Retinal Contrast Transfer Functions in Adults With and Without ADHD.

Retinal Contrast Transfer Functions in Adults with and without ADHD.

PLoS One. 2013; 8(5): e61728
Bubl E, Dörr M, Philipsen A, Ebert D, Bach M, van Elst LT

In previous studies, we found a strong reduction in contrast perception and retinal contrast gain in patients with major depression, which normalized after remission of depression. We also identified a possible role of the dopaminergic system in this effect, because visual contrast perception depends on dopaminergic neurotransmission. Dopamine is also known to play an important role in the pathogenesis of attention deficit hyperactivity disorder (ADHD). Therefore, in order to explore the specificity of retinal contrast gain as a marker of depression in comparison with other psychiatric diseases, we recorded the pattern electroretinogram (PERG) in patients with ADHD. Twenty patients diagnosed with ADHD and 20 matched healthy subjects were studied. Visual pattern electroretinograms were recorded from both eyes. The contrast gain of the patients with attention deficit disorder (ADD) did not differ from the control group, nor did the contrast gain of any ADHD subgroup (predominantly inattentive or combined patients). In the healthy subjects, a significant correlation between depression score and contrast gain was found. As the contrast gain in an earlier study clearly separated the patients with depression from the controls, we assume that retinal contrast gain might be a specific marker in depression. HubMed – depression


Factors associated with depression and suicide among patients with diabetes mellitus and essential hypertension in a Nigerian teaching hospital.

Afr Health Sci. 2013 Mar; 13(1): 68-77
Igwe M, Uwakwe R, Ahanotu C, Onyeama G, Bakare M, Ndukuba A

Diabetes mellitus (DM) and essential hypertension are chronic medical conditions that place a lot of burden on patients. The presence of depression and suicidal behaviour may worsen the prognosis.To assess the prevalence of depression and suicidal behaviour in subjects with diabetes mellitus and essential hypertension and also determine the socio-demographic correlates.Major depressive episode and suicidality modules of Mini-International Neuropsychiatric Interview were used to assess depression and suicidal behaviour respectively.The prevalence of depression for the subjects with DM was 27.8% and 26.7% for essential hypertension. The subjects with DM had prevalence of 6.3% for suicidal behaviour while essential hypertension had 7.8%. Depression was higher in subjects with DM if they were not married or had no education while the subjects with essential hypertension were more likely to have depression if they were not married, had no education or not employed. Suicidal behaviour was higher in subjects with DM if they had no education while in essential hypertension suicidal behaviour was higher in females, those not married and those not educated.Depression and suicidal behaviour occur with DM and essential hypertension. HubMed – depression


Initiation, labile, and stabilization phases of experience-dependent plasticity at neocortical synapses.

J Neurosci. 2013 May 8; 33(19): 8483-93
Wen JA, Deblois MC, Barth AL

Alteration of sensory input can change the strength of neocortical synapses. Selective activation of a subset of whiskers is sufficient to potentiate layer 4-layer 2/3 excitatory synapses in the mouse somatosensory (barrel) cortex, a process that is NMDAR dependent. By analyzing the time course of sensory-induced synaptic change, we have identified three distinct phases for synaptic strengthening in vivo. After an early, NMDAR-dependent phase where selective whisker activation is rapidly translated into increased synaptic strength, we identify a second phase where this potentiation is profoundly reduced by an input-specific, NMDAR-dependent depression. This labile phase is transient, lasting only a few hours, and may require ongoing sensory input for synaptic weakening. Residual synaptic strength is maintained in a third phase, the stabilization phase, which requires mGluR5 signaling. Identification of these three phases will facilitate a molecular dissection of the pathways that regulate synaptic lability and stabilization, and suggest potential approaches to modulate learning. HubMed – depression


A Myosin va mutant mouse with disruptions in glutamate synaptic development and mature plasticity in visual cortex.

J Neurosci. 2013 May 8; 33(19): 8472-82
Yoshii A, Zhao JP, Pandian S, van Zundert B, Constantine-Paton M

Myosin Va (MyoVa) mediates F-actin-based vesicular transport toward the plasma membrane and is found at neuronal postsynaptic densities (PSDs), but the role of MyoVa in synaptic development and function is largely unknown. Here, in studies using the dominant-negative MyoVa neurological mutant mouse Flailer, we find that MyoVa plays an essential role in activity-dependent delivery of PSD-95 and other critical PSD molecules to synapses and in endocytosis of AMPA-type glutamate receptors (AMPAR) in the dendrites of CNS neurons. MyoVa is known to carry a complex containing the major scaffolding proteins of the mature PSD, PSD-95, SAPAP1/GKAP, Shank, and Homer to dendritic spine synapses. In Flailer, neurons show abnormal dendritic shaft localization of PSD-95, stargazin, dynamin3, AMPARs and abnormal spine morphology. Flailer neurons also have abnormally high AMPAR miniature current frequencies and spontaneous AMPAR currents that are more frequent and larger than in wild-type while numbers of NMDAR containing synapses remain normal. The AMPAR abnormalities are consistent with a severely disrupted developmental regulation of long-term depression that we find in cortical Flailer neurons. Thus MyoVa plays a fundamentally important role both in localizing mature glutamate synapses to spines and in organizing the synapse for normal function. For this reason Flailer mice will be valuable in further dissecting the role of MyoVa in normal synaptic and circuit refinement and also in studies of neurological and neuropsychiatric diseases where disruptions of normal glutamate synapses are frequently observed. HubMed – depression



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