Introduction: Aluminium is an important voltage sensitive calcium channels blocker and enter the body from different sources. This ion interfere with biological function of Ca2+ ion. Because the arcuate nucleuse has beta-endorphin neuron which effect on pain control, this experiment was performed to study the effect of aluminium microinjection on male rat's pain threshold.Materials and method: The experiment performed on four group of male rats (n=36), that the actuate nucleus were bilateral cannulated by sterotaxic surgery. Test group received 100 nl ACSF containing 0.15 pmol aluminium in each side of the arcuate nucleus for 15 days. Two series of these animals after cannulation received the same volume of ACSF with pH =7.2 and 3.4. The shame control group did not received any agent after cannulation. At the end of experiment, animals pain threshold was measured by tail emmersion method. Statistic test was student t-test. The results are expressed as mean±SE and P<0.05 were significant.Results: Results showed that the pain threshold in that group received aluminum in arcuate nucleus (6.78±0.34 mse) decrease significantly compared with shame control pain threshold (8.61±0. mse) group (p<0.05).Conclusion: These result indicate that injection of aluminum in male rat's arcuate nucleus, can be affect on pain threshold. Further studies will probably show the exact mechanism of aluminum ion on pain threshold.

Background and Aim: Although the degeneration of nucleus pulposus cells (NPCs) is one of the main causes of intervertebral disc degeneration, the molecular complications of this disease have yet to be clarified. The ability of stem cells to differentiate into different types of cells, especially NPCs, has attracted much attention. This study aimed to investigate the role of genes with differential expressions in stem cell differentiation into NPCs and to identify the salient signaling pathways involved. Since there has not been an extensive study on the important genes of NPC cell differentiation, it is necessary to investigate this process. Methods: RNA-sequencing raw files of stem cell samples and differentiated NPCs with the accession number GSE122429 from the GEO database. The samples were analyzed, and genes with differential expressions were isolated in the R programming language with the Limma package via logarithmic fold changes (logFC) ≠, 3 and adjusted P-values < 0. 05. Functional analysis was conducted on the signaling pathways and biological processes of the differentially expressed genes using the Enrichr database. Results: In NPCs, 170 genes were upregulated, and 102 genes were downregulated. The functional analysis revealed that the differentially expressed genes were mostly involved in the extracellular matrix organization, collagen organization, and positive cellular processes. The study of signaling pathways identified the neural crest differentiation pathway as the most significant pathway in the evaluated samples. Considering logFC ≠, 3, overexpression was detected in MSX2, OLIG3, WNT3A, TWIST1, PAX3, RHOB, CDH6, COL2A1, CDH1, ZIC1, PMP22, SNAI2, and MSX1, all of which are involved in the neural crest differentiation pathway. Conclusion: Our results should expand the knowledge of the molecular pathways involved in stem cell differentiation into NPCs and proffer new clues to the treatment of intervertebral disc degeneration. Nonetheless, more detailed molecular studies are needed to determine the reliable biomarkers of NPCs.

Introduction: The septal region is part of the telencephalon and is a component of the limbic system. The lateral septal area (LS); largest nuclear mass in this region, plays a pivotal role in various physiological processes, such as aggression, emotion, thermoregulation, water and food intake and sexual behaviour. To support the functional analysis of this brain area in the rat, the sources of its afferents were determined using HRP retrograde tract tracing technique. Materials and Methods: One microliter of HRP (25%, sigma) injected by stereotaxic surgery and through hamilton syringe septum (LS) 48 hours after surgery. Perfusion fixation and sectioning on animal brain, were performed. TMB histochemistry reaction using HRP was used for this purpose. Results: Retrogradely labeled perikarya was observed ipsilaterally in diagonal band of Broca and hippocampus in telencephalon, paraventricular, parataenial, reuniens, lateroposterior, interanterodorsal and mediodorsal nuclei of the thalamus, lateral preoptic area, anterior and dorsal hypothalamus, lateral hypothalamus/tuber cinereum, perifornical area, posterior hypothalamus, submammillothalamic, supramammillary and lateral mammillary nuclei in diencephalon, ventral tegmental area, interfascicularis nucleus, interpeduncular nucleus, raphe nuclei, tegmental nuclei, central gray area and locus coeruleus in brain stem. Conclusion: These results indicate that according to its connections, the LS is an integrative center that receives cognitive, behavioural and autonomic informations and probably is a center for modulating these informations.

Introduction: The Bed nucleus stria terminalis (BST) is a part of the limbic system. It was recently shown that chemical stimulation of the BST by L-glutamate elicited cardiovascular depressive responses. In the present study, we have investigated the possible cardiovascular role of the GABAergic receptors in BST by microinjection of its agonist and antagonists.Methods: Experiments were performed on 21 anaesthetized rats. Drugs were microinjected into the BST in volume of 50 nl using streotaxic apparatus. Blood pressure and heart rate were recorded before and throughout each experiment. The averages of maximum changes in the arterial pressure and heart rate were compared with control group and with its average in before injections using student t-test and paired t-test, respectively.Results: GABAA receptor antagonist, bicuculline met iodide (BMI, 1 mM), increased both arterial pressure (+14.2±3.08) and heart rate (+9.8± 2.5) (p<0.05). Muscimole, a GABAA agonist (5 mM), caused a significant decrease of the arterial pressure (-10.2 ±4.1) and heart rate (-20.3±9.40) (p<0.01). However, microinjection of phaclofen (5 mM), a GABAB receptor antagonist caused small unsignificant changes of the heart rate and blood pressure.Conclusion: GABAergic inhibitory neurons of the BST seems to cause decrease in the blood pressure and heart rate by GABAA but not GABAB receptors.

Background and objectives: Cuneiform nucleus (CnF) is in midbrain area that has several functions including cardiovascular regulation. It is reported that the cardiovascular effect of CnF nucleus is mediated by rostral ventrolateral medulla (RVLM). However, direct projection from CnF to RVLM is sparse; therefore cardiovascular response of CnF nucleus may be relayed by other nuclei such as Kolliker—Fuse nucleus (KF). To test this hypothesis, KF was inactivated by cobalt chloride (CoCl2) and its effect on long cardiovascular response of glutamate in CnF was evaluated.Materials and Method: Rats were anesthetized and arterially canuulated. Blood pressure (BP) and heart rate (HR) were recorded throughout the experiment. The drugs were microinjected into the nuclei and maximum change was compared with that prior to injection and with the control group using descriptive statistics and unpaired t-test for data analysis. Results were given as the mean±SEM.Results: Microinjection of glutamate into the CnF nucleus caused a long term response (high blood pressure and tachycardia). Inactivation of KF nucleus significantly attenuated the blood pressure effect of long term response reaching 10.39±2.25 mmHg which is a significant decrease compared to glutamate (19.62±2.09 mmHg) (P<0.01). Maximum change in heart rate (16.33±4.8 bpm) showed no significant difference compared to glutamate (21.6±11.9 bpm).Conclusion: Our results showed that long term high blood pressure effect of CnF nucleus was mediated by KF nucleus. However, since inactivation of KF cannot completely block this response, another area may also be involved in relaying this effect. Tachycardia response was not affected by inactivation of KF nucleus. This finding indicates that the pathway of tachycardia response of CnF is probably independent of KF nucleus.