Discoveries in Retina Physiology and Disease Biology Using Single-Cell RNA Sequencing

The retina, a component of the central nervous system, is composed of six distinct neuronal types and various types of glial cells. A technique for single-cell transcriptome analysis called single-cell RNA sequencing (scRNA-seq) can be employed to study the complicated dynamics of several types of retinal cells. It meticulously examines how various cell types express their genes, shedding light on all biological processes. scRNA-seq is an alternative to regular RNA-seq, which cannot identify cellular heterogeneity. Understanding retinal diseases requires research on retinal cell heterogeneity. The identification of novel cell subpopulations can provide information about disease occurrence and progression as well as the specific biological functions of particular cells. We currently have a better understanding of the interactions among the brain, the retina, and its visual pathways thanks to the use of scRNA-seq to examine retinal development and disease pathogenesis. Additionally, this technology offers fresh perspectives on the sensitivity and molecular basis of cell subtypes linked to retinal diseases. Thanks to scRNA-seq technology, we now have a better understanding of the most recent developments and difficulties in retinal development and disorders. We believe that scRNA-seq is an important tool for developing cutting-edge treatments for retinal diseases. This paper presents a systematic review of the history of sRNA-seq technology development and provides an overview of the unique subtypes of retinal cells and the specific gene markers this technology identifies

Dual- vs. Single-Plane Ultrasonic Scan-Assisted Positioning during Lumbar Spinal Puncture in Elderly Patients: A Randomized Controlled Trial

The purpose of this study was to investigate the ability of single- versus dual-plane ultrasound scan-assisted spinal anesthesia techniques to improve the success rate and efficacy of spinal anesthesia in elderly patients undergoing lower extremity surgery. A total of 120 elderly patients undergoing lower extremity surgery were randomly assigned to either receive single-plane (Group A) or dual-plane ultrasonic scan-assisted spinal anesthesia (Group B). The primary outcome analyzed by this study was first-attempt success rate. Secondary outcomes analyzed included number of needle insertion attempts, needle redirections, locating time, procedural time, total time, puncture depth, quality of ultrasound images, level of block, adverse reactions, and complications. The first-attempt success rate was significantly higher in Group B compared to Group A (88.3% vs. 68.3%, p = 0.008). In comparison with Group A, the number of needle insertion attempts (1 (1–2) vs. 1 (1–1), p = 0.005) and needle redirections (2 (1–3) vs. 1 (0–2), p p p < 0.001). The dual-plane ultrasonic scan-assisted spinal anesthesia technique warrants consideration for application in elderly patients

Brain-Derived Neurotrophic Factor Ameliorates Learning Deficits in a Rat Model of Alzheimer's Disease Induced by Aβ1-42

<div><p>An emerging body of data suggests that the early onset of Alzheimer’s disease (AD) is associated with decreased brain-derived neurotrophic factor (BDNF). Because BDNF plays a critical role in the regulation of high-frequency synaptic transmission and long-term potentiation in the hippocampus, the up-regulation of BDNF may rescue cognitive impairments and learning deficits in AD. In the present study, we investigated the effects of hippocampal BDNF in a rat model of AD produced by a ventricle injection of amyloid-β1-42 (Aβ1-42). We found that a ventricle injection of Aβ1-42 caused learning deficits in rats subjected to the Morris water maze and decreased BDNF expression in the hippocampus. Chronic intra-hippocampal BDNF administration rescued learning deficits in the water maze, whereas infusions of NGF and NT-3 did not influence the behavioral performance of rats injected with Aβ1-42. Furthermore, the BDNF-related improvement in learning was ERK-dependent because the inhibition of ERK, but not JNK or p38, blocked the effects of BDNF on cognitive improvement in rats injected with Aβ1-42. Together, our data suggest that the up-regulation of BDNF in the hippocampus via activation of the ERK signaling pathway can ameliorate Aβ1-42-induced learning deficits, thus identifying a novel pathway through which BDNF protects against AD-related cognitive impairments. The results of this research may shed light on a feasible therapeutic approach to control the progression of AD.</p></div

Effect of intra-hippocampal injections of BDNF (0.05, 0.25 and 1.0 μg/side), NGF (0.25 μg/side) and NT-3 (0.25 μg/side) on spatial learning function in the Aβ1-42-treated rat model of Alzheimer's disease.

<p>(A) Representative swim traces of each group in the fifth training trial. (B) Escape latency and (C) swimming speed in each training trial were also analyzed. (D) The time spent in the target quadrant in the probe task. (E) The number of times crossing the platform in the probe task. (F) The total distance traveled in the open field test after the probe task. n = 8/group. For panel B, * <i>P</i> < 0.05, ** <i>P</i> < 0.01, Aβ1–42 + saline <i>vs</i> sham control group; # <i>P</i> < 0.05, Aβ1–42 + NGF <i>vs</i> sham control group; § <i>P</i> < 0.05, Aβ1–42 + NT-3 <i>vs</i> sham control group. For the other panels, * <i>P</i> < 0.05, ** <i>P</i> < 0.01, and *** <i>P</i> < 0.0001, compared with sham controls. # <i>P</i> <0.05 as compared with Aβ1–42 + saline group.</p

Effect of intra-hippocampal injections of BDNF (1.0 μg), NGF (0.25 μg), and NT-3 (0.25 μg) on MAPK expression in the hippocampus in a rat model of Alzheimer's disease.

<p>(A) representative western blots of each group. GAPDH was used as the internal loading control. (B) relative expression of phosphorylated ERK. (C) and (D) relative expression of phosphorylated JNK and p38. * <i>P</i> < 0.05, ** <i>P</i> < 0.01, and *** <i>P</i> < 0.0001 compared with sham controls. # <i>P</i> <0.05 as compared with Aβ1–42 + saline group.</p

Effect of intra-hippocampal injections of BDNF, ERK activator ceramide C6 and the ERK inhibitor PD98059 on spatial learning function in the rat model of Alzheimer's disease.

<p>(A) Representative swim traces of each group in the fifth training trial. (B) Escape latency and (C) swimming speed in each training trial were also analyzed. (D) The time spent in the target quadrant in the probe task. (E) The number of times crossing the platform in the probe task. (F) The total distance traveled in the open field test after the probe task. n = 8 each group. For panel B, * <i>P</i> < 0.05, ** <i>P</i> < 0.01, Aβ1–42 + PD98059 + BDNF <i>vs</i> Aβ1–42 + BDNF group; # <i>P</i>< 0.05, Aβ1–42 + ceramide C6 <i>vs</i>. Aβ1–42 + BDNF group. For the other panels, * <i>P</i> < 0.05 and *** <i>P</i> < 0.0001 compared with the Aβ1–42 + BDNF group.</p