It is well known that nitric oxide (NO), within the paraventricular nucleus (PVN) of the hypothalamus, mediates sympatho-inhibition via an inhibitory GABA-ergic mechanism. Furthermore, the inhibitory GABA-ergic mechanism is impaired in the spontaneously hypertensive rat (SHR). These data suggest that the NO system, within the PVN, may also be impaired in the SHR. In addition, previous studies have documented that daily exercise attenuates the development of tachycardia, hypertension and blood pressure related cardiovascular disease risk factors in SHR. These data suggest that daily exercise enhances the inhibitory GABA-ergic and/or NO systems. Therefore, this study was designed to test the hypothesis that hypertension, in the SHR, is associated with a lower number of NADPH-diaphorase (a commonly used marker for neuronal NOS activity) positive neurons within the PVN and that daily exercise increases the number of NOS positive neurons. Using a standard histochemical protocol, NOS positive neurons were measured in the PVN, supraoptic nucleus, median preoptic area, lateral hypothalamus, nucleus of the tractus solitarius and rostral ventrolateral medulla. Results document that SHR have significantly fewer NOS-positive neurons in the PVN than their genetic control, the Wistar-Kyoto (WKY) rats (110+/-11 versus 139+/-17). Furthermore, daily exercise increased the number of NOS positive neurons in the SHR to levels seen in the WKY rats. These data demonstrate that hypertension, in the SHR, is associated with a lower number of NOS positive neurons within the PVN and that daily exercise increases the number of NOS positive neurons within the PVN.
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http://dx.doi.org/10.1016/s0006-8993(02)03400-5 | DOI Listing |
Brain
January 2025
Translational Neuroimaging Laboratory, Montreal Neurological Institute, H3A 2B4, Montreal, Canada.
Plasma phosphorylated tau biomarkers open unprecedented opportunities for identifying carriers of Alzheimer's disease pathophysiology in early disease stages using minimally invasive techniques. Plasma p-tau biomarkers are believed to reflect tau phosphorylation and secretion. However, it remains unclear to what extent the magnitude of plasma p-tau abnormalities reflects neuronal network disturbance in the form of cognitive impairment.
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January 2025
Neuroimmunology Research Group, Netherlands Institute for Neuroscience, Amsterdam, Netherlands.
Introduction: Remyelination of demyelinated axons can occur as an endogenous repair mechanism in multiple sclerosis (MS), but its efficacy varies between both MS individuals and lesions. The molecular and cellular mechanisms that drive remyelination remain poorly understood. Here, we studied the relation between microglia activation and remyelination activity in MS.
View Article and Find Full Text PDFJ Med Biochem
November 2024
People's Hospital of Xuyi County, Department of Pathology, Huaian, Jiangsu Province, China.
Background: Serum neuritin and neuron-specific enolase (NSE) have predictive value for the prognosis of patients with combined traumatic brain injury (TBI) and spinal cord injury (SCI). Studying their predictive effects has positive value for disease control and treatment.
Methods: Sixty patients with combined TBI and SCI were recruited and rolled into three groups according to prognosis: Group I (n=42, favourable prognosis), Group II (n=11, poor prognosis), and Group III (n=7, death).
Spine (Phila Pa 1976)
January 2025
Department of Orthopedics, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People's Republic of China.
Study Design: Subgroup analysis of a retrospective clinical and animal trial [Study of different doses of methylprednisolone on functional recovery of spinal cord injury].
Objective: The aimed to investigate the efficacy of low-dose methylprednisolone regimens in promoting neural repair after SCI.
Summary Of Background Data: Spinal cord injury (SCI) can result in sensory, motor, and autonomic nerve dysfunction, often leading to disability or death.
Ann Neurol
January 2025
Neuroscience Research Center, Department of Medical and Surgical Sciences, University "Magna Graecia", Catanzaro, Italy.
Objective: Progressive Supranuclear Palsy (PSP) is a severe neurodegenerative disease characterized by tangles of hyperphosphorylated tau protein and tufted astrocytes. Developing treatments for PSP is challenging due to the lack of disease models reproducing its key pathological features. This study aimed to model sporadic PSP-Richardson's syndrome (PSP-RS) using multi-donor midbrain organoids (MOs).
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