The distribution of Fos, the protein product of the immediate early gene c-fos, was studied with immunocytochemistry in the adult male rat brain after nerve growth factor (NGF) administration. NGF was injected in the lateral cerebral ventricle through a previously implanted cannula. The total number of Fos-immunoreactive (ir) neurons in the brain was 2-3 times higher after NGF administration than in control animals (untreated or injected with cytochrome c). With respect to control rats, in the NGF-treated cases Fos-ir cells were more numerous in the anterior olfactory nucleus, in the medial prefrontal and anterior cingulate cortices, in the basal forebrain, in the preoptic and ventromedial nuclei of the hypothalamus, as well as anterior hypothalamic area, in the thalamic midline nuclei, and in some brainstem structures, such as the parabrachial nucleus. The relative quantitative increase of Fos-ir neurons varied in the different structures. In addition, Fos-ir neurons were evident after NGF administration in areas devoid of immunopositive cells in control animals. These included: frontoparietal and occipital cortical fields, the hypothalamic arcuate nucleus, and many brainstem structures, such as the dorsal nucleus of the lateral lemniscus, posterodorsal tegmental, medial and lateral vestibular, ventral cochlear, and prepositus hypoglossal nuclei. These findings demonstrate that the intracerebroventricular administration of NGF can induce c-fos expression in neurons in vivo. The distribution of Fos-ir neurons indicates that NGF can induce activation of functionally and chemically heterogeneous neuronal subsets in the brain.
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http://dx.doi.org/10.1016/0006-8993(93)91138-i | DOI Listing |
Neuroscience
December 2024
Institute of Translational Medicine, School of Medicine, Yangzhou University, Yangzhou 225009, China; Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, Yangzhou University, Yangzhou 225009, China. Electronic address:
Vascular obstruction often causes inadequate oxygen and nutrient supply to the brain. This deficiency results in cerebral ischemic injury, which significantly impairs neurological function. This review aimed to explore the neuroprotective and regenerative effects of nerve growth factor (NGF) in cerebral ischemic injury.
View Article and Find Full Text PDFCell Signal
December 2024
Research Service, Edward Hines Jr. Veterans Administration Hospital, Hines, IL, USA; Department of Molecular Pharmacology and Neuroscience, Loyola University Chicago, Health Sciences Division, Maywood, IL, USA.
The nerve growth factor (NGF) receptor TrkA is a tightly regulated receptor tyrosine kinase that activates neuronal signaling pathways promoting cell survival in addition to axonal and dendritic outgrowth. Previously, we showed that NGF and TrkA signaling is altered in neuron-like PC12 cells that overexpress Nogo-A, a protein known to influence axonal outgrowth and dendritic arborization associated with neuronal plasticity. In the present report, we provide evidence for changes in NGF-mediated receptor-level and downstream signaling that occur in cells overexpressing Nogo-A.
View Article and Find Full Text PDFJ Pain Res
November 2024
Department of Clinical Laboratory Science, College of Health Sciences, Catholic University of Pusan, Busan, 46252, Republic of Korea.
Background: Paclitaxel (PTX) can induce chemotherapy-induced peripheral neuropathy (CIPN) as a side effect. The aim of this study was to understand the neurochemical changes induced by NGF/TrkA signaling in PTX-induced neuropathic pain.
Methods: The PTX-induced CIPN mouse model was evaluated using nerve conduction velocity (NCV) and behavioral tests.
Mol Psychiatry
November 2024
Department of Pharmacology, School of Medicine, University of Crete, Heraklion, 71003, Greece.
Alzheimer's Disease (AD) is an incurable and debilitating progressive, neurodegenerative disorder which is the leading cause of dementia worldwide. Neuropathologically, AD is characterized by the accumulation of Aβ amyloid plaques in the microenvironment of brain cells and neurovascular walls, chronic neuroinflammation, resulting in neuronal and synaptic loss, myelin and axonal failure, as well as significant reduction in adult hippocampal neurogenesis. The hippocampal formation is particularly vulnerable to this degenerative process, due to early dysfunction of the cholinergic circuit.
View Article and Find Full Text PDFGen Physiol Biophys
November 2024
Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
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