Effects of excitotoxic injury to the thoracic gray matter on sensitivity to below-level nociceptive stimulation were evaluated for female and male Long-Evans rats. Operant escape and lick/guard (L/G) reflex responses to thermal stimulation were evaluated before and for 13-15 weeks after: 1) injections of quisqualic acid (QUIS) into the thoracic gray matter (T8-9), 2) laminectomy and spinal exposure and penetration without injection (sham) or 3) no surgical procedure (control). L/G responding to heat stimulation (44 °C) was unaffected for females and males following thoracic QUIS injections. Similarly, male escape performance was not significantly altered for 44 °C or 10 °C stimulation after QUIS injections or sham surgery. However, escape testing following QUIS and sham injections revealed increased heat sensitivity (44 °C) and decreased cold sensitivity (10 °C) for females. This selective effect is indicative of altered sympathetic activation by the thoracic injections. The effect of sham surgery suggests that female rats are vulnerable to ischemic injury during exposure and manipulation of the spinal cord. Escape from nociceptive heat and cold sensitivity of control males and females was unchanged over 13-15 weeks of testing.
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http://dx.doi.org/10.1016/j.brainres.2011.08.072 | DOI Listing |
Neurochem Res
January 2025
Huazhong University of Science and Technology, Tongji Medical College, Wuhan, Hubei, 430000, China.
Epilepsy (EP) is a neurological disorder characterized by abnormal, sudden neuronal discharges. Seizures increase extracellular glutamate levels, causing excitotoxic damage. Glutamate transporter type 1 (GLT-1) and its human homologue excitatory amino acid transporter-2 (EAAT2) clear 95% of extracellular glutamate.
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December 2024
School of Medical & Allied Sciences, K.R. Mangalam University, Gurugram, Haryana, India.
Background: Parkinson's disease is a hypokinetic disorder characterized by selective loss of dopaminergic in substantia nigra pars compacta (SNPc) region of mid-brain. Dopaminergic degeneration of neurons is considered to be due to oxidative stress, neuroinflammation, neurons mitochondrial dysfunction and glutamate excitotoxicity etc. Inosine a purine nucleoside has been reported to produce anti-oxidant, anti-inflammatory and neuromodulatory actions in previous studies.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Vanderbilt University Medical Center, Nashville, TN, USA.
Background: Manganese (Mn) is an essential metal that serves as a cofactor for metalloenzymes important in moderating the glutamate/glutamine cycle and other oxidative stress pathways. Typically, Mn is acquired through the diet, however, Mn overexposure can arise through drinking inadequately treated well water or inhalation of Mn-containing industrial byproducts. Mn toxicity disrupts dopaminergic neurotransmission resulting in a Parkinsonian disorder referred to as manganism.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Alabama at Birmingham, Birmingham, AL, USA.
Progranulin is a secreted pro-protein that is necessary for maintaining lysosomal function and exerts anti-inflammatory and neurotrophic effects in the brain. Loss-of-function GRN mutations, most of which cause progranulin haploinsufficiency, are a major autosomal dominant cause of frontotemporal dementia (FTD). Other GRN variants are associated with risk for FTD, Alzheimer's disease (AD) and Parkinson's disease.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
Background: Single nucleus RNA sequencing (snRNA-seq) has revolutionized our ability to dissect transcriptional profiles in specific cell types. While nuclear sequencing enhances analysis robustness, it captures only 20-50% of the cellular transcriptional information, limiting our comprehensive understanding of the cellular transcriptional ensemble. Therefore, we propose a computational approach to extract the cellular signal from bulk transcriptomic data from brain tissue, allowing us to investigate cell type-specific transcriptomic programs underlying neurodegeneration.
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