[NET WATER TRANSPORT VIA RAT COLON EPITELIUM UNDER THE EXPERIMENTAL DYSBIOSIS].

The aim of the present study was to investigate the effect of cephalosporin antibiotic ceftriaxone (50 mg/kg, i/m) and mac- rolide antibiotic azithromycin (15 mg/kg, per.os.) on net water transport across rat colonic epithelium. Study was done on male Wistar rats (180-250 g). Azithromycin or ceftriaxone was injected daily for 5 days. Net water transport was evaluated on the 6th day by isolated colonic loop perfusion technique in vivo on anaesthetized rats. Treatment with azithromycin increased 2,4-fold the absorption of water, while ceftriaxone caused decrease 1,9-fold water absorption. The antibiotics treatment within five days didn't change the composition of the fecal and colonic parietal microbiota. Azithromycin-induced increase in water absorption was associated with upregulation of AQP 8 water channel expression (P < 0.05) in colonic mucosa. Ceftriaxone treatment didn't change protein level of AQP8 but induced pro-inflammatory changes in colonic mucosa structure and mast cells degranulation. We showed for the first time the opposite effects ofmacrolide and cephalosporin antibiotics on net water transport across rat colonic epithelium.

Inducible nitric oxide synthase gene deficiency counteracts multiple manifestations of peripheral neuropathy in a streptozotocin-induced mouse model of diabetes.

AIMS/HYPOTHESIS: Evidence for the importance of peroxynitrite, a product of superoxide anion radical reaction with nitric oxide, in peripheral diabetic neuropathy is emerging. The role of specific nitric oxide synthase isoforms in diabetes-associated nitrosative stress and nerve fibre dysfunction and degeneration remains unknown. This study evaluated the contribution of inducible nitric oxide synthase (iNOS) to peroxynitrite injury to peripheral nerve and dorsal root ganglia and development of peripheral diabetic neuropathy. METHODS: Control mice and mice with iNos (also known as Nos2) gene deficiency (iNos ( -/- )) were made diabetic with streptozotocin, and maintained for 6 weeks. Peroxynitrite injury was assessed by nitrotyrosine and poly(ADP-ribose) accumulation (immunohistochemistry). Thermal algesia was evaluated by paw withdrawal, tail-flick and hot plate tests, mechanical algesia by the Randall-Selitto test, and tactile allodynia by a von Frey filament test. RESULTS: Diabetic wild-type mice displayed peroxynitrite injury in peripheral nerve and dorsal root ganglion neurons. They also developed motor and sensory nerve conduction velocity deficits, thermal and mechanical hypoalgesia, tactile allodynia and approximately 36% loss of intraepidermal nerve fibres. Diabetic iNos ( -/- ) mice did not display nitrotyrosine and poly(ADP-ribose) accumulation in peripheral nerve, but were not protected from nitrosative stress in dorsal root ganglia. Despite this latter circumstance, diabetic iNos ( -/- ) mice preserved normal nerve conduction velocities. Small-fibre sensory neuropathy was also less severe in diabetic iNos ( -/- ) than in wild-type mice. CONCLUSIONS/INTERPRETATION: iNOS plays a key role in peroxynitrite injury to peripheral nerve, and functional and structural changes of diabetic neuropathy. Nitrosative stress in axons and Schwann cells, rather than dorsal root ganglion neurons, underlies peripheral nerve dysfunction and degeneration.

[Effect of monoamines and testosterone on hypothalamo-gonadal complex of Japanese quail (an electrophysiological and morphometric study)]. / Vplyv monoaminiv i testosteronu na hipotalamo-honadnyi kompleks iapons'kykh perepeliv (elektrofiziolohichne ta morfometrychne doslidzhennia).

Effects of biogenic amines, testosterone and melatonin both on the developing electrical activity of hypothalamic arcuate nucleus (NA) and morphology of testis and NA neurocytes during maturation in birds (Coturnix coturnix japonica) were tested. Slow [symbol: see text]-frequency was shown to prevail at quail NA electrical activity. NA spectral power gradually enlarges during maturation. The data confirm the evidence that catecholamines induce acceleration of sexual maturation in birds mainly via brain alpha-adrenoreceptors, while dopamine- and serotoninergic brain systems cause deceleration of maturation. Morning or evening treatments with melatonin (5 mkg/100 g bw) and evening ones (50 mkg/100 g bw) were revealed to result in activation of hypothalamic-testicular axis, and high-dose morning melatonin injections don't have any influence. Significant correlation was registered between the spectral power of NA neurocytes and profile area of their cellular nuclei. Total EA was demonstrated to vary at [symbol: see text]1- and, lesser, [symbol: see text]2-, [symbol: see text]-, and 6-ranges of spectrum, and was insignificant at B-range.

[The electrical activity of the hypothalamic arcuate nucleus and the morphofunctional characteristics of the gonads in birds during blockade and stimulation of the beta-adrenergic receptors]. / Elektrichna aktyvnist' arkuatnoho iadra hipotalamusa ta morfofunktsional'na kharakterystyka honad ptakhiv pry blokadi ta stymuliatsiï beta-adrenerhichnykh retseptoriv.

Beta-adrenoreceptors agonist isadrine as shown by measurement of hypothalamic arcuate nucleus (AN) summary electrical activity and by morphometry of its neurons and testis does not result in significant acceleration of maturation in maturing (4-6 week old) male japanese quails (Coturnix coturnix japonica). Anapryline-induced blockade of beta-adrenoreceptors leads to small inhibiting of the reproductive complex. This findings confirm our previous works, according to which brain beta-adrenergic system does not play leading role in regulation of maturation in birds. The direct correlation between morphometrical and electrophysiological features of AN neurosecretory cells was demonstrated as well.