Dora Zelena, Ophelie Menant, Frederic Andersson and Elodie Chaillou
The periaqueductal gray (PAG) is less referred in relationship with emotions than other parts of the brain (e.g. cortex, thalamus, amygdala), most probably because of the difficulty to reach and manipulate this small and deeply lying structure. After defining how to evaluate emotions, we have reviewed the literature and summarized data of the PAG contribution to the feeling of emotions focusing on the behavioral and neurochemical considerations. In humans, emotions can be characterized by three main domains: the physiological changes, the communicative expressions, and the subjective experiences. In animals, the physiological changes can mainly be studied. Indeed, early studies have considered the PAG as an important center of the emotions-related autonomic and motoric processes. However, in vivo imaging have changed our view by highlighting the PAG as a significant player in emotions-related cognitive processes. The PAG lies on the crossroad of networks important in the regulation of emotions and therefore it should not be neglected. In vivo imaging represents a good tool for studying this structure in living organism and may reveal new information about its role beyond its importance in the neurovegetative regulation.
Heba A. Abdel-Hamid, Mona M. I. Abdalla, Nagwa M. Zenhom and Rasha F. Ahmed
Objective. The aim of the present study was to assess the effect of the PYY3–36, as a potential therapy for the type 2 diabetes mellitus (T2DM), induced by high fat diet (HFD) and an intraperitoneal (i.p.) administration of streptozotocin (STZ) in albino rats.
Methods. Forty adult male albino Wistar rats were divided into: 1) control group (C, in which the rats were fed with a standard diet and received vehicle; 2) diabetic group (D, in which T2DM was induced by feeding the rats with HFD for four weeks followed by a single i.p. injection of 35 mg/kg STZ, this group was also allowed to have HFD till the end of the study; and 3) D+PYY3–36 group (in which the diabetic rats were treated with 50 µg/kg i.p. PYY3–36 twice a day for one week). Food intake, water intake, body weight (b.w.), visceral fat weight (VFW), liver glycogen content, serum levels of glucose, insulin, and interleukin-6 (IL-6), were measured. Homeostatic-model assessment of insulin resistance (HOMA-IR) was estimated. The gene expression of the hypothalamic neuropeptide Y (NPY) and visceral nuclear factor kappa B (NF-κB) were assessed by a reverse transcription polymerase chain reaction (RT-PCR).
Results. The PYY3–36 administration to the diabetic group of rats significantly increased the serum insulin levels and liver glycogen content, decreased the body weight, VFW, food intake, water intake, serum levels of the glucose, IL-6, and HOMA-IR. It also decreased the expression of both the hypothalamic NPY and the visceral fat NF-κB.
Conclusion. With respect to the fact of improved insulin release and enhanced insulin sensitivity (an effect that may be mediated via suppressing accumulation of visceral fat and inflammatory markers), in the rats treated with PYY3–36, the PYY3–36 might be considered for the future as a promising therapeutic tool in T2DM.
Objective. A disturbance of sensorimotor gating measured by prepulse inhibition of acoustic startle (PPI) is one of the best tests of the schizophrenia-like behavior. Vasopressin was implicated in the development of schizophrenia; therefore, the naturally occurring vasopressin-deficient Brattleboro rat has been suggested to be a reliable non-pharmacological animal model. However, previous studies focusing on PPI deficit did not use proper control and despite clear gender differences in the development of the disorder, the effect of gender has been mostly neglected.
Methods. First, we compared the „noise” and „tone” type prepulse at 73-77-81 dB intensity during the light or dark phase using small (~150 g) or big (~500 g) Wistar rats. The test parameters were validated by a pharmacological schizophrenia model (30 mg/kg ketamine i.p.). Than male, female, and lactating vasopressin-deficient animals were compared with +/+ ones.
Results. We established that the prepulse “noise” type is not optimal for PPI testing. The cycle of the day as well as the body weight had no effect on PPI. Even if we compared vasopressin-deficient animals with their closely related +/+ controls, the PPI deficiency was visible with more pronounced effect at 77 dB prepulse intensity similarly to pharmacological schizophrenia model. Despite our expectation, the gender as well as lactation had no effect on the vasopressin-deficiency induced PPI deficit.
Conclusions. The present data confirmed and extended our previous studies that vasopressin-deficient rat is a good model of schizophrenia. It seems that female as well as lactating Brattleboro rats are useful tools for testing putative novel antipsychotics in line with special attention required for schizophrenic women.
Shokoufeh Taherkhani, Fatemeh Moradi, Masoumeh Hosseini, Mohsen Alipour and Hadi Feizi
Objective. Ghrelin, a 28 amino acid peptide, has diverse physiological roles. Phosphatidylino-sitol-bisphosphate 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) are involved in some of the recognized actions of ghrelin. It has been shown that ghrelin upregulates HOXB4 gene expression but the real mechanism of this effect is not clear.
Methods. Rat bone marrow stromal cells (BMSCs) were cultured in DMEM. BMSCs were treated with ghrelin (100 μM) for 48 h. Real-time PCR for HOXB4 was performed from Control (untreated BMSCs), BG (BMSCs treated with 100 µM ghrelin), PD (BMSCs treated with 10 µM PD98059, a potent inhibitor of mitogen-activated protein kinase, and 100 µM ghrelin), LY (BM-SCs treated with 10 µM LY294002, a strong inhibitor of phosphoinositide 3-kinase, and 100 µM ghrelin) and SY (BMSCs treated with 10 µM LY294002 plus 10 µM PD98059, and 100 µM ghrelin) groups. Relative gene expression changes were determined using Relative expression software tool 9 (REST 9).
Results. HOXB4 gene has been overexpressed in ghrelin-treated BMSCs (p<0.05). PI3K inhi-bition by LY294002 significantly downregulated the ghrelin-induced overexpression of HOXB4 (p<0.05).
Conclusion. We can conclude that ghrelin, through PI3K/Akt pathway, may improve BMSC transplantation potency by reducing its apoptosis. Moreover, upregulating HOXB4 in BMSC and its possible differentiation to HSCs might in the future open the doors to new treatment for hematologic disorders. Therefore, activating the PI3K/Akt pathway, instead of using a non-specific inducer, could be the principal point to increase the efficiency of BMSC-based cell therapies in the future.
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