Ontogeny of receptors for thyrotropin-releasing hormone in the rat brain

Blanchard, Louise M.; Barden, Nicholas

doi:10.1016/0165-3806(86)90175-6

Cited by 14 publications

(3 citation statements)

References 18 publications

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“…LDH release is associated with plasma membrane damage and is highly correlated with neuronal cell death as assessed by Trypan Blue staining in vitro [5,54]. Glutamate-induced neurodegeneration involves a dynamic process associated with elements of both necrosis and apoptosis [2] The period of peak TRH receptor expression in the rat central nervous system occurs shortly after the first week of birth [1], and TRH receptor mRNA has been localized primarily to ventral hippocampal granule cells, as well as pyramidal and subicular neurons [22]. Since the ontogeny of the TRH receptor parallels the development of Glu susceptibility and the media is known to select for neurons, this culture procedure should facilitate studies aimed at more clearly defining the neuroprotective mechanism of TRH/analogs.…”

Section: Discussionmentioning

confidence: 99%

An analog of thyrotropin-releasing hormone (TRH) is neuroprotective against glutamate-induced toxicity in fetal rat hippocampal neurons in vitro

et al. 2007

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TRH has been found to be efficacious in treating certain neurodegenerative disorders such as epilepsy, Alzheimer's disease, neurotrauma and depression, however, its mechanism of action is poorly understood. Since Glutamate (Glu) toxicity has been implicated in these disorders, we utilized primary enriched cultures of rat fetal (E 17) hippocampal neurons to test the hypothesis that an analog of TRH, 3-Methyl-Histidine TRH (3Me-H TRH), given concurrently with Glu would protect such neurons against cell damage and cell death. Cell viability was assessed via Trypan Blue exclusion cell counts and neuronal damage was determined by assaying lactic acid dehydrogenase (LDH) released in the conditioned media. Fetal hippocampal neurons were cultured in neurobasal media for 7 days. On day 7, neurons (10 6 /well) were treated with: control media, 10 μM 3Me-H TRH, 500 μM Glu, or 500 μM Glu with either 10, 1, 0.1, 0.01 or 0.001 μM 3Me-H TRH. Both media and neurons were harvested 16 hr after treatment. Prolonged exposure to 10 μM 3Me-H TRH was not toxic to the cells, whereas, neurons exposed to 500 μM Glu resulted in maximal cell death. Notably, 10, 1 and 0.1 μM 3Me-H TRH, when co-treated with 500 μM Glu protected fetal neurons against cell death in a concentration-dependent manner. These results provide support for an important neuroprotective effect of TRH/analogs against glutamate toxicity in primary hippocampal neuronal culture, and implicate a potentially beneficial role of TRH/analogs in neurodegenerative diseases.

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Section: Discussionmentioning

confidence: 99%

An analog of thyrotropin-releasing hormone (TRH) is neuroprotective against glutamate-induced toxicity in fetal rat hippocampal neurons in vitro

et al. 2007

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“…The hypothalamic-pituitary-adrenal axis has been reported to be impaired during the neonatal period and aging, and this effect has been attributed to lack or decrease of CRH receptor mRNA, respectively (7)(8)(9). Likewise, it has been reported that TRH binding sites change with aging (10). Most studies in this regard have focused on expression of a single HRH receptor in a particular physiologic situation such as aging or puberty, and receptor expression has been estimated at the level of mRNA in tissue extracts rather than the functional protein at the single cell level.…”

mentioning

confidence: 99%

Changes in Expression of Hypothalamic Releasing Hormone Receptors in Individual Rat Anterior Pituitary Cells during Maturation, Puberty and Senescence

Senovilla¹,

García‐Sancho²,

Alonso³

2005

Endocrinology

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Anterior pituitary (AP) is formed by five different cell types, each one producing a different AP hormone whose secretion is regulated by a specific hypothalamic-releasing hormone (HRH). On the other hand, a significant number of AP cells express multiple HRH receptors (multiresponsive cells). Plastic changes in expression of HRH receptors in individual AP cells are involved in critical endocrine events. Here we have characterized the changes in functional responses to CRH, LHRH, TRH, and GHRH in individual AP cells throughout the whole life span of the rat. To this end, calcium responses to the HRHs were followed by single-cell imaging in freshly dispersed AP cells prepared from rats of different ages (0-540 postnatal days). Three different cell pools were identified: 1) monoresponsive cells, holding a single class of HRH receptor; 2) multiresponsive cells; and 3) nonresponsive cells. The relative abundance of each pool changed with age. Nonresponsive cells were abundant at birth, multiresponsive cells were abundant at puberty, and monoresponsive cells dominated at senescence. The relative abundance of each HRH receptor changed largely with age but not gender. In addition, the contribution of monoresponsive and multiresponsive cells to responses to each HRH changed very much with age. Thus, the anterior pituitary shows large changes in cell populations typed by functional responses to HRHs during maturation, puberty, and senescence.

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“…Previous studies have shown that TRH receptors are also expressed at birth and that their density increases postnatally (41,42). Concurrently, the number of TRH-producing neurons in the paraventricular nucleus increases during the first week of life (43,44).…”

Section: Discussionmentioning

confidence: 94%

Distribution, Cellular Localization, and Ontogeny of Preprothyrotropin-Releasing Hormone-(160–169) (Ps4)-Binding Sites in the Rat Pituitary¹

et al. 1998

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Ontogeny of receptors for thyrotropin-releasing hormone in the rat brain

Cited by 14 publications

References 18 publications

An analog of thyrotropin-releasing hormone (TRH) is neuroprotective against glutamate-induced toxicity in fetal rat hippocampal neurons in vitro

An analog of thyrotropin-releasing hormone (TRH) is neuroprotective against glutamate-induced toxicity in fetal rat hippocampal neurons in vitro

Changes in Expression of Hypothalamic Releasing Hormone Receptors in Individual Rat Anterior Pituitary Cells during Maturation, Puberty and Senescence

Distribution, Cellular Localization, and Ontogeny of Preprothyrotropin-Releasing Hormone-(160–169) (Ps4)-Binding Sites in the Rat Pituitary¹

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Ontogeny of receptors for thyrotropin-releasing hormone in the rat brain

Cited by 14 publications

References 18 publications

An analog of thyrotropin-releasing hormone (TRH) is neuroprotective against glutamate-induced toxicity in fetal rat hippocampal neurons in vitro

An analog of thyrotropin-releasing hormone (TRH) is neuroprotective against glutamate-induced toxicity in fetal rat hippocampal neurons in vitro

Changes in Expression of Hypothalamic Releasing Hormone Receptors in Individual Rat Anterior Pituitary Cells during Maturation, Puberty and Senescence

Distribution, Cellular Localization, and Ontogeny of Preprothyrotropin-Releasing Hormone-(160–169) (Ps4)-Binding Sites in the Rat Pituitary1

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Distribution, Cellular Localization, and Ontogeny of Preprothyrotropin-Releasing Hormone-(160–169) (Ps4)-Binding Sites in the Rat Pituitary¹