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Neural Circuit Development and Function in the Healthy and Diseased Brain

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Neuron Networks in Healthy and Diseased Brains

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Studies in rodents offer insights into bipolar disorder that may help understanding and treatment of this common and debilitating condition. Kihoon Han and colleagues at Korea University in Seoul review research using mice and rats to model the episodes of mania in patients with bipolar disorder. The research supports an emerging hypothesis implicating specific problems with nervous transmission in the brain in the onset of mania.

The hypothesis suggests that the transmission of signals between particular nerve cells whose normal function is either to excite or to inhibit other nerve cells may be involved. It also indicates regions of the brain most involved in manic episodes. Changes at the affected nerve junctions—called synapses—brought about by mood-stabilizing drugs are examined. The hypothesis suggests new approaches to treatment options for researchers to explore.


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Insights into how the brain responds to environmental stimuli during early infancy may inform brain disorder therapies. This phase, if disrupted, may impact on healthy development. Se-Young Choi at Seoul National University School of Dentistry, South Korea reviewed current understanding of the mechanisms involved in this critical period, particularly in the primary sensory cortex. Certain neurons and genes are known to play key roles, and it is possible that manipulating sensory inputs at specific times could achieve specific developmental results. Novel technologies will reveal how the body regulates neural circuits and could one day enable scientists to restore normal functioning in patients with brain disorders such as autism.

Further analysis of synaptic proteins will provide insights into the functioning of neural circuits and associated brain disorders. The brain houses numerous highly specialized neuron types, which transfer and process information via a complex network of synaptic connections. Taken with the evidence that astrocytes strongly control synapse formation and the in vitro evidence for the role of astrocytes in Rett syndrome and fragile X syndrome, this raises the question of whether abnormal astrocyte development could contribute to the pathogenesis of these common neurodevelopmental diseases.

Thus, these results show that astrocytes might have an underappreciated role in many neurodevelopmental diseases and raise the question of whether targeting astrocytes might lead to the development of new therapeutic agents for these diseases. Astrocytes can no longer be thought of as passive support cells. Over the past 10 years, many compelling lines of evidence have shown that astrocytes powerfully control every stage of synapse formation, maturation and elimination to support the development and maintenance of neural circuits.

One important area for future investigation is to determine how specific astrocyte-secreted signals interact with the neuronal signalling pathways that regulate synapse development and plasticity. Furthermore, advances in our understanding of how astrocytes respond to neuronal activity to regulate the release of secreted signals should improve our understanding of the molecular mechanisms that control synapse formation and function.

Another exciting area of research will be the study of human astrocytes to determine how they differ from their rodent counterparts. An understanding of the unique characteristics of human astrocytes might provide a new insight into the basis of human cognition. This molecular insight might also further our understanding of the pathological changes in astrocytes that lead to several neurodevelopmental disorders. As astrocytes are so essential to the normal structure and function of synapses, it has been difficult to dissect their role in synapse development and function in vivo.


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  • However, with the identification of astrocyte-specific markers 89 and the molecules they release, the advent of optogenetics and improvements in imaging techniques, it might now be possible to manipulate astrocytes in specific brain regions and at different times during development in vivo. Furthermore, advances in cell culture techniques and induced pluripotent stem cell technology 32 will allow researchers to purify astrocytes and neurons from patients with neurodevelopmental disorders.

    Synapses, Circuits and Behaviour

    These studies might shed new light on the contributions made by astrocytes to the formation of neural circuits in both healthy and diseased human brains. Competing interests statement. See Web version for details. Europe PMC requires Javascript to function effectively. Recent Activity. The snippet could not be located in the article text. This may be because the snippet appears in a figure legend, contains special characters or spans different sections of the article.

    Nat Rev Neurosci. Author manuscript; available in PMC May PMID: Laura E. Clarke and Ben A. Correspondence to L. Copyright notice. The publisher's final edited version of this article is available at Nat Rev Neurosci. See other articles in PMC that cite the published article. Abstract Astrocytes are now emerging as key participants in many aspects of brain development, function and disease. Table 1 Synaptogenic molecules secreted by astrocytes.

    Cholesterol is thought to act as a building material to enhance dendrite and presynaptic terminal differentiation 10 , 33 Ephrins EPH receptor tyrosine kinase Ephrin—EPH interactions modulate dendritic spine dynamics. Activation of the receptor EPH type A4 EPHA4 by ephrin A3 induces spine retraction, whereas inhibition of ephrin—EPHA4 interactions distorted spine shape and organization 69 , 70 EPHA4- and ephrin A3-knockout mice showed irregularities in the morphology of their dendritic spines 69 , 70 Glypican Unknown Glypicans converted silent synapses to functional ones by increasing the amplitude and frequency of glutamatergic synaptic events in cultured RGCs.

    This conversion was achieved by increasing the surface level of AMPA receptors 1 Genetic deletion of glypicans in vivo led to defective synapse formation, with decreased amplitude of excitatory synaptic currents and reduced recruitment of AMPA receptors 1 Hevin Neuroligins and neurexins S.