Neuroscience
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Previous research has suggested that balance impairments may be linked to anxiety in PD, yet there is little empirical evidence to support this link in PD. This study aimed to evaluate the influence of anxiety on balance, and also examine whether dopaminergic treatment modulates the influence of anxiety on balance. Forty-two participants (10 high anxious PD [HA-PD]; 11 low anxious PD [LA-PD], 21 controls [HC]) performed 10 quiet standing trials on a force platform in two virtual environments: LOW threat; on a plank located on the ground; HIGH threat; on an elevated plank. ⋯ Although dopaminergic medication significantly reduced self-reported anxiety, it had limited effects on balance. In conclusion, this study provides strong evidence that anxiety does influence balance control in PD, especially those who are highly anxious. Dopamine appears to modulate anxiety, but further research is needed to evaluate whether dopaminergic treatment is optimal for anxiety induced balance deficits.
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Neuronal gap junctions are ubiquitous in the brain, but their precise positions in actual neuronal circuits have been uncertain, and their functional roles remain unclear. In this study, I visualized connexin36-immunoreactive gap junctions and examined the structural features of the interconnected dendrites arising from parvalbumin (PV)-positive interneurons in layer 4 of the feline visual cortex. I observed evidence for net-like dense linkages of dendrites among virtually all PV neurons (56/58 cells, 96.6%) in the tissue. ⋯ In contrast, gap junctions formed between nearby cells were close to both somata. Thalamocortical afferents established synapses densely on somata of layer 4 PV neurons, indicating the possible involvement of proximal gap junctions in visual stimulus-driven feedforward regulation. These findings provide a new structural basis for cortical investigations.
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Comparative Study
The significance of rotational behavior and sensitivity of striatal dopamine receptors in hemiparkinsonian rats: A comparative study of lactacystin and 6-OHDA.
A growing body of evidence indicates that impairment of the ubiquitin-proteasome (UPS) system in the substantia nigra (SN) plays an important role in the pathogenesis of Parkinson's disease (PD). The aim of our study was to compare two unilateral rat models, one produced by intranigral administration of the UPS inhibitor lactacystin or the other induced by 6-OHDA, in terms of their effect on the amphetamine- and apomorphine-induced rotational behavior, striatal dopamine (DA) D1 and D2 receptor sensitivity and tissue levels of DA and its metabolites. We found that these models did not differ in the intensity of ipsilateral rotations induced by amphetamine. ⋯ Binding of [3H]raclopride to D2 receptors was increased in the lesioned striatum in both investigated (PD) models six weeks after lesion. In turn, binding of [3H]SCH23390 to the striatal D1 receptors was not changed in the lactacystin group but was increased bilaterally in the 6-OHDA group. The present results add a new value to the study of DA receptor sensitivity and are discussed in the context of the validity of the lactacystin model as a suitable model of Parkinson's disease.
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Equivocal evidence indicates that high-intensity muscle contractions can affect the corticospinal responses in muscles not directly involved in the task. In the present study, the responsiveness of corticomotor pathway innervating non-dominant biceps brachii was measured in eleven healthy participants before and after: (i) two 100-s isometric unilateral knee extension maximal voluntary contractions (MVCs) on dominant leg (FATIGUE) and (ii) rest (CONTROL). Transcranial magnetic stimulation, transmastoid electrical and brachial plexus electrical stimulation were used to evoke motor evoked potential (MEP), cervicomedullary motor evoked potential (CMEP) and compound muscle action potential (Mmax) in biceps brachii muscle. ⋯ Yet, the elbow flexor MVC force did not exhibit any difference between FATIGUE and CONTROL conditions. These results suggest that the upper limb muscles' corticomotor pathway responsiveness recorded during voluntary contractions were modulated by lower limbs fatiguing contractions and this modulation depends on the force produced during testing, i.e. level of central motor drive. However, these changes have little effect on upper limb muscle maximal performance.
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The Ts65Dn mouse model of Down syndrome (DS) and Alzheimer's disease (AD) exhibits cognitive impairment and degeneration of basal forebrain cholinergic neurons (BFCNs). Our prior studies demonstrated that maternal choline supplementation (MCS) improves attention and spatial cognition in Ts65Dn offspring, normalizes hippocampal neurogenesis, and lessens BFCN degeneration in the medial septal nucleus (MSN). Here we determined whether (i) BFCN degeneration contributes to attentional dysfunction, and (ii) whether the attentional benefits of perinatal MCS are due to changes in BFCN morphology. ⋯ MCS did not normalize any of these morphological abnormalities in the NBM/SI or MSN. Finally, correlational analysis revealed that attentional performance was inversely associated with BFCN volume, and positively associated with BFCN density. These results support the lifelong attentional benefits of MCS for Ts65Dn and 2N offspring and have profound implications for translation to human DS and pathology attenuation in AD.