piperidines has been researched along with Brain-Concussion* in 4 studies
4 other study(ies) available for piperidines and Brain-Concussion
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A Novel Highly Sensitive Method for Measuring Inflammatory Neural-Derived APC Activity in Glial Cell Lines, Mouse Brain and Human CSF.
Neural inflammation is linked to coagulation. Low levels of thrombin have a neuroprotective effect, mediated by activated protein C (APC). We describe a sensitive novel method for the measurement of APC activity at the low concentrations found in neural tissue.. APC activity was measured using a fluorogenic substrate, Pyr-Pro-Arg-AMC, cleaved preferentially by APC. Selectivity was assessed using specific inhibitors and activators. APC levels were measured in human plasma, in glia cell lines, in mice brain slices following mild traumatic brain injury (mTBI) and systemic lipopolysaccharide (LPS) injection, and in cerebrospinal fluid (CSF) taken from viral meningoencephalitis patients and controls.. Selectivity required apixaban and alpha-naphthylsulphonylglycyl-4-amidinophenylalanine piperidine (NAPAP). APC levels were easily measurable in plasma and were significantly increased by Protac and CaCl. This method is selective and sensitive for the measurement of APC activity that significantly changes during inflammation in cell lines, animal models and human CSF. Topics: Animals; Brain; Brain Concussion; Cell Line; Cerebrospinal Fluid; Dipeptides; Endothelial Protein C Receptor; Humans; Inflammation; Lipopolysaccharides; Male; Mice; Mice, Inbred ICR; Models, Animal; Neuroglia; Piperidines; Protein C; Pyrazoles; Pyridones; Receptor, PAR-1; Thrombin | 2020 |
Post-blast treatment with Nociceptin/Orphanin FQ peptide (NOP) receptor antagonist reduces brain injury-induced hypoxia and signaling proteins in vestibulomotor-related brain regions.
Mild traumatic brain injury (mTBI) diagnoses have increased due to aggressive sports and blast-related injuries, but the cellular mechanisms and pathology underlying mTBI are not completely understood. Previous reports indicate that Nociceptin Orphanin/FQ (N/OFQ), an endogenous neuropeptide, contributes to post-injury ischemia following mechanical brain injury, yet its specific role in cerebral hypoxia, vestibulomotor function and injury marker expression following blast-induced TBI is not known. This study is the first to identify a direct association of N/OFQ and its N/OFQ peptide (NOP) receptor with TBI-induced changes following a single 80psi head blast exposure in male rats. N/OFQ and NOP receptor expression increased in brain tissue and plasma following TBI, concurrent with vestibular dysfunction but preceding hypoxia and appearance of injury markers compared to sham rats. A single post-blast treatment with the NOP receptor antagonist, SB-612111, transiently improved acute vestibulomotor performance. It also prevented increases in markers of TBI-induced hypoxia, pro-apoptotic proteins and injury seen 8-10days post-blast. This study reveals an apparent role for the N/OFQ-NOP receptor system in blast TBI and suggests potential therapeutic utility of NOP receptor antagonists for mTBI. Topics: Animals; Blast Injuries; Brain; Brain Concussion; Cycloheptanes; Hypoxia, Brain; Male; Motor Activity; Narcotic Antagonists; Neuroprotective Agents; Nociceptin Receptor; Piperidines; Proteome; Rats, Sprague-Dawley; Receptors, Opioid | 2018 |
Inhibition of Endocannabinoid Degradation Improves Outcomes from Mild Traumatic Brain Injury: A Mechanistic Role for Synaptic Hyperexcitability.
Topics: Animals; Astrocytes; Benzodioxoles; Brain Concussion; Endocannabinoids; Excitatory Postsynaptic Potentials; Male; Motor Activity; Piperidines; Rats; Rats, Sprague-Dawley; Rats, Wistar; Synapses; Treatment Outcome | 2017 |
Neuroprotective and antiamnesic effect of donepezil, a nicotinic acetylcholine-receptor activator, on rats with concussive mild traumatic brain injury.
In this study we evaluated the effect of donepezil on the neurodegeneration and behavioral impairments induced by mild traumatic brain injury (MTBI). Donepezil is an acetylcholinesterase inhibitor that is used to treat Alzheimer's disease. Donepezil was given orally to rats subjected to MTBI. Treatment with a single oral dose of donepezil (12mg/kg) immediately after injury significantly attenuated MTBI-induced neuronal death and cognitive impairment as measured by preservation of neurons in the CA1 region of the hippocampus and a water maze test respectively. However, these neuroprotective effects were prevented by concomitant injection of mecamylamine, a nicotinic acetylcholine-receptor (nAChR) antagonist, indicating that protection is mediated by nAChR activation. Topics: Animals; Brain; Brain Concussion; Brain Injuries; Cholinesterase Inhibitors; Disease Models, Animal; Donepezil; Hippocampus; Indans; Male; Maze Learning; Memory Disorders; Nerve Degeneration; Neuroprotective Agents; Nicotinic Agonists; Nicotinic Antagonists; Nootropic Agents; Piperidines; Rats; Rats, Sprague-Dawley; Receptors, Nicotinic; Treatment Outcome | 2008 |