bibd helper tools work

OMEGA.bib

@@ -254,11 +254,6 @@
 	File = {papers/Tallinen_NaturePhysics2016.pdf},
 	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nphys3632}}
 
-@article{cite-key,
-	Date-Added = {2018-04-05 22:32:31 +0000},
-	Date-Modified = {2018-04-05 22:32:31 +0000},
-	File = {papers/Tallinen_NaturePhysics2016.pdf}}
-
 @article{Tallinen:2014,
 	Abstract = {The exterior of the mammalian brain--the cerebral cortex--has a conserved layered structure whose thickness varies little across species. However, selection pressures over evolutionary time scales have led to cortices that have a large surface area to volume ratio in some organisms, with the result that the brain is strongly convoluted into sulci and gyri. Here we show that the gyrification can arise as a nonlinear consequence of a simple mechanical instability driven by tangential expansion of the gray matter constrained by the white matter. A physical mimic of the process using a layered swelling gel captures the essence of the mechanism, and numerical simulations of the brain treated as a soft solid lead to the formation of cusped sulci and smooth gyri similar to those in the brain. The resulting gyrification patterns are a function of relative cortical expansion and relative thickness (compared with brain size), and are consistent with observations of a wide range of brains, ranging from smooth to highly convoluted. Furthermore, this dependence on two simple geometric parameters that characterize the brain also allows us to qualitatively explain how variations in these parameters lead to anatomical anomalies in such situations as polymicrogyria, pachygyria, and lissencephalia.},
 	Author = {Tallinen, Tuomas and Chung, Jun Young and Biggins, John S and Mahadevan, L},
@@ -111411,4 +111406,58 @@ CONCLUSIONS: Centrifugal axons in the macaque retina are part of the system of a
 	Volume = {8},
 	Year = {1997}}
 
-@Comment{jabref-meta: databaseType:bibtex;}
+@article{Smith2017,
+  title = {Cadherin-10 Maintains Excitatory/Inhibitory Ratio through Interactions with Synaptic Proteins.},
+  author = {Smith, Katharine R and Jones, Kelly A and Kopeikina, Katherine J and Burette, Alain C and Copits, Bryan A and Yoon, Sehyoun and Forrest, Marc P and Fawcett-Patel, Jessica M and Hanley, Jonathan G and Weinberg, Richard J and Swanson, Geoffrey T and Penzes, Peter},
+  journal = {J Neurosci},
+  volume = {37},
+  number = {46},
+  year = {2017},
+  month = {Nov},
+  pages = {11127-11139},
+  abstract = {Appropriate excitatory/inhibitory (E/I) balance is essential for normal cortical function and is altered in some psychiatric disorders, including autism spectrum disorders (ASDs). Cell-autonomous molecular mechanisms that control the balance of excitatory and inhibitory synapse function remain poorly understood; no proteins that regulate excitatory and inhibitory synapse strength in a coordinated reciprocal manner have been identified. Using super-resolution imaging, electrophysiology, and molecular manipulations, we show that cadherin-10, encoded by CDH10 within the ASD risk locus 5p14.1, maintains both excitatory and inhibitory synaptic scaffold structure in cultured cortical neurons from rats of both sexes. Cadherin-10 localizes to both excitatory and inhibitory synapses in neocortex, where it is organized into nanoscale puncta that influence the size of their associated PSDs. Knockdown of cadherin-10 reduces excitatory but increases inhibitory synapse size and strength, altering the E/I ratio in cortical neurons. Furthermore, cadherin-10 exhibits differential participation in complexes with PSD-95 and gephyrin, which may underlie its role in maintaining the E/I ratio. Our data provide a new mechanism whereby a protein encoded by a common ASD risk factor controls E/I ratios by regulating excitatory and inhibitory synapses in opposing directions.SIGNIFICANCE STATEMENT The correct balance between excitatory/inhibitory (E/I) is crucial for normal brain function and is altered in psychiatric disorders such as autism. However, the molecular mechanisms that underlie this balance remain elusive. To address this, we studied cadherin-10, an adhesion protein that is genetically linked to autism and understudied at the cellular level. Using a combination of advanced microscopy techniques and electrophysiology, we show that cadherin-10 forms nanoscale puncta at excitatory and inhibitory synapses, maintains excitatory and inhibitory synaptic structure, and is essential for maintaining the correct balance between excitation and inhibition in neuronal dendrites. These findings reveal a new mechanism by which E/I balance is controlled in neurons and may bear relevance to synaptic dysfunction in autism.},
+  keywords = {CDH10; PSD-95; adhesion; cadherin-10; dendritic spines; inhibitory synapses; },
+  mesh = {Animals; Cadherins; Cells, Cultured; Disks Large Homolog 4 Protein; Excitatory Postsynaptic Potentials; Female; HEK293 Cells; Humans; Inhibitory Postsynaptic Potentials; Male; Mice; Protein Binding; Rats; Rats, Sprague-Dawley; Synapses; },
+  pubmed = {29030434},
+  pii = {JNEUROSCI.1153-17.2017},
+  doi = {10.1523/JNEUROSCI.1153-17.2017},
+  pmc = {PMC5688522},
+  url = {https://www.ncbi.nlm.nih.gov/pubmed/29030434},
+  file = {papers/Smith_JNeurosci2017-29030434.pdf},
+  nlmuniqueid = {8102140}
+}
+
+@Article{Forrest2018,
+  author      = {Forrest, Marc P and Parnell, Euan and Penzes, Peter},
+  title       = {Dendritic structural plasticity and neuropsychiatric disease.},
+  journal     = {Nat Rev Neurosci},
+  year        = {2018},
+  volume      = {19},
+  number      = {4},
+  pages       = {215-234},
+  month       = {Mar},
+  abstract    = {The structure of neuronal circuits that subserve cognitive functions in the brain is shaped and refined throughout development and into adulthood. Evidence from human and animal studies suggests that the cellular and synaptic substrates of these circuits are atypical in neuropsychiatric disorders, indicating that altered structural plasticity may be an important part of the disease biology. Advances in genetics have redefined our understanding of neuropsychiatric disorders and have revealed a spectrum of risk factors that impact pathways known to influence structural plasticity. In this Review, we discuss the importance of recent genetic findings on the different mechanisms of structural plasticity and propose that these converge on shared pathways that can be targeted with novel therapeutics.},
+  doi         = {10.1038/nrn.2018.16},
+  file        = {papers/Forrest_NatRevNeurosci2018-29545546.pdf},
+  nlmuniqueid = {100962781},
+  pii         = {nrn.2018.16},
+  pubmed      = {29545546},
+  url         = {https://www.ncbi.nlm.nih.gov/pubmed/29545546},
+}
+
+@article{Johnson1981,
+  title = {Neural mechanisms of spatial tactile discrimination: neural patterns evoked by braille-like dot patterns in the monkey.},
+  author = {Johnson, K O and Lamb, G D},
+  journal = {J Physiol},
+  volume = {310},
+  year = {1981},
+  month = {Jan},
+  pages = {117-44},
+  abstract = {1. The experiments reported here were designed to investigate the responses of cutaneous mechanoreceptive afferents to spatially configured dot patterns scanned across the skin. Braille-like patterns were selected because the discrimination of Braille characters must depend on spatial patterning rather than some other facet of the afferent discharge. 2. A multifactorial experimental design was used in which each afferent fibre was studied using every combination of six dot patterns, two dot sizes, two dot spacings, two contact forces and two scanning velocities. Two other factors, scanning direction relative to the skin ridges and intermittent versus continuous scanning, were studied. 3. Beside the general question concerning the response properties of the mechanoreceptive afferents, three major questions were addressed here. (i) What is the critical spatial dimension at which neural spatial patterning breaks down and below which tactual discrimination must depend on facets of the afferent discharge other than spatial neural patterning? (ii) Which mechanoreceptive population sets this critical dimension? (iii) Why is tactual discrimination enhanced by lateral scanning? 4. The results presented here suggest that the critical dimension, below which spatial neural patterning breaks down, is of the order of 1.0 mm and that the slowly adapting (SA) afferent fibres are responsible for this limit. 5. At dimensions above approximately 1.0 mm the spatial contrast between peaks and troughs in the SA discharge is markedly enhanced during scanning. When the skin is stationary the discharge rates in the SA population drop rapidly to low levels. A second possible reason for enhanced tactual discrimination during scanning is related to the increased spatiotemporal information in a coherent pattern of neural activity moving across a discrete population of afferent fibres. 6. The effects of variations in conduction velocity are analysed and it is shown that they place serious constraints on the transmission of spatiotemporal information.},
+  pubmed = {7230030},
+  pmc = {PMC1274731},
+  url = {https://www.ncbi.nlm.nih.gov/pubmed/7230030},
+  file = {papers/Johnson_JPhysiol1981-7230030.pdf},
+  nlmuniqueid = {0266262}
+}
+