The prevalence of migraines in females is 3 times greater than in males. Current research has implicated the calcitonin gene-related peptide (CGRP) as a significant factor in the pathophysiology of migraines. This study investigated the sex differences associated with the expression of three protein components of the calcitonin gene-related peptide receptor: calcitonin receptor-like receptor (CLR), receptor activity-modifying protein 1 (RAMP1), and receptor component protein (RCP). The research included comparing baseline protein levels in the spinal trigeminal nucleus caudalis (SpVc) and upper cervical spinal cord between male and female rats and whether or not knock-down of the expression of RCP in the SpVc mitigates pain induced by chemical noxious stimulation of the meninges. The dataset includes western blot images (embedded within the associated article), protein expression analysis, and data associated with pain assessment and tests of facial mechanical hypersensitivity and allodynia in males versus females.

This study was undertaken to investigate the neuropathological mechanisms associated with spinal cord injury (SCI) pain. The research focused on the possible abnormal functional connectivity between the thalamus and cortex believed to be the etiology of SCI pain. A total of 14 rats were included in the research separated into 2 groups: SCI (8) and sham-operated (6). Resting-state functional magnetic resonance imaging scans were performed before surgery and postoperatively at 3, 7, 14, and 21 days. Dataset includes neuroimages and Seed-Based Correlation Analysis values.

This study tested the viability of using MRI-guided transcranial focused ultrasound (MRgFUS) to modify the interstitial space in the living brain. As a non-invasive technique, success in generating spatially controlled, non-destructive changes could lead to clinical applications such as enhancing delivery of therapeutics and altering fluid and pressure dynamics. The research involved the use of computer simulations for treatment planning and MRI acoustic radiation force impulse imaging for target validation. Additionally, Evans blue dye or nanoparticle probes were utilized to assess changes in the interstitium.This dataset includes a variety of histological, acoustic simulation, and electrophysiological images and tabular data of compressional acoustic properties of skull and brain tissue and physiochemical properties of nanoparticles.

Nonarthritic anterior ischemic optic neuropathy (NAION) commonly causes sudden optic nerve (ON)-related vision loss. The rodent NAION model (rAION) closely resembles NAION in presentation and physiological responses. Researchers hypothesized that blocking pro-inflammatory prostaglandin (PGE2) production by inhibiting monoacylglycerol lipase or cyclooxygenase activity and co-administering PGJ2 would potentiate RGC survival following ischemic neuropathy. This study identified early rAION-associated optic nerve head (ONH) inflammatory gene expression responses and the anti-inflammatory prostaglandin PGJ2’s effects on those responses. Deep sequencing was performed on vehicle- and PGJ2-treated ONHs 3d post-rAION induction. Results were compared against responses from a retinal ischemia model. Animals were treated with PGJ2 and MAGL inhibitor KML29, or PGJ2 + COX inhibitor meloxicam. RGC survival was quantified by stereology.

Fiber optics were implanted into the dorsal bed nucleus of the stria terminalis (dBNST) of 8-week-old male and female Sprague Dawley rats. Dopamine activity was measured using GRABda signals in the dBNST during a series of behavioral experiments. Experiments includes a Pavlovian lever autoshaping (PLA) training, a reward prediction error (RPE) probe session, and a satiety test. Rats were injected with fentanyl prior to the PLA session.

Primary hippocampal neuron cultures obtained from Sprague-Dawley rat embryos were infected with lentivirus expressing EGFP. Immunostaining with specific antibodies was performed on fixed neurons. Confocal and DNA-PAINT microscopy were used for imaging, and custom analysis methods were applied to analyze the acquired images. Statistical analyses were conducted using GraphPad PRISM.

This dataset was generated to investigate long-lasting neurobiological adaptations to drugs of abuse. This dataset specifically supported the study of cocaine exposure impact of mitochondrial dynamics and morphology through early growth response factor 3 (Egr3) transcriptional regulation of mitochondria-related nuclear gene transcripts. Mitochondria-related nuclear genes were assayed following contingent or non-contingent cocaine exposure in rodents and were also examined in postmortem nucleus accumbens (NAc) of cocaine dependents.

Supplemental data in tabular forms include human demographics, DNA sequencing primers, mitochondrial statistical analysis, and gene regulations.

The following data elements were observed over a period of 7-10 days: Egr3 change in response to cocaine vs saline between rats and human postmortem issue; Egr3 binding changes in various genes promoting mitochondria in response to cocaine vs saline between rats and human postmortem issue; mRNA change in response to cocaine and saline between rats and human postmortem issue and between cocaine addict and control group; mRNA change in response to cocaine and saline between rats and human dead issue; Ribosome (the RNA binding proteins) associated mRNA changes in dopamine receptor-1 containing medium spiny neurons (D1 MSNs) and D2 MSNs in response to cocaine and saline between cocaine addict and control group.