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Questions: Does neuromuscular electrical stimulation (NMES) applied during haemodialysis sessions improve functional capacity in people with end-stage renal disease? Does NMES used in this way also improve muscle strength, muscle mass/architecture, psychological outcomes, cardiovascular outcomes and biochemical variables? Does it have any adverse effects?, Design: Systematic review of randomised controlled trials with meta-analysis. PubMed, Web of Science, Scopus and SPORTDiscus were searched from inception to 15 October 2019., Participants: Patients receiving haemodialysis for end-stage renal disease., Intervention: NMES administered during haemodialysis sessions versus control., Outcomes Measures: Functional capacity, muscle strength, muscle mass, psychological outcomes, cardiovascular outcomes, biochemical variables and adverse events., Data Analysis: Data were meta-analysed where possible and results were expressed as the pooled mean difference between groups with a 95% confidence interval., Results: Eight studies (221 patients) were included in the analysis. Overall, the methodological quality of the studies was fair to good. NMES improved functional capacity as assessed by the 6-minute walk distance test (MD 31 m, 95% CI 13 to 49) and peak workload attained in incremental exercise (MD 12.5 W, 95% CI 3.2 to 21.9). NMES increased knee extensor muscle strength (MD 3.5 kg, 95% CI 2.3 to 4.7) and handgrip strength (MD 2.4 kg, 95% CI 0.4 to 4.4). Muscle mass/architecture was not substantially affected. NMES was estimated to be beneficial for several domains of quality of life in several studies, although most of these estimates were imprecise. No benefits were found for cardiovascular outcomes. The available data did not establish any clear effects on cardiovascular outcomes or biochemical variables (dialysis efficiency, urea and creatinine). No major NMES-related adverse events were observed., Conclusions: NMES is safe, practical and effective for improving functional capacity and muscle strength in haemodialysis patients. Further research is needed to confirm the clinical relevance of these findings., Registration: PROSPERO CRD42018107323., (Copyright © 2020 Australian Physiotherapy Association. Published by Elsevier B.V. All rights reserved.)

Background and Purpose: Vascular endothelial and smooth muscle cell phenotypes may change dramatically after isolation and in cell cultures. This study was designed to investigate gap junctions coupling in an integrated intact preparation and to test if K(IR) channels modulate resting membrane conductance in "in situ" endothelial cells (EC), and acetylcholine (ACh)-evoked relaxation of the rat superior mesenteric artery., Experimental Approach: Whole cell blind patch recordings of ionic currents from in situ EC, dye-coupling experiments, and functional studies were performed in rat superior mesenteric artery., Key Results: EC were dye-coupled through gap junctions. 18β-glycyrretinic acid (25 μM) decreased outward and inward currents, the 80% decay of time and time constant of the capacitative transients, capacitance, and increased input resistance. Barium chloride (30 μM) decreased resting and ACh-evoked inward currents, the sensitivity of ACh-evoked relaxation, and decreased both the sensitivity and the maximal relaxation to S-nitroso-N-acetyl penicillamine in arteries with, but not in arteries without endothelium., Conclusions: The present results suggest that the EC layer of this large artery is electrically coupled, and that K(IR) channels regulate resting inward conductance, hence suggesting that they are of importance for resting membrane potential in in situ EC. Moreover, EC K(IR) channels are involved in ACh-evoked relaxation., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Changes in the retino-collicular projection and in the number of optic nerve (ON) axons in adult rats were analyzed after partial loss of retinal ganglion cells (RGCs), induced by intravitreal injections of kainic acid (KA) on postnatal days 2-3 (P2-P3) or 10-12 (P10-P12). KA injected at P2-P3 decreased the volume of the adult contralateral superior colliculus (SC) and the density of the retino-collicular contralateral projection, but maintained the neonatal pattern in the ipsilateral projection from the un-injected eye. ON axon number was significantly increased in the un-injected eye but decreased in the KA-injected eye. Thus, restriction of the ipsilateral retino-collicular projection and RGC death in the un-injected eye are modified by KA at P2-P3, during the postnatal critical period, but not at P10-P12, after it is over. We suggest that, in the SC contralateral to the KA-injected eye, the disappearance of axon terminals belonging to RGC killed by KA would decrease competition between ipsilateral and contralateral terminals, thus contributing to maintaining the neonatal pattern in the ipsilateral retino-collicular projection. The reduction in RGC death in the un-injected eye could also be related to the disappearance of RGC terminals in the contralateral SC, which would have increased neurotrophic factor availability.

Gamma-amino butyric acid (GABA) has been characterized as an inhibitory neurotransmitter acting through chloride mediated channels in the adult nervous system. Using gramicidin-perforated patch clamp recordings from horizontal cells dissociated from the retinas of adult rabbits, we found that GABA is able to induce cell depolarization. Ionic currents induced by GABA in dissociated horizontal cells showed a reversal potential close to -30 mV. This value is more positive than the resting potential of these cells (ca. -70 mV). Therefore, according to the Nernst equation, the intracellular chloride concentration in horizontal cells was estimated to be of 44 mM. The depolarizing effect of GABA at the dendrites of horizontal cells may serve to shape the center-surround organization of the receptive fields in retinal cells, thereby securing the shape discrimination of visual input.

We propose a mathematical model of rabbit retinal horizontal cell based on the ionic current mechanisms. Five types of ionic currents in rabbit retinal horizontal cell, I(Na), I(Ca), I(Kv), I(A) and I(Ka), are described by Hodgkin-Huxley type equations based on voltage clamp measurements. In simulation the model reproduced similar responses to voltage and current clamp experiments. Under the current clamp experiment a repetitive action potential was found on A-type rabbit horizontal cells. Our result suggests that the repetitive action potential is generated by an interaction Of I(Ca) and I(Kv).

In the vertebrate retina, the rod bipolar cells make reciprocal synapses with amacrine cells at the axon terminal. Amacrine cells may perform a fine control of the transmitter release from rod bipolar cells by means of GABAergic synapses acting on different types of GABA receptors. To clarify this possibility GABA-induced currents were recorded by the patch-clamp whole cell method in rod bipolar cells enzymatically dissociated from the mouse retina. All cells tested showed a desensitising chloride-sensitive GABA-induced current. When GABA 30 microM was applied in presence of 100 microM biccuculine, a blocker of the GABA(A) receptors, a slow-desensitising component of the current still remains. This current was blocked when GABA 30 microM was applied in presence of 100 microM 3-aminopropylphosphonic acid, an antagonist of the GABA(C) receptors. The current mediated by GABA(C) receptors showed an EC50 of less that 5 microM; the ionic current through the GABA(A) receptor showed an EC50 of ca. 30 microM. Two pieces of evidence demonstrated that the GABA(C)-mediated current was localised at the axon terminal of rod bipolar cells: (1) cells lacking the axon terminal only showed the biccuculine-sensitive GABA-induced current; and (2) after mechanical section of the axon terminal, bipolar cells lost the slow-desensitising component of the GABA-induced current. We conclude that the rod bipolar cells express two types of ionotropic GABA receptors, and that the high sensitive GABA(C) receptors are mainly localised at the level of the axon terminal and therefore may contribute to the modulation of the transmitter release from the rod bipolar cell.