Seasonal variations of the β-endorphin neuronal system in the mediobasal hypothalamus of the jerboa (Jaculus orientalis)
Laboratoire de Physiologie Animale, Faculté des Sciences Dhar Mehrez -Fès, Université Sidi Mohamed Ben Abdellah, B.P.1796 Fès-Atlas, Morocco.Neuroscience Letters (Impact Factor: 2.03). 04/2005; 376(2):107-10. DOI: 10.1016/j.neulet.2004.11.035
The distribution of neurons expressing beta-endorphin immunoreactivity was explored in the brain of adult jerboa during two distinct periods characterizing its reproductive cycle. A large presence of cell bodies displaying beta-endorphin immunoreactivity occured within different parts of the mediobasal hypothalamus along its rostrocaudal extent, from the retrochiasmatic area to the posterior arcuate nucleus. Quantitatively, the highest density of immunoreactive beta-endorphin neurons was noted at the medial level of the arcuate nucleus. Furthermore, a seasonal study showed that the number of IR-beta-endorphin neurons was highest in the anterior portion of the arcuate nucleus of jerboas sacrificed in autumn as compared to those sacrificed during spring-summer. Quantitatively, the number of beta-endorphin containing neurons in autumn was 200% in comparison to that found in spring-summer. These results suggest that beta-endorphin containing neuronal population especially localized in the anterior part of arcuate nucleus, exerts an inhibitory influence on the GnRH neurosecretory system in the jerboa, notably in autumn, probably via an increasing expression of its products. The results provide morphofunctional arguments in favour of inhibitory opioid control of GnRH neurons activity and hence the neuroendocrine events regulating reproduction in jerboa.
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ABSTRACT: The corticotropin-releasing hormone (CRH) neurons of the hypothalamic parvocellular paraventricular nucleus (PVN) have a high potential for phenotypical plasticity, allowing them to rapidly modify their neuroendocrine output, depending upon the type of stressors. Indeed, these neurons coexpress other neuropeptides, such as cholecystokinin (CCK), vasopressin (VP), and neurotensin, subserving an eventual complementary function to CRH in the regulation of the pituitary. Unlike in rats, our previous data showed that in jerboas, CCK is not coexpressed within CRH neurons in control as well as stressed animals. The present study explored an eventual VP participation in the phenotypic plasticity of CRH neurons in the jerboa. We analyzed the VP expression within the PVN by immunocytochemistry in male jerboas submitted to acute stress. Our results showed that, contrary to CRH and CCK, no significant change concerned the number of VP-immunoreactive neurons following a 30-min immobilization. The VP/CRH coexpression within PVN and median eminence was investigated by double immunocytochemistry. In control as well as stressed animals, the CRH-immunopositive neurons coexpressed VP within cell bodies and terminals. No significant difference in the number of VP/CRH double-labeled cells was found between both groups. However, such coexpression was quantitatively more important into the posterior PVN as compared with the anterior PVN. This suggests an eventual autocrine/paracrine or endocrine role for jerboa parvocellular VP which is not correlated with acute immobilization stress. VP-immunoreactive neurons also coexpressed CCK within PVN and median eminence of control and stressed jerboas. Such coexpression was more important into the anterior PVN as compared with the posterior PVN. These results showed the occurrence of at least two VP neuronal populations within the jerboa PVN. In addition, the VP expression did not depend upon acute immobilization stress. These data highlight differences in the neuroendocrine regulatory mechanisms of the stress response involving CRH/CCK or VP. They also underline that adaptative physiological mechanisms to stress might vary from one mammal species to another.Neuroendocrinology 02/2006; 84(6):396-404. DOI:10.1159/000100509 · 4.37 Impact Factor
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ABSTRACT: The present study aimed to determine whether beta-endorphin immunoreactivity (bEP-ir) in the neurones of the nucleus lateralis tuberis (NLT) is linked to the seasonal cycle and shows correlation with the number of luteinising hormone (LH) cells in the pituitary gland and ovaries in the teleost, Cirrhinus mrigala. Although LH cells were moderately immunostained during the resting phase (December to January), the morphological profile suggested increased synthetic and secretory activity during the preparatory (February to April) and prespawning (May to June) phases. However, LH immunoreactivity was greatly reduced (P < 0.001) in the spawning (July to August) phase, suggesting massive discharge of the hormone; this pool was partly replenished in the postspawning (September to November) phase. The ovaries grew rapidly in the preparatory and prespawning phases; maximal size was attained during spawning, when ovulation occurred. Thereafter, the ovaries regressed. The NLT of C. mrigala is divisible into the pars lateralis (NLTl) and medialis (NLTm). During the postspawning and resting phases, bEP-ir was readily detectable in the NLTm as well as NLTl neurones. However, a steady reduction in the immunoreactivity was observed in the NLTm neurones during the preparatory through spawning phases (P < 0.001), suggesting a negative correlation with the LH cells-ovary axis. Thus, the inhibitory influence of beta-endorphin on the gonadotrophin-releasing hormone (GnRH)-LH axis appears to be attenuated during the preparatory through spawning phases. This may be necessary for the rapid stimulation of the axis culminating in spawning. Neurones of the NLTl also showed a gradual reduction in bEP-ir during the preparatory and prespawning phases (P < 0.01) and may therefore play a similar role. However, significant augmentation of the immunoreactivity was noticed in these neurones during the spawning phase (P < 0.001), the physiological significance of which is unknown. Although the present study demonstrated a temporal correlation between the beta-endorphin in the NLT, LH cells and the ovary, we suggest that the peptide in the NLTl and NLTm may show functional duality during the spawning phase.Journal of Neuroendocrinology 05/2006; 18(5):319-29. DOI:10.1111/j.1365-2826.2006.01421.x · 3.14 Impact Factor
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ABSTRACT: The hypothalamic response to an environmental stress implicates the corticotrophin-releasing hormone (CRH) neuroendocrine system of the hypothalamic parvicellular paraventricular nucleus (PVN) in addition to other neuropeptides coexpressed within CRH neurones and controlling the hypothalamo-pituitary-adrenal (HPA) axis activity as well. Such neuropeptides are vasopressin, neurotensin and cholecystokinin (CCK). It has previously been demonstrated that the majority of the CRH neuronal population coexpresses CCK after a peripheral stress in rats. In the present study, we explored such neuroendocrine plasticity in the jerboa in captivity as another animal model. In particular, we studied CCK and CRH expression within the hypothalamic PVN by immunocytochemistry in control versus acute immobilisation stress-submitted jerboas. The results show that CCK- and CRH-immunoreactive neuronal systems are located in the hypothalamic parvicellular PVN. The number of CCK-immunoreactive neurones within the PVN was significantly increased (138% increase) in stressed animals compared to controls. Similarly, the number of CRH-containing neurones was higher in stressed jerboas (128%) compared to controls. These results suggest that the neurogenic stress caused by immobilisation stimulates CCK as well as CRH expression in jerboas, which correlates well with previous data obtained in rats using other stressors. The data obtained also suggest that, in addition to CRH, CCK is another neuropeptide involved in the response to stress in jerboa, acting by controlling HPA axis activity. Because CCK is involved in the phenotypical plasticity of CRH-containing neurones in response to an environmental stress, we also explored their coexpression by double immunocytochemistry within the PVN and the median eminence (i.e. the site of CRH and CCK corelease in the rat) following jerboa immobilisation. The results show that CCK is not coexpressed within CRH neurones in either control or stressed jerboa, suggesting differences between jerboas and rats in the neuroendocrine regulatory mechanisms of the stress response involving CRH and CCK. The adaptative physiological mechanisms to environmental conditions might vary from one mammal species to another.Journal of Neuroendocrinology 11/2006; 18(10):767-75. DOI:10.1111/j.1365-2826.2006.01474.x · 3.14 Impact Factor
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