Journal
SCIENCE
Volume 340, Issue 6129, Pages 157-161Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1231828
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Funding
- UK Medical Research Council [G070149]
- Royal Society [Hirth2007/R2]
- Parkinson's UK [G-0714]
- Motor Neurone Disease Association [Hirth/Mar12/6085, Hirth/Oct07/6233]
- Alzheimer Research UK [Hirth/ARUK/2012]
- Fondation Thierry Latran (DrosALS)
- Air Force Research Laboratories [NJS/AFRL FA86511010001]
- Center for Insect Science, University of Arizona, Tucson
- MRC [G0701498] Funding Source: UKRI
- Alzheimers Research UK [ARUK-PhD2012-18] Funding Source: researchfish
- Medical Research Council [G0701498] Funding Source: researchfish
- Parkinson's UK [G-0714] Funding Source: researchfish
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The arthropod central complex and vertebrate basal ganglia derive from embryonic basal forebrain lineages that are specified by an evolutionarily conserved genetic program leading to interconnected neuropils and nuclei that populate the midline of the forebrain-midbrain boundary region. In the substructures of both the central complex and basal ganglia, network connectivity and neuronal activity mediate control mechanisms in which inhibitory (GABAergic) and modulatory (dopaminergic) circuits facilitate the regulation and release of adaptive behaviors. Both basal ganglia and central complex dysfunction result in behavioral defects including motor abnormalities, impaired memory formation, attention deficits, affective disorders, and sleep disturbances. The observed multitude of similarities suggests deep homology of arthropod central complex and vertebrate basal ganglia circuitries underlying the selection and maintenance of behavioral actions.
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