ATR-FTIR spectroscopy to evaluate serum protein expression in a murine cerebral ischemia model.

Stroke is a prevalent vascular disease that causes disability and death worldwide. Molecular techniques have been developed to assess serum concentrations of biomarkers associated with this disease, such as some proteins. ATR-FTIR was proposed as an alternative technique to determine protein expression during the early stages of stroke. Serum samples from sham, ischemic, and ischemic treated with estradiol benzoate (EB; as a neuroprotective agent) male rats were evaluated at 0, 2-, 4-, 6-, 12-, and 24-hours post-ischemia. The analysis was developed in the mid-infrared region but mainly focused on the protein region (1500-1700 cm-1), where it was possible to observe the modulation in the absorbance intensity. The peaks at 1545, 1645, 1635, and 1650 cm-1 associated with amide II, amide I, ß-sheets, and α-helixes, respectively, were prominent peaks where protein modulation was observed. The results demonstrate that infrared spectroscopy could be a good alternative technique to determine the modulation of protein expression during stroke events.

Apelin-13 facilitates lordosis behavior following infusions to the ventromedial hypothalamus or preoptic area in ovariectomized, estrogen-primed rats.

In normal hormonal conditions, increased neuronal activity in the ventromedial hypothalamus (VMH) induces lordosis whereas activation of the preoptic area (POA) exerts an opposite effect. In the present work, we explored the effect of bilateral infusion of different doses of the apelin-13 (0.37, 0.75, 1.5, and 15 µg) in both brain areas on the expression of lordosis behavior. Lordosis quotient and lordosis reflex score were performed at 30, 120, and 240 min. Weak lordosis was observed following the 0.37 µg dose of apelin-13 at 30 min in the VMH of EB-primed rats; however, the rest of the doses induced significant lordosis relative to the control group. At 120 min, all doses induced lordosis behavior, while at 240 min, the highest dose of 15 µg did not induce significant differences. Interestingly, only the 0.75 µg infusion of apelin in the POA induced significant lordosis at 120 and 240 min. These results indicate that apelin-13 acts preferably in HVM and slightly in POA to initiate lordosis behavior in estrogen-primed rats.

Chronobiotic effect of melatonin in experimental optic neuritis.

Optic neuritis (ON) is an inflammatory condition of the optic nerve, which leads to retinal ganglion cell (RGC) loss. A subset of RGCs expressing the photopigment melanopsin regulates non-image-forming visual system (NIFVS) functions such as pupillary light reflex (PLR) and circadian rhythms. Melatonin is a chronobiotic agent able to regulate the circadian system. We analyzed the effect of ON on the NIFVS, and the effect of melatonin on the NIFVS alterations induced by ON. For this purpose, optic nerves from male Wistar rats received vehicle or bacterial lipopolysaccharide (LPS), and one group of animals received a subcutaneous pellet of melatonin or a sham procedure. The NIFVS was analyzed in terms of: i) blue light-evoked PLR, ii) the communication between the retina and the suprachiasmatic nuclei (by anterograde transport, and ex vivo magnetic resonance images), iii) locomotor activity rhythm, and iv) Brn3a(+) and melanopsin(+) RGC number (by immunohistochemistry). Experimental ON significantly decreased the blue light-evoked PLR, induced a misconnection between the retina and the suprachiasmatic nuclei, decreased Brn3a(+) RGCs, but not melanopsin(+) RGC number. A bilateral injection of LPS significantly increased the light (but not dark) phase locomotor activity, rhythm periodicity, and time of offset activity. Melatonin prevented the decrease in blue light-evoked PLR, and locomotor activity rhythm alterations induced by ON. These results support that ON provoked alterations of the circadian physiology, and that melatonin could restore the circadian system misalignment.

Tibolone facilitates lordosis behavior through estrogen, progestin, and GnRH-1 receptors in estrogen-primed rats.

A dose-response study was made of the broad-spectrum gonadal steroid agonist tibolone (TBL) on lordosis behavior in estradiol benzoate (EB: 5 µg) primed rats. Doses of TBL (0, 1, 4, and 16 µg) were infused to the right lateral ventricle 2 h before testing. The highest dose increased lordosis quotients significantly at 240 min and 360 min following infusion. However, the intensity of lordosis was weak. In experiment 2, the TBL dose of 16 µg was selected to determine whether tamoxifen (TMX), RU486, or antide could modify the lordosis response to TBL. Infusions of the three compounds, before TBL, significantly attenuated the TBL-induced facilitation of lordosis. The results suggest that TBL stimulates lordosis by activating estrogen, progesterone, and may do so by downstream stimulation of GnRH release. The physiological role TBL plays in controlling lordosis behavior remains to be determined.