Search Results - (Author, Cooperation:T. L. Horvath)

2015-02-25

Nature Publishing Group (NPG)

0028-0836

1476-4687

Biology

Chemistry and Pharmacology

Medicine

Natural Sciences in General

Physics

Animals ; Cannabinoids/*pharmacology ; Eating/*drug effects/*physiology ; Energy Metabolism/drug effects ; Hypothalamus/*cytology/drug effects/physiology ; Ion Channels/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondria/drug effects/metabolism ; Mitochondrial Proteins/metabolism ; Naloxone/pharmacology ; Neurons/*drug effects/*metabolism ; Pro-Opiomelanocortin/*metabolism ; Receptor, Cannabinoid, CB1/agonists/metabolism ; Satiety Response/drug effects/physiology ; alpha-MSH/secretion ; beta-Endorphin/metabolism

2014-01-07

Nature Publishing Group (NPG)

0028-0836

1476-4687

Biology

Chemistry and Pharmacology

Medicine

Natural Sciences in General

Physics

Administration, Intranasal ; Animals ; Animals, Newborn ; Anoxia/genetics/metabolism/pathology/physiopathology ; Brain Injuries/*congenital/*drug therapy/pathology/prevention & control ; Cell Differentiation/drug effects ; Cell Division/drug effects ; Cell Lineage/drug effects ; Cell Survival/drug effects ; Demyelinating Diseases/congenital/metabolism/pathology/prevention & control ; Disease Models, Animal ; Epidermal Growth Factor/administration & dosage/*pharmacology/*therapeutic use ; Humans ; Infant, Premature, Diseases/drug therapy/metabolism/pathology ; Male ; Mice ; Molecular Targeted Therapy ; Oligodendroglia/cytology/*drug effects/metabolism/pathology ; Receptor, Epidermal Growth Factor/genetics/metabolism ; Regeneration/drug effects ; Signal Transduction/drug effects ; Stem Cells/cytology/drug effects/metabolism ; Time Factors

2011-06-11

American Association for the Advancement of Science (AAAS)

0036-8075

1095-9203

Biology

Chemistry and Pharmacology

Computer Science

Medicine

Natural Sciences in General

Physics

Alkaloids/metabolism ; Animals ; Azocines/metabolism ; Eating/*drug effects ; Ganglionic Stimulants/*pharmacology ; Male ; Melanocortins/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neurons/drug effects/metabolism ; Nicotine/*pharmacology ; Nicotinic Agonists/pharmacology ; Pro-Opiomelanocortin/*metabolism ; Quinolizines/metabolism ; Receptors, Nicotinic/metabolism

1365-2826

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

The effects of leptin on food intake, metabolism, sleep patterns and reproduction may be mediated, in part, by the midbrain serotonergic systems. Here, we report on the distribution of neurones that accumulate leptin in the raphe nuclei of male and female rats after intracerebroventricular administration of mouse recombinant leptin labelled with digoxigenin. Direct leptin-targeted cells were present in the periventricular grey, pontine and raphe nuclei. Confocal microscopy revealed that raphe neurones which accumulated leptin were predominantly serotonergic. The temporal pattern of leptin accumulation by raphe neurones showed a marked gender difference: 6 h after leptin administration, all male and female rats showed massive leptin binding in the dorsal raphe, while 30 min after leptin treatment, only 10% of male rats exhibited leptin-labelled cells in contrast to 50% of females. The present observations reveal that leptin can be selectively accumulated by serotonergic neurones in the raphe nuclei and that this mechanism is gender specific. These findings support the idea that the midbrain serotonergic system is an important mediator of the effects of leptin on brain function and may provide an explanation for gender differences in metabolism regulation and its coordination with higher functions of the brain.

Electronic Resource

1365-2826

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

To assess their role in the regulation of gonadotropin secretion in primates, we determined the number of synaptic connections on gondotropin releasing hormone (GnRH)- and non-GnRH neurones of the arcuate nucleus of ovariectomized (OVX) and OVX plus oestradiol benzoate-treated African green monkeys. After 24 h (day 1), 48 h (day 2) and 8 days (day 8), we performed immunostaining for GnRH. Using electron microscopy, synapses on GnRH- and randomly selected non-GnRH neurones were counted and characterized according to the classification of Gray (symmetric/inhibitory or asymmetric/excitatory). Serum concentrations of oestradiol (OVX) needed to 232 pg/ml on day 1, 63 pg/ml on day 2 and 45 pg/ml on day 8. Concentrations of luteinizing hormone (LH) fell after ovariectomy to 9 µg/ml on day 1, surged to 93 µg/ml on day 2 and declined again by day 8. (a) Ten days after ovariectomy, there were no synapses on GnRH neurones, whereas non-GnRH cells received substantial inhibitory innervation and moderate excitatory input. (b) On day 1, GnRH neurones had highest numbers of inhibitory synapses, while inhibitory synapses on non-GnRH neurones decreased, whereas numbers of excitatory synapses remained relatively unchanged compared to OVX monkeys. (c) By day 2, synapses on GnRH neurones decreased, while synapses increased on non-GnRH cells compared to day 1. (d) On day 8, the most pronounced alteration on GnRH cells was an elevated inhibitory input while non-GnRH neurones received the fewest synapses compared to day 2. We conclude that during an oestrogen-induced LH surge, synapses on GnRH- and mixed non-GnRH neurones are differentially regulated. These findings suggest that oestrogen modulation of arcuate nucleus synapses may be important in the regulation of gonadotropin secretion in monkeys.

Electronic Resource

1573-6830

estradiol ; arcuate nucleus ; gonadotropin releasing hormone ; ovarian cycle ; synaptogenesis ; synaptic plasticity ; GABA ; dopamine ; β-endorphin ; neural cell adhesion molecule ; insulin-like growth factor I

Springer Online Journal Archives 1860-2000

Biology

Summary 1. Studies conducted on the rat arcuate nucleus, an area involved in the development and control of LH and FSH secretion, have shown the existence of hormonally regulated developmental sex differences in synaptic patterns and estrogen-induced synaptic plasticity during adult life. Several questions raised by these findings are examined in this review: 2. The mechanisms of estrogen-regulated developmental synaptogenesis. These include the role of glycocalyx glycoproteins in neuronal membranes, neural cell adhesion molecules, and insulin-like growth factor I. 3. The relationship among circulating estrogen, gonadotropin levels, and hypothalamic synaptic plasticity. Recent evidence for the role of GABAergic and dopaminergic synaptic inputs and POMC projections from the arcuate nucleus to the GnRH cells is discussed. 4. The synaptologic basis of age-related failure of positive feedback. The role of the cumulative effect of repeated preovulatory synaptic retraction and reapplication cycles on sensescent constant estrus is analyzed.

Electronic Resource