Cellular organization of the lateral and postinfundibular regions of the median eminence in the rat

Rodríguez, Estéban M.; González, Carlos B.; Delannoy, Luis

doi:10.1007/bf00236998

Cited by 91 publications

(107 citation statements)

References 43 publications

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“…2 E and F, arrows). This corresponds to the known distribution of ependymal tanycytes (24,25), a specialized population of glial cells implicated in the transport of hormones, and other substances in the hypothalamus (26). The relative amounts of D2 mRNA in the hypothalamus and layers 1-4 of the parietal cortex were compared by measuring the optical density of these regions on a lowexposure autoradiograph (Fig.…”

Section: Resultssupporting

confidence: 54%

The type 2 iodothyronine deiodinase is expressed primarily in glial cells in the neonatal rat brain

Guadaño-Ferraz

Obregón

Germain

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

332

194

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Thyroid hormone plays an essential role in mammalian brain maturation and function, in large part by regulating the expression of specific neuronal genes. In this tissue, the type 2 deiodinase (D2) appears to be essential for providing adequate levels of the active thyroid hormone 3,5,3-triiodothyronine (T3) during the developmental period. We have studied the regional and cellular localization of D2 mRNA in the brain of 15-day-old neonatal rats. D2 is expressed in the cerebral cortex, olfactory bulb, hippocampus, caudate, thalamus, hypothalamus, and cerebellum and was absent from the white matter. At the cellular level, D2 is expressed predominantly, if not exclusively, in astrocytes and in the tanycytes lining the third ventricle and present in the median eminence. These results suggest a close metabolic coupling between subsets of glial cells and neurons, whereby thyroxine is taken up from the blood and͞or cerebrospinal f luid by astrocytes and tanycytes, is deiodinated to T3, and then is released for utilization by neurons.Thyroid hormone controls a number of metabolic and developmental processes and, in particular, is an essential factor for normal mammalian brain maturation (1). In humans and other species, thyroid deficiency during the perinatal period results in irreversible brain damage and mental retardation (1, 2). The effects of thyroid hormone result primarily from changes in gene expression mediated through the binding of the active compound 3,5,3Ј-triiodothyronine (T3) to specific nuclear receptors of the steroid-retinoic acid-thyroid hormone superfamily. Previous studies have demonstrated that T3 nuclear receptors are expressed in a complex temporal pattern in specific regions of the brain that include the cerebral cortex, hippocampus, striatum, cerebellum, and hypothalamus (3, 4). These receptors are found predominantly in neurons and oligodendrocytes (5-7), and a number of neuronal genes have been shown to be regulated by thyroid hormone during development (8, 9).The majority of T3 in the brain is produced locally within the central nervous system by the 5Ј-deiodination of thyroxine (T4) (10). The type 2 deiodinase (D2) appears to be of particular importance in catalyzing the conversion of T4 to T3 in the brain during fetal and early neonatal life (11)(12)(13). During this period in the rat, the expression of D2 activity in brain increases at the end of gestation and is highest at 15-20 days of postnatal life (14). This pattern of activity corresponds temporally to the period when the developing brain is most dependent on thyroid hormone and correlates with increasing brain T3 concentrations, which peak at 2 weeks of age (13).An important property of the D2 is that its activity is markedly increased by thyroid hormone deficiency (15). This enhanced D2 activity serves to maintain T3 production in the brain in the face of limiting amounts of the prohormone T4 (16). Brain T3 levels thus appear to be protected to a considerable extent by alterations in circulating thyroid hormone levels (12...

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Section: Resultssupporting

confidence: 54%

The type 2 iodothyronine deiodinase is expressed primarily in glial cells in the neonatal rat brain

Guadaño-Ferraz

Obregón

Germain

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

332

194

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“…The appearance of DII mRNA in the ependymal zone and the ME (6) together with our recent observation of glial fibrillary acidic protein in cells expressing DII mRNA (29) and a previous report (30) on the expression of DII in glial cells in neonatal rat brain strongly indicate that DII-producing cells are astrocytes and tanycytes. These glial cells provide an extensive network of cellular processes in the ARC (31)(32)(33)(34) and suggest a paracrine action on PVN-projective ARC neurons via the production of thyroid hormones. In our previous study (29), we have shown that neurons in the ARC heavily project to neuroendocrine TRH cells in the PVN, and we recently found that a robust NPY innervation of TRH cells (35) originates from the ARC (36).…”

Section: Discussionmentioning

confidence: 99%

Fasting-Induced Increase in Type II Iodothyronine Deiodinase Activity and Messenger Ribonucleic Acid Levels Is Not Reversed by Thyroxine in the Rat Hypothalamus

Diano

1998

Endocrinology

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The importance of local formation of T 3 in the feedback effect of the thyroid gland on hypothalamic TRH-producing cells has been established. Primary failure of the thyroid gland results in a fall in circulating T 4 and T 3 levels, leading to an elevation in the production and release of TRH in the hypothalamic paraventricular nucleus. In contrast, during short term fasting, declining plasma levels of thyroid hormones coincide with suppressed TRH production and release. In the brain, the prevalent enzyme that converts T 4 to T 3 is type II iodothyronine deiodinase (DII). The present study was undertaken to determine whether a differential hypothalamic expression of type II deiodinase may exist in fasted rats and in animals that are hypothyroid due to the failure of the thyroid gland. Using in situ hybridization, we assessed type II deiodinase messenger RNA (mRNA) levels in the hypothalamus of rats that were control euthyroid, hyperthyroid (T 4 ), hypothyroid induced by propylthiouracil (PTU), and fasted. A group of fasted rats also received exogenous T 4 . DII mRNA was detected around the third ventricle, including the ependymal layer and adjacent periventricular regions as well as in the arcuate nucleus and the external layer of the median eminence. Quantitative in situ hybridization analysis demonstrated that PTU treatment and short term fasting resulted in significant elevations in DII messenger levels compared with those in euthyroid controls. Three weeks of PTU administration induced a consistent decline in circulating T 3 and undetectable T 4 levels, whereas 3 days of fasting resulted in only a 50% fall in the concentration of serum thyroid hormones. Interestingly, however, the expression of the DII mRNA was more than 2-fold higher in fasted animals compared with the values in PTU-treated rats. Furthermore, although T 4 administration repressed DII mRNA expression in euthyroid animals, the same treatment had no effect on the fasting-induced elevations of DII message.To assess whether DII enzymatic activity is also affected during food deprivation, hypothalami were dissected out, and DII activity was measured in control euthyroid, fasted, and fasted plus T 4 -treated rats. To determine whether comparable changes in plasma thyroid hormone levels induced by fasting and PTU treatment could have affected DII enzymatic activity in a similar manner, animals were injected ip with PTU for 5 days to decrease plasma thyroid hormones to levels similar to those caused by fasting. DII enzymatic assay showed a significant increase in DII activity in fasted and fasted plus T 4 -treated animals compared with those in euthyroid controls and PTU-treated rats. No significant changes were found in PTU-treated rats compared with euthyroid animals. These data indicate that during short term fasting, a signal of nonthyroid origin underlies the robust elevation of DII production and activity in the hypothalamus. Thus, we propose that during the initial phase of food deprivation, an increased negative thyroid feedback exis...

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“…l-pm thick serial sections were obtained of the whole ME-PT (about 2 mm long), from the cephalic end up to the caudal end (pituitary stalk). Every 100 um a few ultrathin sections of the ME-PT were obtained [31]. Thus, ultrathin frontal sections were obtained from 20 different lev els in the cephalic-caudal direction.…”

Section: Immunocytochemistrymentioning

confidence: 99%

Changes in the Luteinizing Hormone Content of the Rat Pars tuheralis during the Estrus Cycle and after Lesions in the Preoptic Area

Aguado¹,

Hancke²,

Rodrı́guez³

et al. 1982

Neuroendocrinology

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The rat pars tuberalis was studied with conventional electron microscopy and immunocytochemistry for the demonstration of luteinizing hormone (LH). The LH-secreting cells were preferentially located in two regions of the pars tuberalis (PT), namely, that surrounding the neural stalk and that occupying the tuberoinfundibular sulci. Dialyzed extracts of PT prepared after removal of the pituitary stalk, had the capacity to induce ovulation in chlorpromazine-blocked rats in proestrus. In radioimmunoassays carried out under the same conditions, the PT extracts yielded displacement curves parallel to those of standard LH. The immunoreactive LH content of the female PT was determined at three phases of the estrous cycle: diestrus, afternoon of proestrus and estrus. The lowest values were found in rats sacrificed in the evening of proestrus (18.00 h), and they were about one sixth of the peak values found at estrus. 1 month after inducing lesions in the preoptic area of female rats, the LH content of the PT was four times higher than the highest values found during the estrous cycle. The results suggest that the rat PT does secrete LH, and that this secretory activity fluctuates with the estrous cycle, but in a manner that differs from that reported for LH secretion of the pars distalis.

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Cellular organization of the lateral and postinfundibular regions of the median eminence in the rat

Cited by 91 publications

References 43 publications

The type 2 iodothyronine deiodinase is expressed primarily in glial cells in the neonatal rat brain

The type 2 iodothyronine deiodinase is expressed primarily in glial cells in the neonatal rat brain

Fasting-Induced Increase in Type II Iodothyronine Deiodinase Activity and Messenger Ribonucleic Acid Levels Is Not Reversed by Thyroxine in the Rat Hypothalamus

Changes in the Luteinizing Hormone Content of the Rat Pars tuheralis during the Estrus Cycle and after Lesions in the Preoptic Area

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