Memorizing significant locations in the environment is a fundamental capacity of the brain. In this issue, Turi et al. (2019) present multidisciplinary evidence for a critical involvement of disinhibitory interneurons in hippocampal CA1 in this process.
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| http://dx.doi.org/10.1016/j.neuron.2019.03.006 | DOI Listing |
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Altered firing output of VIP interneurons and early dysfunctions in CA1 hippocampal circuits in the 3xTg mouse model of Alzheimer's disease.
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Article Synopsis
- - Alzheimer's disease (AD) causes memory loss and early changes in hippocampal function, particularly involving GABAergic interneurons (INs) that help regulate network activity.
- - Type 3 interneuron-specific (I-S3) cells in the hippocampus, which play a key role in memory by disinhibiting excitatory cells, show altered firing patterns in AD-affected mice.
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Studies of COMT ValMet suggest that the neural circuitry subserving inhibitory control may be modulated by this functional polymorphism altering cortical dopamine availability, thus giving rise to heritable differences in behaviors. Using an anatomically-constrained magnetoencephalography method and stratifying the sample by COMT genotype, from a larger sample of 153 subjects, we examined the spatial and temporal dynamics of beta oscillations during motor execution and inhibition in 21 healthy Met/Met (high dopamine) or 21 Val/Val (low dopamine) genotype individuals during a Go/NoGo paradigm. While task performance was unaffected, Met homozygotes demonstrated an overall increase in beta power across regions essential for inhibitory control during early motor preparation (∼100 ms latency), suggestive of a global motor "pause" on behavior.
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