802
                Publication date (Electronic): 30 January 2023
                Publication date (Electronic preprint): 30 January 2023
                Publication date Collection: 01 April 2023
                Volume: 12
                Issue: 2
                Electronic Location Identifier: e220225
                Affiliations
                [1 ]ENS de Lyon , INRAE, CNRS, Institut de Génomique Fonctionnelle de Lyon, Lyon, France
                Author notes
                Correspondence should be addressed to F Flamant: Frederic.flamant@ 123456ens-lyon.fr
                Author information
                http://orcid.org/0000-0002-3360-2345
                Article
                Publisher ID: ETJ-22-0225
                DOI: 10.1530/ETJ-22-0225
                PMC ID: 10083660
                PubMed ID: 36715693
                SO-VID: 8f1b9cc0-ca0c-44a4-83db-98b06e48fb83
                Copyright © © the author(s)
                License:

                This work is licensed under a Creative Commons Attribution 4.0 International License.

                History
                Date received : 23 January 2023
                Date accepted : 30 January 2023
                Categories
                Subject: Review

                Keywords: thyroid hormone,mouse,postnatal development,metamorphosis
                Data availability:
                Keywords: thyroid hormone, mouse, postnatal development, metamorphosis

                Comments

                Comment on this article

                Related Documents Log