Showing papers on "Hypothalamus published in 1979"
TL;DR: Simultaneous recording from two extracellular electrodes indicated neural activity at two sites in the brain, one of which is in or near the suprachiasmatic nucleus and the other in one of many other brain locations, which indicated clear circadian rhythmicity of spontaneous neural activity.
Abstract: The experimental work described tested the prosposition that the suprachiasmatic nucleus of the hypothalamus is an autonomous circadian pacemaker. Simultaneous recording from two extracellular electrodes indicated neural (multiple unit) activity at two sites in the brain, one of which is in or near the suprachiasmatic nucleus and the other in one of many other brain locations. Both sites in intact rats displayed clear circadian rhythmicity of spontaneous neural activity. In experimental animals, a Halasz knife was used to create an island of hypothalamic tissue that contained the suprachiasmatic nuclei. In such animals that were also blinded by bilateral ocular enucleation, circadian rhythmicity was lost at all brain locations recorded outside the island, but it persisted within the island that contained the suprachiasmatic nuclei. The rhythmicity of the island is thus not dependent on afferent inputs from elsewhere in the brain.
975 citations
TL;DR: Preliminary observations indicate that the EOP may increase serotonin and decrease dopamine metabolism in the hypothalamus, which could account for practically all of their effects on pituitary hormone secretion.
436 citations
TL;DR: Insulin-binding sites were localized in the rat brain by means of light microscopic radioautography and the radioautographic reactions over the circumventricular organs, the medial basal hypothalamus, and the paravagal region were reduced, indicating the presence of competitive binding sites.
Abstract: Insulin-binding sites were localized in the rat brain by means of light microscopic radioautography. Male rats were injected intracardially with [125I]iodoinsulin in the absence and presence of excess unlabeled insulin, insulin analogs, or structurally unrelated polypeptide hormones. Five minutes after injection, the brains were preserved in vivo by perfusion and subjected to radioautographic procedures. Radioautographic reactions caused by [125I]iodoinsulin occurred over all circumventricular organs lacking a blood-brain barrier. In addition, the medial basal hypothalamus, the medial paravagal region, and the choroid plexus were labeled. In the presence of a 500-fold excess of coinjected unlabeled insulin, the radioautographic reactions over the circumventricular organs, the medial basal hypothalamus, and the paravagal region were reduced by 56–78%, indicating the presence of competitive binding sites. In the external contact zone of the median eminence and in the hypothalamic arcuate nucleus, the effect...
327 citations
TL;DR: The results of these studies suggest that endogenous opioids exist in brain tissue which normally inhibit activity in the hypothalamic-pituitary-LH axis and participate in the androgen-dependent feedback control of LH elaboration by this axis.
Abstract: Two narcotic antagonists, naloxone and naltrexone, significantly elevated serum LH levels in male rats within minutes after their sc injection. The peak increase in serum LH occurred 20 min after the injection. Naloxone increased LH levels up to a dose of 1 mg/kg, after which no further increases were found. A dose of 0.35 mg/kg produced a half-maximal response. The exogenous opioid morphine blocked the increase in LH produced by naloxone in a dose-dependent fashion, suggesting that the specific receptor-blocking effects of the antagonist could account for its enhancement of serum LH levels. The locus of action of naloxone within the hypothalamic-pituitary-LH axis appeared to be at the level of the hypothalamus since the drug had no effect on LHRH-stimulated release of LH by the anterior pituitary and did not block dihydrotestosterone's suppression of pituitary LH release in vitro. Naloxone also prevented testosterone's negative feedback inhibition of serum LH in the castrated male rat. The results of the...
319 citations
TL;DR: It appears that the peptide demonstrated in most parts of the brain is identical with CCK-8, however, in the neurosecretory cell bodies of the hypothalamus, the median eminence and the neurohypophysis, the immunoreactive material is probably identical with gastrin.
Abstract: The distribution of gastrin and CCK-like peptides in the rat brain was studied by immunocytochemistry using an antiserum reacting equally well with both groups of peptides. Immunoreactive nerve cell bodies were detected in all cortical areas, in the hippocampus where they were particularly numerous, in the mesencephalic central gray and in the medulla oblongata. After colchicine treatment immunoreactive material appeared also in cell bodies of the magnocellular hypothalamic system. Immunoreactive nerve fibers were widely distributed in the brain. Particularly dense accumulations were seen in the hippocampus near the ventral surface of the brain, in the caudate nucleus, in the interpeduncular nucleus, the parabrachial nucleus, the dorsal part of the medulla oblongata and in the dorsal horn of the spinal cord. In the hypothalamus immunoreactive nerve fibers were observed in all nuclei, being most frequent in the ventromedial, dorsal and lateral hypothalamic nuclei. A rich supply of nerve fibers was seen in the outer zone of the median eminence and in the neurohypophysis. From previous immunochemical analysis it appears that the peptide demonstrated in most parts of the brain is identical with CCK-8. In the neurosecretory cell bodies of the hypothalamus, the median eminence and the neurohypophysis, however, the immunoreactive material is probably identical with gastrin.
257 citations
TL;DR: Findings suggest a link between the neuroendocrine mechanisms that initiate such episodic secretion and those responsible for the onset of flush episodes.
Abstract: Menopausal flush episodes were found to be invariably associated with the initiation of pulsatile pituitary release of luteinizing hormone. This was not accompanied by a significant change in circulating catecholamine or prolactin concentrations. Since pulsatile luteinizing hormone release results from episodic secretion of luteinizing hormone releasing factor by the hypothalamus, these findings suggest a link between the neuroendocrine mechanisms that initiate such episodic secretion and those responsible for the onset of flush episodes.
252 citations
TL;DR: (ir)-enkephalins in the pituitary are concentrated in nerve fibres projecting from the hypothalamus to the pars nervosa and that this pathway may be involved in the regulation of neurohypophysial neurosecretion.
Abstract: WE have previously reported that significant amounts of immunoreactive (ir)-Leu5-enkephalin were present in extracts of the neurointermediate lobe of the rat pituitary1. Negligible amounts of the pentapeptide were detected in the anterior lobe. In these assays, the concentration of Leu5-enkephalin in the neurointermediate lobe was higher than in the globus pallidus, the brain region reported to contain the densest enkephalinergic innervation2. The high content of (ir)-Leu-enkephalin in the neurointermediate lobe of the pituitary led us to further investigation of its distribution and possible function. We report here that (ir)-enkephalins in the pituitary are concentrated in nerve fibres projecting from the hypothalamus to the pars nervosa and that this pathway may be involved in the regulation of neurohypophysial neurosecretion.
247 citations
TL;DR: The experiments are consistent with the notion that brain progestin receptors mediate at least some of the behavioral effects of progesterone.
203 citations
TL;DR: Based on the treatment of serial paraffin sections with various antisera, it was clearly shown that MSH, ACTH, and LPH occur in the same cells located in the pars distalis as in the Pars intermedia.
Abstract: The ontogenesis of cells containing polypeptide hormones (ACTH, MSH, LPH, GH and Prolactin) was investigated in the fetal rat hypophysis by immunohistochemistry using the peroxidase-antiperoxidase complex. Corticotrophs, melanotrophs and lipotropic cells were revealed earlier in the pars distalis than in the pars intermedia. In the pars distalis, cells producing LPH were found in the morning of day 15 of gestation using anti-γ- or anti-β-LPH sera, and in the afternoon using anti-α- or β-endorphin sera. Cells containing β-MSH were observed from the afternoon of day 15. The cells stainable with the anti-α-MSH, anti-β-(17-39)ACTH and anti-β-(l-24)ACTH sera appeared on day 16. In the pars intermedia, the cells producing α-MSH, β MSH, α- and β-endorphin, γ and β-LPH were observed in the morning of day 17, while cells containing ACTH were only revealed in the afternoon of the same day of gestation. Based on the treatment of serial paraffin sections with various antisera, it was clearly shown that MSH, ACTH, and LPH occur in the same cells located in the pars distalis as in the pars intermedia. The development of the corticotrophs, melanotrophs and lipotropic cells does not require the presence of the fetal hypothalamus or other central nervous structures. The pituitary glands of 21 day-old fetuses encephalectomized on day 16 showed as many reactive cells as those of the littermate controls. The somatotrophs were first revealed in the pars distalis in the afternoon of day 19. The cells producing prolactin were not observed before day 21 of gestation. On some cases GH and prolactin were found together in one cell. The cytodifferentiation of GH and prolactin cells is apparently not under hypothalamic control.
187 citations
TL;DR: The results indicate that amphetamines may influence behavior through effects on specific regions of the brain through effects of amphetamine on release and uptake of catecholamine neurotransmitters.
Abstract: Amphetamine, a potent sympathomimetic amine, has powerful stimulant actions in the central nervous system. These actions are believed to be related to the influence of amphetamine on release and uptake of catecholamine neurotransmitters. The [14C]deoxyglucose method makes it possible to study changes in cerebral metabolic rate in different areas of gray and white matter. Because of the close relationship between metabolic rate and functional activity, this method may be used to identify specific structures in the brain in which functional activity is altered. The [14C]deoxyglucose method was used to explore for changes in metabolic rate produced by d-and l-amphetamine (5 mg/kg) in forty gray and four white matter structures in normal conscious rats. d-Amphetamine produced increases in local cerebral glucose utilization in a number of components of the extrapyramidal motor system, as well as in some other structures known to contain dopamine-producing and/or dopaminoceptive cells. The largest increases after d-amphetamine administration occurred in the subthalamic nucleus and the zona reticulata of the substantia nigra. l-Amphetamine produced increases in some but not all of these same structures, and these were generally smaller than those observed with d-amphetamine. Decreases in local cerebral glucose utilization after either d- or l-amphetamine administration were found in the habenula and the suprachiasmatic nuclei of the hypothalamus. The effects in the suprachiasmatic nuclei may reflect their normal diurnal rhythm in metabolic rate. These results indicate that amphetamines may influence behavior through effects on specific regions of the brain. Only some of these regions have previously been studied as possible sites of action of amphetamine.
183 citations
TL;DR: Data is presented showing that injected estrogens have a longer half-life in newborn rats than in 3-week-old animals and that estrogens such as diethylstilbestrol and moxestrol, which do not bind strongly to alpha-fetoprotein, gain access to brain estrogen receptors at lower doses compared to estradiol-17 beta.
TL;DR: The estrogen receptor system of the rat brain is not detected at 15 and 19 days of gestation, even though estrogen receptors can be measured in the maternal hypothalamus, and this is consistent with the protective role of alpha-fetoprotein in scavenging circulating maternal estradiol and keeping it from reaching intracellular receptor sites.
TL;DR: In an attempt to localize estrogen-sensitive brain sites sufficient to prime feminine sexual behavior, 30-gauge cannulae containing approximately 9 ng high specific activity [3H]-estradiol were implanted unilaterally or bilaterally into the ventromedial region of the hypothalamus of ovariectomized rats.
Abstract: In an attempt to localize estrogen-sensitive brain sites sufficient to prime feminine sexual behavior, 30-gauge cannulae containing approximately 9 ng high specific activity [3H]-estradiol were implanted unilaterally or bilaterally into the ventromedial region of the hypothalamus of ovariectomized rats. Tests for lordosis behavior were conducted on days 3 and 6 postimplantation, 4–6 h after progesterone treatment. Brain, pituitary, and uterine tissue were then sampled for radioactivity. Cannulae delivered, on the average, 3 ng [3H]estradiol during 8 days. Radioactivity was localized almost exclusively to the hypothalamus or hemihypothalamus in which the implant was placed. This was true regardless of whether tissue radioactivity or radioactivity in cell nuclei was analyzed. In the bilateral implant experiments, average hypothalamic [3H]estradiol radioactivity amounted to 56 pg/rat in tissue and 220 fg in purified cell nuclei. The latter is 4% of the estimated estrogen eceptor capacity of cell nuclei of th...
TL;DR: LHRH and LHRH agonists cause a decrease in testicular LH/hCG receptors and inhibit testicular steroidogenesis in hypophysectomised male rats, indicating a direct effect on the Leydig cells.
Abstract: Luteinising hormone releasing hormone (LHRH), produced by the hypothalamus, stimulates gonadotropin production by the pituitary1–3. Paradoxically, chronic treatment with large doses of LHRH or its agonists causes a decline in testicular steroidogenesis and testicular LH/human chorionic gonadotropin (hCG) receptors; they also cause a decrease in the weight of testes, seminal vesicles and ventral prostate4–7. There are three possible mechanisms for the inhibitory action of LHRH and its agonists. At the pituitary level, prolonged action of LHRH or its agonists may make the pituitary refractory to further stimulation by LHRH, with a decrease in serum gonadotropins and subsequent atrophy of the male reproductive organs8,9. It is also possible that pharmacological doses of LHRH stimulate the release of a large amount of LH, which in turn ‘desensitises’ the testis to further LH10–14. We have tested a third possibility, namely that LHRH and its agonists act directly on the testis. We report here that LHRH and LHRH agonists cause a decrease in testicular LH/hCG receptors and inhibit testicular steroidogenesis in hypophysectomised male rats, indicating a direct effect on the Leydig cells. This is consistent with our demonstration that LHRH and its agonists act independently of the pituitary to inhibit ovarian steroidogenesis in cultured rat granulosa cells and in hypophysectomised female rats in vivo15.
TL;DR: The present findings suggest that the PVST neurons are distinct from the PVHT neurons and that the neuronal groups of both systems form different cell columns within the nucleus.
Abstract: The distribution of labeled neurons in the paraventricular nucleus of the hypothalamus (PVN) was studied following injections of horseradish peroxidase (HRP) into the spinal cord (C8 to T1) or the hypophysis in the rat. Injections were also made in the spinal cord in another group of animals, which were subjected to water deprivation for a period of 3 days, and the PVN of these animals was examined with the electron microscope. Spinal projection neurons (paraventriculospinal tract, PVST, neurons) formed two groups; the dorsal and the ventral groups. They were located within the parvocellular part of the PVN and fused into one at the caudal level. The neurons of the dorsal group were well assembled whereas those of the ventral group were intermingled with paraventriculohypophyseal tract (PVHT) neurons, which were concentrated in the magnocellular part. Electron microscopic observations revealed that HRP-labeled neurons after spinal injections did not contain neurosecretory granules and that they were not affected by water deprivation. On the other hand, neurons containing a number of neurosecretory granules displayed a significant degree of dilatation of the endoplasmic reticulum as the result of water deprivation. These neurons contained no HRP granules. The present findings suggest that the PVST neurons are distinct from the PVHT neurons and that the neuronal groups of both systems form different cell columns within the nucleus.
TL;DR: Analysis of the regional and subcellular distribution of vasoactive intestinal peptide in the brain of adult male rat, using a specific radioimmunoassay, suggests that hypothalamic nerve endings containing the peptide derive from neuronal cell bodies located both outside and within the MBH.
TL;DR: Using neonatal sodium glutamate administration to produce such arcuate nucleus destruction in rats, the content of ACTH and β-endorphin-like material in the hypothalamus and other brain regions is markedly reduced in the absence of any change in whole pituitary, anterior lobe or plasma ACTH concentrations.
Abstract: IMMUNOASSAY and immunocytochemical techniques, in some instances with additional characterisation by bioassay and gel filtration, have demonstrated the presence of ACTH-like1–10, β-lipotropin (LPH)-like6,8,9,11–13 and beta-endorphin-like6,14,15 activity within the central nervous system. However, the source of these peptides in the central nervous system is uncertain3. Hypophysectomy is not associated with any change in hypothalamic content of ACTH1,5,10 or of beta-endorphin-like material14, suggesting a non-pituitary, presumably central nervous system, origin. Immunoreactive perikarya containing ACTH-like8–10,16,17, β-LPH-like8,9,11,13,16,17 and β-endorphin-like15–17 material have thus far only been demonstrated in the arcuate nucleus and adjacent lateral areas of the mediobasal hypothalamus. We considered that if the arcuate nucleus were the source of ACTH-like activity within other areas of the central nervous system, its destruction would result in a decrease of such activity. Neonatal administration of sodium glutamate produces central nervous system lesions, restricted largely to neurones of the arcuate nucleus and to the retina18, while sparing fibres of passage19. We report here that, using neonatal sodium glutamate administration to produce such arcuate nucleus destruction in rats, the content of ACTH and β-endorphin-like material in the hypothalamus and other brain regions is markedly reduced in the absence of any change in whole pituitary, anterior lobe or plasma ACTH concentrations.
TL;DR: The rat hypothalamus was studied at the light microscopic level with the use of single and double immunocytochemical staining methods and it was shown that the rat supraoptic and paraventricular hypothalamic nuclei, and their accessory neurosecretoryuclei, do not contain magnocellular somatostatin neurons.
Abstract: The rat hypothalamus was studied at the light microscopic level with the use of single and double immunocytochemical staining methods. It was shown that the rat supraoptic and paraventricular hypothalamic nuclei, and their accessory neurosecretory nuclei, do not contain magnocellular somatostatin neurons. The distribution of the hypothalamic parvocellular somatostatin cells is described. The parvocellular component of the rat hypothalamic paraventricular nucleus is, at least partly, composed of somatostatin cells: they form a fairly well circumscribed periventricular cell mass. The rat suprachiasmatic nuclei contain separate somatostatin neurons and vasopressin neurons. Scattered somatostatin cells are present in the entire arcuate nucleus. In addition to the periventricular somatostatin cells located in the preopticanterior hypothalamic area and in the arcuate nucleus, the rat hypothalamus also contains numerous scattered somatostatin cells located distant from the third ventricle.
TL;DR: It is suggested that the perifornical hypothalamus plays a role in the process of inhibiting food consumption in response to increased dopaminergic and adrenergic activity.
TL;DR: Pregnant rats were injected with two successive daily doses of 3H‐thymidine from gestational days 13 and 14 until the day before birth and this progressively delayed comprehensive labelling procedure determined the time of origin of neurons in the nuclei of the epithalamus, thalamic and ventral thalamus.
Abstract: Groups of pregnant rats were injected with two successive daily doses of 3H-thymidine from gestational days 13 and 14 (E13+14) until the day before birth (E21+22) With this progressively delayed comprehensive labelling procedure we determined the time of origin of neurons in the nuclei of the epithalamus, thalamus, and ventral thalamus The zona incerta, subtha- lamic nucleus, reticular nucleus, posterior nucleus, and ventral lateral genicu- late nucleus are composed of the earliest arising neurons (E13, or before, to E15) The neurons of the lateral habenular nucleus are produced between days E13-16 The neurons of the medial geniculate and lateral geniculate nuclei, the ventrobasal and ventrolateral complexes, and the nucleus lateralis, pars poste- rior, arise rapidly on days E14-15; the medial geniculate nucleus with a peak on day E14, the others with a peak on day El5 Neurons of a group of nuclei, with ill-defined boundaries medial to the sensory relay nuclei, arise apparently on days E15-16, with a peak on day E15; these may represent the intralaminar nu- clei The next group is generated on days E15-16 but with peak formation time on day E16: this includes the anteroventral, anterodorsal, anteromedial and mediodorsal nuclei The rhomboid, reuniens and paratenial nuclei, and the paraventricular nucleus, pars anterior, arise next (E16-17) The medial haben- ular nucleus forms last and over a protracted period (E15-19) With their lengthy generation time the lateral and medial habenular nuclei resemble more the nuclei of the hypothalamus than the nuclei of the dorsal thalamus In three preceding papers of this series (Altman and Bayer, '78a,b,c) we dealt with the time and site of origin of neurons of the hypothalamus and of the cells of its special- ized ventricular linings The time of origin of cells in different regions of the hypothalamus was determined quantitatively in adult rats that were tagged with 3H-thymidine from the early embryonic through the early postnatal period Internuclear and intranuclear gradi- ents in autoradiographic labelling patterns were noted and interpreted as directional "ar- rows" that point to the possible site of origin and route of dispersion of the settled cells This information obtained in adult rats was then used, in an attempt to identify the neuro- epithelial source and early differentiation of various components of the hypothalamus, in a series of normal and X-irradiated rat embryos
TL;DR: It is demonstrated that some of the catecholamine-containing cells in the rabbit dorsal hypothalamus project directly to the thoracic spinal cord, which indicates that these cells may be involved in the integration of pituitary hormonal secretion and peripheral autonomic nervous regulation.
TL;DR: Findings are consistent with the hypothesis that a population of neuronal cell bodies producing alpha-MSH originate in the arcuate region of the hypothalamus and that they send axonal projections to many areas of the limbic system and brain stem.
TL;DR: The results suggest that the same neurons of the rat hypothalamus synthesize several neuropeptides identical with or immunologically related to endorphins, ACTH, α-MSH and β-LPH, probably arising from a common precursor molecule similar to that found in the corticotropic cells of the pituitary.
Abstract: In rat brains intraventricularly injected with colchicine, the same discrete neurons of the arcuate and ventromedial nuclei can be stained with antisera against α- and β-endorphins, (1-24)ACTH, (17-39)ACTH, α- and β-MSH, and β-LPH, as demonstrated by comparative studies in consecutive serial sections. These neurons are strongly reactive with anti-(17-39)ACTH, anti-β-endorphin, anti-α-MSH and anti-β-MSH, and more faintly stained with anti-α-endorphin, anti-β-LPH and anti-(1-24)ACTH. Exceptionally, neurons reactive with anti-(17-39)ACTH and anti-β-endorphin are poorly stained or completely negative with anti-α-MSH and anti-β-MSH. Immunoreactive fibers end in the lateral median eminence and in the arcuate nucleus proper, or form ascending pathways along the third ventricle. Comparative studies with other antisera or with the Falck and Hillarp technique show that these neurons differ from the elements producing LH-RH, somatostatin, neurophysin, oxytocin, vasopressin and dopamine.
TL;DR: This selective reaction, which involved approximately 1000 neurons on each side of the third ventricle, was unaltered by concomitant administration of 10 (-3) M non-radioactive norepinephrine, and was absent after intraventricular injection of 10(-5) or 10(-4) M tritiated nore Alpinephrine.
TL;DR: A hypothetical scheme for feedback actions on target hypothalamic and pituitary actions by gonadotropins is proposed, and present state of knowledge in this respect is presented.
Abstract: PIP: A hypothetical scheme for feedback actions on target hypothalamic and pituitary actions by gonadotropins is proposed, and present state of knowledge in this respect is presented. A stimulatory effect of target organ hormones on the hypothalamo-adenohypophysial system (HAS) was shown only to operate in the case of gonadotropin surge. In spontaneous ovulators, at low plasma progesterone levels, estradiol 1st increases pituitary responsiveness and then permits the expression of a daily neural signal that results in the increased release of gonadotropin-releasing hormone (GRH) into portal vessel blood. Increased GRH in portal vessel blood releases luteinizing hormone (LH), and at the same time further increases pituitary responsiveness by its priming effect. The increased plasma LH concentration stimulates the secretion of progesterone, which further increases pituitary responsiveness. This series of events leads to the LH surge. The priming effect of GRH obviates the need for a massive release of GRH and ensures that the peak of the GRH surge coincides with the peak in pituitary responsiveness. To be affected fully by estradiol and progesterone, the gonadotropins must be exposed to GRH; this is why neural blocking agents can inhibit the effect of these steroids. Secretion of LH but not FSH is dependent on continuous exposure of the gonadotropins to GRH. The factors that terminate the GRH surge are not known, though progesterone may play a role. This scheme also operates in the production of the 1st LH surge in rats.
TL;DR: Findings suggest that the synthesis, and transport, of ACTH and beta-End are linked in the brain as well as in the pituitary, possibly through a common precursor.
Abstract: Immunoreactive ACTH and beta-endorphin (beta-End) were localized in the brain and pituitaries of normal and colchicine-treated rats, using the immunoperoxidase method at the light microscopic level. On adjacent serial 5-micron paraffin sections of anterior pituitaries, both ACTH and beta-End could be found in the same cells. On adjacent 5-micron paraffin sections of brains of colchicine-treated rats, both ACTH and beta-End could be found in the same perikarya of hypothalamic arcuate nucleus neurons. It appeared that all perikarya containing beta-End contained ACTH as well, suggesting that neurons producing beta-End also produce ACTH. Pathways of ACTH fibers corresponded to pathways of beta-End fibers. These findings suggest that the synthesis, and transport, of ACTH and beta-End are linked in the brain as well as in the pituitary, possibly through a common precursor.
TL;DR: Evidence of a somatostatin (SRIF)-like antigen has been found in the brain and digestive tract of rainbow trout and in the gut, where material immunoreactive for luteinizing hormone-releasing hormone has the same distribution in the pituitary as SRIF.
TL;DR: The zone of fibers essential for the active components of maternal behavior, i.e., nest building and retrieving, is determined and appear to enter/leave MPO dorsolaterally beneath the crossing of the anterior commissure in the region of the bed nucleus of the stria terminalis.
TL;DR: These experiments demonstrate the feasibility of using a neuropharmacologic approach to the mechanisms underlying mammalian circadian rhythms, and suggest that light and carbachol presumably act on the suprachiasmatic nucleus of the hypothalamus.
Abstract: Environmental lighting regulates numerous circadian rhythms, including the cycle in pineal serotonin N-acetyltransferase activity. Brief exposure of rats to light can shift the phase of this enzyme's circadian rhythm. Light also rapidly reduces nocturnal enzyme activity. Intraventricular injections of carbachol, a cholinergic agonist, can mimic both of these effects. Light and carbachol presumably act on the suprachiasmatic nucleus of the hypothalamus. These experiments demonstrate the feasibility of using a neuropharmacologic approach to the mechanisms underlying mammalian circadian rhythms.
TL;DR: Female freshwater eels injected with estradiol-17β (E2) for 15–78 days appear paler and secrete more mucus than controls and vitellogenin synthesis occurs in the liver, which shows a significant hypertrophy, an increased vacuolization and glycogen depletion.
Abstract: Female freshwater eels injected with estradiol-17β (E2) for 15–78 days appear paler and secrete more mucus than controls. The resulting strongly opalescent blood plasma indicates that vitellogenin synthesis occurs in the liver, which shows a significant hypertrophy, an increased vacuolization (lipid material) and glycogen depletion. Plasma sodium is lowered, but calcium levels are considerably increased. The gonosomatic index increases (0.92±0.1 to a maximum of 2.21). Oocytes are enlarged, but the incorporation of vitellogenin remains discrete. Gonadotrophs (GTH cells), small and scarcely visible in the pituitary of control eels, are hypertrophied and contain numerous glycoprotein granules after E2-administration. E2 may act on the pituitary and/or hypothalamus via a positive feedback to induce gonadotrophin (GTH) synthesis; GTH release seems to be very limited as indicated by the ovarian response. The differentiation of GTH cells in eels treated with fish pituitary extracts is most probably due to secretion of E2 by the ovary, which reacts on the pituitary. Various hypotheses are considered to explain the low GTH release. Thyrotrophs, somatotrophs and prolactin cells of the pituitary are stimulated. In the pars intermedia, MSH and PAS-positive cells appear less active. A possible antidopaminergic effect of E2 is discussed. E2 administration constitutes a simple and economic technique to induce the synthesis of GTH and will facilitate the biochemical and biological study of the latter hormone in eels.