Effects of acute insulin deficiency on catecholamine and indoleamine content and catecholamine turnover in microdissected hypothalamic nuclei in streptozotocin-diabetic rats

Oliver, E.H.; Sartin, J. L.; Dieberg, Gudrun; Ch, Rahe; Dn, Marple; Kemppainen, R.J.

doi:10.1530/acta.0.1200343

Cited by 17 publications

(6 citation statements)

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“…A direct, central action of insulin is possible, as insulin receptors are widely distributed in the brain including sites that are important in the control of GnRH secretion, i.e., the arcuate nucleus and the median eminence within the medial basal hypothalamus [30,31]. Insulin inhibits uptake of norepinephrine in dissociated rat brain cells [32] and alters catecholamine kinetics in the hypothalamus [33]. Moreover, insulin receptors are present on catecholaminergic terminals in the hypothalamus [34], at sites where such neurotransmitters are known to regulate GnRH secretion in sheep [35].…”

Section: Discussionmentioning

confidence: 99%

Central Action of Insulin Regulates Pulsatile Luteinizing Hormone Secretion in the Diabetic Sheep Model1

Tanaka

Nagatani

Bucholtz

et al. 2000

Biology of Reproduction

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This study tested the hypothesis that central mechanisms regulating luteinizing hormone (LH) secretion are responsive to insulin. Our approach was to infuse insulin into the lateral ventricle of six streptozotocin-induced diabetic sheep in an amount that is normally present in the CSF when LH secretion is maintained by peripheral insulin administration. In the first experiment, we monitored cerebrospinal fluid (CSF) insulin concentrations every 3-5 h in four diabetic sheep given insulin by peripheral injection (30 IU). The insulin concentration in the CSF was increased after insulin injection, and there was a positive relationship between CSF and plasma concentrations of insulin (r = 0.80, P < 0.01). In the second experiment, peripheral insulin administration was discontinued, and the sheep received either an intracerebroventricular (i.c.v.) infusion of insulin (12 mU/day in 2.4 ml saline) or saline (2.4 ml/day) for 5 days (n = 6) in a crossover design. The dose of insulin (i.c.v.) was calculated to approximate the increase in CSF insulin concentration found after peripheral insulin treatment. To monitor LH secretory patterns, blood samples were collected by jugular venipuncture at 10-min intervals for 4 h on the day before and 5 days after the start of i.c.v. insulin infusion. To monitor the increase in CSF insulin concentrations, a single CSF sample was collected one and four days after the start of the central infusion. The i.c.v. insulin infusion increased CSF insulin concentrations above those in saline-treated animals (P < 0.05) and maintained them at or above the peak levels achieved after peripheral insulin treatment. Central insulin infusion did not affect peripheral (plasma) insulin or glucose concentrations. LH pulse frequency in insulin-treated animals was greater than that in saline-treated animals (3.5 +/- 0.2 vs. 2.3 +/- 0.3 pulses/4 h, P < 0.01), but it was less than that during peripheral insulin treatment (4.8 +/- 0.2 pulses/4 h, P < 0.01). Our findings suggest that physiologic levels of central insulin supplementation are able to increase pulsatile LH secretion in diabetic sheep with low peripheral insulin. These results are consistent with the notion that central insulin plays a role in regulating pulsatile GnRH secretion.

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Section: Discussionmentioning

confidence: 99%

Central Action of Insulin Regulates Pulsatile Luteinizing Hormone Secretion in the Diabetic Sheep Model1

Tanaka

Nagatani

Bucholtz

et al. 2000

Biology of Reproduction

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“…This was espe cially perplexing, and we are presently pursu ing this finding. It may be that medullary 5-HT levels are significantly depressed by as much as 71% in diabetic rats [15,19,22,[42][43][44][45], therefore, less 5-HT is available for re lease in our slices. These 5-HT neurons clearly possess functional ci2-adrenergic receptors be cause clonidine depresses S2 release in both normal and diabetic slices.…”

Section: Discussionmentioning

confidence: 94%

“…All of the reported changes in neu rotransmitter concentrations brought about by the diabetic state were returned towards normal levels with insulin perfusion therapy. Streptozotocin-induced diabetes in rats mark edly reduces the synthesis [22,23], as well as content, of 5-HT in selective brain regions such as hypothalamus, brain stem, and corpus callosum [15. 22.…”

Section: Introductionmentioning

confidence: 99%

Effect of Insulin and Clonidine on the Evoked Release of Norepinephrine and Serotonin from the Nucleus tractus solitarius of the Diabetic Rat

Dunbar

Clough-Helfman²,

Barraco³

et al. 1995

Pharmacology

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Dorsal medullary brain slices containing primarily the nucleus tractus solitarius (NTS) were obtained from normal or 40- to 50-day streptozotocin-diabetic rats and employed for superfusion studies of evoked transmitter release. Electrically stimulated (25 mA, 2-ms pulses, 3 Hz, 1 min) release of [³H]norepinephrine ([³H]NE) or [³H]5-hydroxytryptamine ([³H]5-HT) from 400-µm NTS slices stimulated at 75 min (S₁) and 130 min (S₂) resulted in S₂/S₁ release ratios that were not different between normal controls or diabetic control groups. Perfusion of normal [³H]NE-loaded slices with 0.1 µmol/l clonidine reduced the S₂/S₁ ratio by 23% (p < 0.05) which was uniform in the caudal, subpostremal, and intermediate segment levels of the NTS. In diabetic NTS slices, the S₂/S₁ ratio was significantly less reduced by clonidine in both the subpostremal (–3%) and intermediate (–11%) slice regions. Blockade of α₂-adrenoceptors with yohimbine (0.1 µmol/l) enhanced (p < 0.05) [³H]NE release (S₂/S1 ratios) in slices from both normal and diabetic rats. Perfusion of [³H]NE-loaded slices with 5 mU/ml insulin did not affect S₂ release. Evoked S₂/S₁ release ratios from NTS slices loaded with [³H]5-HT did not differ between normal control and diabetic control groups. Clonidine (0.1 µmol/l) reduced S₂-evoked release in both normal (–30%) and diabetic (–44%) slices, but the groups were not different from each other. Superfusion with 5 mU/ml insulin did not alter S₂/S₁ ratios in normal [³H]5-HT loaded slices, but did increase the diabetic NTS slice S₂/S₁ ratio to 1.40 ± 0.06 (p < 0.01). In summary, it appears that α₂-adrenoceptor-mediated inhibition of [³H]NE release in the NTS was selectively attenuated in a regionally specific manner in diabetic animals. Release inhibition may be associated with receptor downregulation in NTS regions associated with cardiovascular reflex transmission. Insulin superfusion augmented [³H]5-HT release in the diabetic NTS slices, possibly through increased transmitter synthesis or improved synaptic release.

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“…Besides metabolic changes in peripheral tissues, several central nervous system neurotransmitters are affected by STZ treatment in these animals The concentration of 5-HT is increased in paraventricular nucleus, whereas 5-hydroxyindolic acetic acid (5-HIAA), the deaminated metabolite of 5-HT, is reduced in a number of hypothalamic nuclei suggesting reduced serotonergic activity (Bitar et al, 1987). However, in another study, employing a different methodological approach, STZ did not change the metabolism of 5-HT and 5-HIAA in diverse hypothalamic nuclei (Oliver et al, 1989).…”

Section: Introductionmentioning

confidence: 87%

Hypothalamic 5-Hydroxytryptamine Metabolism Is not Influenced by Streptozotocin-Diabetes Induced at Neonatal Age

Huupponen¹,

Koulu²,

Pesonen³

2009

Exp Clin Endocrinol Diabetes

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Rats were rendered diabetic at neonatal age by an intraperitoneal injection of streptozotocin (90 mg/kg). At 8-10 weeks of age, their 5-HT and 5-HIAA levels in different hypothalamic nuclei (ventromedial, paraventricular, periventricular, supraoptical and suprachiasmatic nuclei) were similar to control animals which received vehicle only. It is concluded that the combination of mild hyperglycemia and hypoinsulinemia does not affect hypothalamic 5-HT metabolism in rats.

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Effects of acute insulin deficiency on catecholamine and indoleamine content and catecholamine turnover in microdissected hypothalamic nuclei in streptozotocin-diabetic rats

Cited by 17 publications

References 0 publications

Central Action of Insulin Regulates Pulsatile Luteinizing Hormone Secretion in the Diabetic Sheep Model1

Central Action of Insulin Regulates Pulsatile Luteinizing Hormone Secretion in the Diabetic Sheep Model1

Effect of Insulin and Clonidine on the Evoked Release of Norepinephrine and Serotonin from the Nucleus tractus solitarius of the Diabetic Rat

Hypothalamic 5-Hydroxytryptamine Metabolism Is not Influenced by Streptozotocin-Diabetes Induced at Neonatal Age

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