Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.14.16.2 (tyrosine hydroxylase)
 14,760 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies have shown that the secretion of several stress-related hormones can be altered by exposure to marihuana or its purified constituents. The purpose of this study was to examine changes in adrenal medullary function caused by acute, subchronic and chronic treatments with two different doses of delta-9-tetrahydrocannabinol (THC). Acute exposure to THC caused a significant decrease in the adrenal medulla contents of both norepinephrine (NE) and epinephrine (E) and a significant increase in the E/NE ratio. These effects were mainly observed with the highest dose of THC, but they were not accompanied by a statistically significant decrease in adrenal medulla tyrosine hydroxylase activity, the rate-limiting enzyme in the catecholamine (CA) synthesis. These effects disappeared after seven or fourteen days of a daily THC treatment, which suggests the development of tolerance to this drug. Analysis of plasma PRL, ACTH and corticosterone levels showed some THC-related changes in these hormones. THC-induced modifications in ACTH and corticosterone were not in parallel to the changes in the adrenal medulla function, whereas those effects of acute THC on PRL release were statistically correlated with decreases of CA contents following acute THC. In conclusion, acute exposure to THC caused an alteration in the adrenal medullary function, reflected by a fall in endogenous stores of both CAs which could influence the adrenal medullary response to stress situations. This acute effect of THC could be mediated by the pituitary secretion of PRL, although the possibility of an effect directly exerted on the adrenal medulla chromaffin cells should be also considered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of delta-9-tetrahydrocannabinol exposure on adrenal medullary function: evidence of an acute effect and development of tolerance in chronic treatments. 168 29

We have previously described hypertrophy of neurons containing estrogen receptor mRNA in the infundibular nucleus of postmenopausal women. In the present investigation we identified peptide mRNAs in the hypertrophied neurons and determined whether postmenopausal neuronal hypertrophy was accompanied by changes in gene expression. In the first study in situ hybridization was performed on sections from hypothalami of postmenopausal women (n = 3) using synthetic 35S-labeled cDNA probes complementary to mRNAs encoding estrogen receptor, substance-P (SP), neurokinin-B (NKB), POMC, cholecystokinin, dynorphin, CRF, enkephalin, galanin, neuropeptide-Y, GH-releasing hormone, and tyrosine hydroxylase. Neuronal cross-sectional areas and cell densities were measured with the aid of a computer microscope system. Neurons labeled with the NKB and SP probes were comparable in size, morphology, and distribution to the hypertrophied neurons containing estrogen receptor mRNA. In contrast, neurons labeled with other cDNA probes were sparsely distributed (CRF and dynorphin), smaller in size (neuropeptide-Y, galanin, GH-releasing hormone, enkephalin, cholecystokinin, and POMC), or located anterior to the hypertrophied population (tyrosine hydroxylase). In the second study sections from hypothalami of premenopausal (n = 3) and postmenopausal (n = 3) women were incubated with cDNA probes complementary to SP or NKB mRNAs. The mean cross-sectional areas of postmenopausal infundibular neurons containing NKB and SP mRNAs increased to 194% and 176% of premenopausal values, respectively. The autoradiographic grain densities of infundibular neurons labeled with either probe were also significantly increased in the postmenopausal group. Finally, the numbers of labeled neurons/tissue increased 6-fold (SP) and 15-fold (NKB) in the postmenopausal infundibular nucleus. These data demonstrate that human menopause is associated with marked increases in hypothalamic NKB and SP gene expression. We propose that neurons containing estrogen receptor, SP, and NKB mRNAs participate in the hypothalamic circuitry regulating estrogen negative feedback in the human.
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PMID:Hypertrophy and increased gene expression of neurons containing neurokinin-B and substance-P messenger ribonucleic acids in the hypothalami of postmenopausal women. 170 31

We have investigated the appearance of the transmitter phenotypes of hypothalamic neurons in grafts transplanted into the third ventricle of adult female rats. The grafts were the mediobasal hypothalamus and the preoptic area of 12.5-day-old rat embryos, and were examined 40-100 days later. Wheat germ agglutinin (WGA) was injected into the jugular vein of several animals for the examination of the existence of neurovascular associations. Three days after the injection, WGA appeared to have been incorporated into the neurons in the paraventricular, periventricular, and arcuate nuclei of the host animals. In the grafts, WGA was also seen incorporated in certain neurons which were found immunoreactive for tyrosine hydroxylase (TH), rat corticotropin-releasing factor (rCRF), substance P (SP), or somatostatin (SRIH). Neurons immunoreactive for neuropeptide Y (NPY) and ACTH did not seem to incorporate WGA. These findings suggest that the neurons containing TH, rCRF, SP, or SRIH link with fenestrated capillaries developed in the grafts. The immunoreactivity for glucocorticoid receptor (GR) was detected mainly in the nucleus of certain neurons and glial cells in the grafts as well as in the host hypothalamic neurons. In the grafts, strong GR immunoreactivity was detected in the cells immunoreactive for TH, NPY, and rCRF as in the host animals. It is concluded that the undifferentiated hypothalamic neurons differentiate to synthesize GR as well as definitive peptides and TH in the grafts.
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PMID:Appearance of neurons with glucocorticoid receptors and neurovascular links in the embryonal rat hypothalamus grafted in the third ventricle. 229 64

The medial preoptic nucleus (MPN) is a sexually dimorphic complex with three major subdivisions. The cell-dense central (MPNc) and medial (MPNm) subdivisions are larger in male rats, while the cell-sparse lateral subdivision (MPNl) occupies a majority of the nucleus in females. In the present study we evaluated the distribution of possible monoaminergic and peptidergic cells and fibers within the MPN, as well as in adjacent regions of the medial preoptic area of the adult male rat. For this, we used an indirect immunohistochemical method with antisera to serotonin (5HT), dopamine beta-hydroxylase (DBH), tyrosine hydroxylase (TH), neuropeptide Y (NPY), cholecystokinin (CCK), vasoactive intestinal polypeptide (VIP), substance P (SP), neurotensin (NT), corticotropin-releasing factor (CRF), luteotropin-releasing hormone (LRH), somatostatin (SS), thyrotropin-releasing hormone (TRH), oxytocin (OXY), vasopressin (VAS), adrenocorticotropic hormone (1-24; ACTH), alpha-melanocyte-stimulating hormone (alpha-MSH), leucine-enkephalin (L-ENK), and calcitonin gene-related peptide (CGRP). The results suggest that cell bodies and/or fibers crossreacting with all of these putative neurotransmitters are differentially distributed within the MPN. Within the MPNm, the densest plexuses of fibers were stained with antisera to SP and NPY, while moderate densities of fibers were stained with anti-DBH, SS, CCK, CGRP, ACTH, and alpha-MSH, and only a few fibers were stained with anti-5HT, TH, NT, VAS, and L-ENK. Moderate numbers of SP- and L-ENK-immunoreactive cell bodies, and a few SS-, NT-, CRF-, and TRH-stained cell bodies were also found within the MPNm. The MPNc contained a dense plexus of CCK-immunoreactive fibers, as well as a few CRF-immunoreactive fibers. Both fiber types were localized almost exclusively to this subdivision, while most of the others studied here appeared to avoid it selectively. This suggests that there are relatively few inputs to the MPNc, and that they tend to avoid other parts of the nucleus, although moderate densities of DBH- and NPY-immunoreactive fibers were found in both the MPNm and MPNc. The MPNc contained several CCK-immunoreactive cell bodies as well as a moderate number of TRH-stained cell bodies. Both cell types were nearly completely localized to the MPNc. The major inputs to the MPNl studied here appear to be stained with antisera to 5HT and L-ENK, although moderate numbers of NT- and CRF- immunoreactive fibers were also found in this part of the nucleus.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neurotransmitter specificity of cells and fibers in the medial preoptic nucleus: an immunohistochemical study in the rat. 242 28

The paraventricular nucleus (PVN) of male albino rats was analyzed for the presence of glucocorticoid receptor-like immunoreactivity (GR-LI) in neuropeptide containing neurons. Using immunohistochemistry, coronal sections trough the entire PVN were double-stained with a mouse monoclonal antibody against GR and one of the following antisera: rabbit antiserum to corticotropin releasing factor (CRF), neurotensin (NT), enkephalin (ENK), cholecystokinin (CCK), thyrotropin releasing hormone (TRH), galanin (GAL), peptide histidine isoleucine (PHI), vasoactive intestinal polypeptide (VIP), somatostatin (SOM) or tyrosine hydroxylase (TH). For comparison the occurrence of GR-LI in NT-, SOM-, NPY- or TH-positive neurons of the arcuate nucleus was also studied. Our results indicate that GR-LI is present in the parvocellular part of the PVN but not in its magnocellular portion. Virtually every parvocellular neuron in the PVN containing one of the above mentioned peptides was also positive for GR, with the exception of SOM neurons, of which only about two thirds showed detectable levels of GR-LI. All TH-positive, presumably dopamine neurons in the PVN were GR-positive. In the arcuate nucleus all TH- and NPY-positive neurons as well as a large proportion of the SOM- and NT-immunoreactive neurons contained GR-LI. The results indicate that in the PVN, in addition to the CRF neurons, certain peptidergic neurons in the parvocellular part of the PVN, without any established role in the control of ACTH synthesis and release, may also be under glucocorticoid control. This seems to be the case also for most arcuate neurons.
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PMID:Coexistence of glucocorticoid receptor-like immunoreactivity with neuropeptides in the hypothalamic paraventricular nucleus. 259 16

Neural input to distinct and separate populations of CRF-immunoreactive (ir) neurons in rat forebrain was investigated. The relationship of opiocortin and/or catecholamine fibers to different groups of CRF-containing neurons was elucidated using single and dual labeling immunocytochemical procedures. Antibodies to CRF, ACTH(1-39) and the catecholamine synthesizing enzymes which are tyrosine hydroxylase (TH), dopamine beta-hydroxylase (DBH) and phenylethanolamine-N-methyltransferase (PNMT) were utilized. CRF-ir neuronal populations are localized predominantly in the following regions of rat forebrain: bed nucleus of stria terminalis, medial preoptic area, suprachiasmatic and paraventricular (PVN) nuclei of hypothalamus and central nucleus of amygdala. The present study demonstrates that CRF-ir neuronal groups in rat forebrain are not homogenous in that each population received a characteristic neural input. CRF-ir neurons in the PVN received a dense input of ACTH-, TH-, DBH-, and PNMT-ir fibers. In contrast, CRF-ir neurons in the central nucleus of amygdala are colocalized predominantly with TH-ir fiber/terminals. In the ventral portion of the bed nucleus of stria terminalis, TH-, ACTH- and DBH-ir fibers are demonstrated in close anatomical proximity to CRF-containing perikarya; in the dorsal portion of this nucleus, TH-ir fiber/terminals are colocalized with CRF-ir neurons. In the suprachiasmatic nucleus, neither opiocortin- nor catecholamine-immunostained fibers are observed in association with CRF-ir neurons. Our data suggest that there is a transmitter specificity of neural input to each CRF-ir neuronal population in rat forebrain.
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PMID:Opiocortin and catecholamine input to CRF-immunoreactive neurons in rat forebrain. 262

A 48 h but not a 72 h or 7 day withdrawal from chronic exposure to cigarette smoke was associated with increased noradrenaline levels (quantitative histofluorimetry) in the subependymal layer (SEL) of the median eminence, the anterior periventricular hypothalamic region (PV I) and the parvocellular part of the hypothalamic nucleus (PA FP) and an increased noradrenaline utilization (tyrosine hydroxylase inhibition by alpha MT) in the SEL and the PV I. Following a 48 h or 72 h but not a 7 day withdrawal from chronic exposure to cigarette smoke an increased catecholamine utilization was found in the medial palisade zone (MPZ) of the median eminence. Reduced serum prolactin, FSH and corticosterone levels were found following a 48 h withdrawal from chronic exposure to cigarette smoke. Following a 72 h withdrawal from chronic exposure to cigarette smoke a reduced concentration of serum prolactin was noted. Chronic exposure to cigarette smoke reduced serum TSH levels and lead to a tolerance development with regard to noradrenaline levels and utilization within the preoptic region with the exception of the periventricular preoptic region. The finding of special interest in the present study is the demonstration of a highly significant lowering of corticosterone serum levels despite maintained blood levels of ACTH as seen 48 h following withdrawal. It is suggested that this type of endocrine change may lead to changes in fear-motivated behaviour and contribute to behavioural withdrawal reactions. The maintained reductions of serum prolactin levels found after 48 h and 72 h of withdrawal from cigarette smoke exposure (cf. Andersson et al. 1985a) is discussed in terms of an increased catecholamine utilization in the medial palisade zone of the median eminance. This activation is suggested to be caused by the development of a prolactin receptor supersensitivity within the medium eminence. The present evidence indicates withdrawal effects mainly in the noradrenaline nerve terminals of the subependymal layer of the median eminence, the anterior periventricular hypothalamic region and the parvocellular part of the paraventricular hypothalamic nucleus which inter alia are involved in regulation of ACTH secretion (cf. Andersson et al. 1985a).
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PMID:Effects of withdrawal from chronic exposure to cigarette smoke on hypothalamic and preoptic catecholamine nerve terminal systems and on the secretion of pituitary hormones in the male rat. 273 53

Male rats were exposed to cigarette smoke (Walton Horizontal Smoking Machine) from one to four cigarettes (Kentucky reference IR-1 type). Catecholamines in the diencephalon were measured by quantitative histofluorimetry in discrete dopamine (DA) and noradrenaline (NA) nerve terminal systems. Blood TSH, prolactin, LH, FSH, ACTH, vasopressin and corticosterone levels were determined by radioimmunoassay procedures. Exposure to unfiltered, but not to filtered (Cambridge glass fibre filters) cigarette smoke resulted in dose-dependent reductions of NA levels in the various hypothalamic NA nerve terminal systems. Evidence was obtained that exposure to unfiltered but not to filtered cigarette smoke resulted in dose-dependent increases of amine turnover (alpha MT-induced CA disappearance experiments) in the various DA and NA nerve terminal systems in the hypothalamus. The lowering of TSH, LH and prolactin secretion induced by unfiltered smoke were probably induced by nicotine and were independent of tyrosine hydroxylase inhibition. Furthermore, unfiltered cigarette smoke produced a dose-related increase in corticosterone secretion. The inhibitory effects of TSH, LH and prolactin secretion were probably in part related to the ability of unfiltered smoke via its nicotine component to activate the lateral and medial tubero-infundibular DA neurons. The increases in corticosterone secretion may at least in part be related to a smoke induced increase in the facilitatory influence of paraventricular NA nerve terminals on CRF activity.
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PMID:Effects of acute intermittent exposure to cigarette smoke on catecholamine levels and turnover in various types of hypothalamic DA and NA nerve terminal systems as well as on the secretion of adenohypophyseal hormones and corticosterone. 286 16

Release of adrenal catecholamine by carbachol has been shown to be coincident with an increase in intracellular cAMP levels. Bovine adrenal medullary (BAM) cells were prepared and maintained in culture and used to examine the role of cAMP in stimulus-secretion coupling. The addition of ACTH to these cells caused a 10- to 50-fold increase in cellular cAMP without an effect on catecholamine secretion, suggesting cortical cell contamination. Percoll density separation of both BAM cells and adrenal cortical cells revealed that the greatest cAMP responses to ACTH corresponded to the catecholamine-containing cell fractions and not to those density layers where cortical cells sedimented. BAM cells isolated on Percoll did not metabolize [14C]cholesterol to steroids as would be expected were the ACTH-stimulated cAMP accumulations due to cortical cell contamination of the cultures. ACTH stimulated protein phosphorylation in 32P-labeled BAM cells in a manner indistinguishable from that induced by carbachol and forskolin. The major soluble phosphoprotein to be affected by these agents had a relative mol wt of 55-57 kdaltons on sodium dodecyl sulfate-gels and corresponded to tyrosine hydroxylase, which is a specific marker enzyme in the adrenal for chromaffin cells. We propose that bovine adrenal chromaffin cells express ACTH receptors which are coupled to adenylate cyclase. While no acute effect of ACTH was found on catecholamine secretion, ACTH may play a direct role in the regulation of catecholamine synthesis by stimulating the phosphorylation of tyrosine hydroxylase by cAMP-dependent protein kinase.
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PMID:Direct effects of adrenocorticotropic hormone on bovine adrenomedullary cells: adenosine 3',5'-monophosphate-dependent phosphorylation of tyrosine hydroxylase. 286 12

The effect of a type A MAO inhibitor, clorgyline, injected alone or with alpha-methyl-p-tyrosine (aMpT) on the plasmatic corticosterone levels estimated at 9 a.m. and 5 p.m. has been studied in male Wistar rats. The clorgyline injected alone produced significant decreases in corticosterone values, especially at 5 p.m., determining a variation lack between the morning and the afternoon levels. When alpha-MpT is associated to IMAO, increases at both points of the day considered in this experiment take place. The amount of NA and 5-HT in the brain was also estimated; clorgyline high increases in Na and 5-HT contents, 5-HT; aMpT reduces the effect of clorgyline, especially as regards content. The results are discussed in relation to this highly specific MAO inhibitor and with the role of these amines as modulators of ACTH secretion. In view of the changes introduced by the aMpT injection, the modifications produced by clorgyline alone are related to NA, but to 5-HT, when the NA synthesis has been interrupted by the tyrosine hydroxylase inhibitor.
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PMID:[Effect of clorgyline and of alpha-methyl-p-tyrosine on the plasma levels of corticosterone in the rat]. 286 53


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