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I MacIntyre

Publications and source records attributed to I MacIntyre.

At least 109 records · Page 6Linked to original sources
PubMed1985

Topographic localization of calcitonin gene-related peptide in the rat brain: an immunohistochemical analysis.

The distribution of immunoreactive calcitonin gene-related peptide in the rat brain was investigated by means of an indirect immunofluorescence method. In addition to previously reported calcitonin gene-related peptide-like immunoreactive structure-containing sites such as the nucleus ambiguus, nucleus originis nervi facialis, nucleus originis nervi hypoglossi, nucleus peripeduncularis and nucleus parabrachialis, the present study demonstrated a far wider distribution of calcitonin gene-related peptide-like immunoreactive structure-containing cells in the rat brain, i.e. the nucleus hypothalamicus lateralis, nucleus ventromedialis thalami, colliculus superior, lemniscus lateralis, gyrus dentatus, nucleus olivaris superior, nucleus tractus solitarii, nucleus cuneiformis, nucleus parabigeminalis and a proportion of the Purkinje cells. We have also demonstrated a more extensive network of calcitonin gene-related peptide-like immunoreactive fibers distributed in various areas throughout the rat brain than has been reported previously such as the colliculus inferior, nucleus olivaris superior, nucleus vestibularis lateralis and inferioris, and nucleus cochlearis dorsalis and ventralis, etc.

Animals↗
PubMed1985

Calcitonin gene-related peptidergic projection from the parabrachial area to the forebrain and diencephalon in the rat: an immunohistochemical analysis.

We investigated ascending fiber projections of calcitonin gene-related peptide from the parabrachial area to the forebrain and diencephalon in the rat using immunocytochemistry. Destruction of the lateral portion of the dorsal parabrachial area resulted in a marked ipsilateral decrease in the fibers containing calcitonin gene-related peptide in the ventromedial hypothalamic nucleus, indicating that cells containing calcitonin gene-related peptide in the lateral portion of the dorsal parabrachial area projected to the ipsilateral ventromedial hypothalamic nucleus. Destruction of the ventral portion of the parabrachial area resulted in a marked decrease of fibers containing calcitonin gene-related peptide in the bed nucleus of the stria terminalis, the central amygdaloid nucleus and the lateral hypothalamus just medial to the crus cerebri (the far-lateral hypothalamus), and a less marked decrease in the ventromedial thalamic nucleus. This means that there are projections from cells containing calcitonin gene-related peptide in the ventral portion of the parabrachial area to the first three regions just mentioned, and to some extent to the last.

Afferent Pathways↗
PubMed1985

Distribution of calcitonin gene-related peptide in the rat peripheral nervous system with reference to its coexistence with substance P.

This immunocytochemical study, using a double-staining method, showed that calcitonin gene-related peptide-like immunoreactive structures are widely distributed in the peripheral nervous system and that many of them coexist with substance P-like immunoreactive structures in single sensory ganglion cells. Neurons positive for calcitonin gene-related peptide but negative for substance P were detected in sensory ganglia. These cells were large (about 30-45 micron in diameter); these primary sensory neurons containing calcitonin gene-related peptide can probably act independently of substance P. There were neurons containing calcitonin gene-related peptide without substance P in the pterygopalatine ganglion, although these cells were less numerous than in the sensory ganglia. In consecutive sections, calcitonin gene-related peptide-like structures occurred in thyroid parafollicular cells, which also contain calcitonin. This suggested that messenger RNA for producing calcitonin gene-related peptide is also present in the thyroid, and like calcitonin, calcitonin gene-related peptide may have a peripheral physiological role.

Animals↗
PubMed1979

A physiological role for calcitonin: protection of the maternal skeleton.

Plasma-calcitonin levels, measured with an established and reliable extraction radioimmunoassay technique, were significantly higher throughout normal pregnancy and lactation than in normal non-pregnant women, and were not immediately influenced by the acute stimulation of breast-feeding. Thus, more calcitonin circulates at times of physiologically increased calcium need. It is suggested that an important function of calcitonin is the protection of the healthy maternal skeleton from excessive resorption by opposing the resorptive action of 1,25-dihydroxycholecalciferol on bone.

Adolescent↗
PubMed1979

The role of the kidney in vitamin D metabolism.

The kidney should be regarded as an organ of central importance in the regulation of calcium metabolism. Its secretion product, 1 alpha,25(OH)2D3, is regulated by several factors, including the calcium and phosphorus content of the diet, parathyroid hormone and the level of 1 alpha,25(OH)2D3 itself. The main occasions in health where 1 alpha,25(OH)2D3 secretion is enhanced are during growth and reproduction. In these situations the secretion of this new renal hormone is under at least partial control of growth hormone and prolactin.

Animals↗
PubMed1978

Effect of oestrogen and 1,25-dihydroxycholecalciferol on 25-hydroxycholecalciferol metabolism in primary chick kidney-cell cultures.

Primary cultures of chick kidney cells convert 25-hydroxycholecalciferol into more-polar metabolites. Cells from vitamin D-deficient chicks have high 25-hydroxycholecalciferol 1 alpha-hydroxylase (1 alpha-hydroxylase) activity, but no 25-hydroxycholecalciferol 24-hydroxylase (24-hydroxylase) activity. Physiological concentrations of 1,25-dihydroxycholeclaciferol suppress 1 alpha-hydroxylase and induce 24-hydroxylase activity. The inhibition of 1 alpha-hydroxylase preceded the induction of 24-hydroxylase. In contrast, oestradiol-17 beta had no effect on the activity of either hydroxylase under a variety of experimental conditions. These results clearly demonstrate that 1,25-dihydroxycholecalciferol, but not oestrogen, acts directly on the kidney cells to regulate the metabolism of 25-hydroxycholecalciferol.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1978

Relative deficiency of plasma-calcitonin in normal women.

A new radioimmunoassay technique was used to measure plasma-calcitonin in normal subjects. Plasma-calcitonin concentrations in women were less than 25% of those in men, and were often undetectable. However, during pregnancy or administration of the oestrogen-progestagen contraceptive pill, plasma-calcitonin equalled or exceeded male concentrations. These findings are consistent with an effect on calcitonin production of normal male testosterone concentrations and concentrations of the sex steroids during pregnancy. Calcitonin may protect the skeleton during calcium stress. Further, although it is unknown whether a deficiency of the hormone plays a role in postmenopausal osteoporosis, this is now a definite possibility which requires urgent investigation.

Adolescent↗
PubMed1978

A survey of the hormonal factors that control calcium metabolism.

(1) Vitamin D is the precursor of an extremely potent calcium regulating hormone, 1,25(OH)2D3, which is secreted by the kidney. (2) The secretion of 1,25(OH)2D3 by the kidney is influenced by the calcium and phosphorus content of the diet, parathyroid hormone, and 1,25(OH)2D3 itself. (3)Prolactin and growth hormone are importnat regulators of vitamin D metabolism during pregnancy and growth.

Animals↗
PubMed1978

Influence of estrogen on renal vitamin D hydroxylases and serum 1alpha,25-(OH)2D3 in chicks.

The influence of estrogen on the metabolism of 25-hydroxyvitamin D3 was studied in 2- to 5-wk-old chicks. Single injections of at least 500 microgram diethylstibestrol (DES) increased the conversion of 25-hydroxyvitamin D3 to 1alpha,25-dihydroxyvitamin D3 (1alpha,25-(OH)2D3) and suppressed the production of 24,25-dihydroxyvitamin D3 in chick kidney homogenates. Acute (one 5-mg) injections of testosterone or progesterone did not enhance the 25-hydroxyvitamin D3-1alpha-hydroxylase, indicating specificity. However, chronic pretreatment with DES appeared to allow the potentiation of previously unstimulatory steroids such as progesterone and testosterone. In addition, the hormonal metabolite of vitamin D3, 1alpha,25-(OH)2D3, was measured in 4- to 6-wk chick plasma after steroid treatment. Greater than 1 mg DES per day for 5 days was necessary to enhance the circulating level of 1alpha,25-(OH)2D3; testosterone alone had no effect. This elevation was rapid, occurring within 12--24 h after injection. These data suggest that estrogen (as evidenced by DES treatment) is a modulator of vitamin D metabolism along with other known regulators such as parathyroid hormone, phosphate, and 1alpha,25-(OH)2D3. The mechanism of the regulation is as yet unknown.

Animals↗