Repeated infusions of 6-hydroxydopamine (6-OHDA) into the third ventricle of the rabbit brain in dosages shown to depress hypothalamic norepinephrine (NE) by more than 80% failed to block the copulation-induced ovulatory surge of LH release from the adenohypophysis in estrogen-primed, multiparous New Zealand White does. Only when infusion of the neurotoxin produced a basal hypothalamic lesion did it intercept the coital stimulus and prevent LH release. In 5 rabbits the initial infusion of 6-OHDA stimulated an LH surge presumably by activating NE release from noradrenergic nerve endings. The failure of chronic depletion of hypothalamic NE to prevent coitally-induced LH release suggests that the transmitter may normally play only a modulatory role in hypothalamopituitary activation in the reflex ovulator, as has also been proposed for its function in cyclic ovulation in the rat. The results suggest that alternative systems may be brought into play to subserve reproductive mechanisms when hypothalamic NE is chronically depleted.
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http://dx.doi.org/10.1159/000123035 | DOI Listing |
J Integr Neurosci
January 2025
Department of Neurosurgery, Affiliated Hospital of Southwest Medical University, 646000 Luzhou, Sichuan, China.
Background: Recent studies suggest that the anterior limb of the internal capsule may be an area of convergence for multiple compulsion loops. In this study, the role of different dopaminergic compulsion loops in the mechanism of obsessive-compulsive disorder (OCD) was investigated by selectively damaging dopaminergic neurons or fibers in the corresponding targets with 6-hydroxydopamine (6-OHDA) and depicting the anatomical map of various compulsion loops located in the anterior limb of the internal capsule.
Methods: A total of 52 male Sprague Dawley (SD) rats were exposed to either saline (1 mL/kg, NS group, n = 6) or quinpirole (QNP, dopamine D2-agonist, 0.
Eur J Neurosci
January 2025
Department of Anatomy, School of Biomedical Sciences, University of Otago, Dunedin, New Zealand.
New therapeutic agents developed for treating neurological disorders are often tested successfully on rodents. Testing in an appropriate large animal model where there is longer lifespan and comparable brain size to humans should improve translational success and is frequently expected by regulatory bodies. In this project, we aimed to establish a novel sheep model of Parkinson's disease as a large-brained experimental model for translational research.
View Article and Find Full Text PDFNeuropharmacology
January 2025
Department of Anatomy & Neuroscience, School of Medicine, University College Cork (UCC), Cork, Ireland; APC Microbiome Ireland, UCC, Cork, Ireland. Electronic address:
Degeneration of midbrain nigrostriatal dopaminergic neurons is a pathological hallmark of Parkinson's disease (PD). Peripheral delivery of a compound(s) to arrest or slow this dopaminergic degeneration is a key therapeutic goal. Pan-inhibitors of histone deacetylase (HDAC) enzymes, key epigenetic regulators, have shown therapeutic promise in PD models.
View Article and Find Full Text PDFEfforts to develop disease-modifying treatments for Parkinson's disease (PD) have been hindered by the lack of animal models replicating all hallmarks of PD and the insufficient attention to extra-nigrostriatal regions pathologically critical for the prodromal appearance of non-motor symptoms. Among PD models, 6-hydroxydopamine (6-OHDA) infusion in mice has gained prominence since 2012, primarily focusing on the nigrostriatal region. This study characterized widespread tyrosine hydroxylase-positive neuron and fiber loss across the brain following a unilateral 6-OHDA (20 μg) infusion into the dorsal striatum.
View Article and Find Full Text PDFBrain Commun
October 2024
Department of Biomedical Engineering, Stevens Institute of Technology, Hoboken, NJ 07030, USA.
Parkinson's disease is a neurodegenerative disease characterized by gait dysfunction in the advanced stages of the disease. The unilateral 6-hydroxydopamine toxin-induced model is the most studied animal model of Parkinson's disease, which reproduces gait dysfunction after >68% dopamine loss in the substantia nigra pars compacta. The extent to which the neural activity in hemi-parkinsonian rats correlates to gait dysfunction and dopaminergic cell loss is not clear.
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