The hypothalamic arcuate nucleus-median eminence complex: Immunohistochemistry of transmitters, peptides and DARPP-32 with special reference to coexistence in dopamine neurons

Everitt, Barry J.; Meister, Björn; Hökfelt, Tomas; Melander, T.; Terenius, Lars; Rökaeus, Åke; Theodorsson‐Norheim, Elvar; Dockray, Graham J.; Edwardson, James A.; Cuello, Claudio; Elde, Robert; Goldstein, Menek; Hemmings, Hugh C.; Ouimet, Charles C.; Walaas, Ivar; Greengard, Paul; Vale, Wylie; Weber, Eckard; Wu, Jang‐Yen; Chang, Kwen‐Jen

doi:10.1016/s0006-8993(86)80192-5

Cited by 101 publications

(62 citation statements)

References 187 publications

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“…POMC-derived peptides such as ␤-endorphin (see Sanger, 1981) and melanocytestimulating hormone (melanocortin) (see below) have been shown to be effectors of feeding and therefore may be important mediators of leptin on the CNS. Similar to the NPY neurons, the large POMC-containing neurons of the arcuate nucleus show rich projections to the PVN (see Everitt et al, 1986). That NPY and POMC neurons project to the PVN suggest that the arcuate neurons, which may be located outside of the BBB (see above), both operate via the PV N to reduce food intake.…”

Section: Discussionmentioning

confidence: 96%

Leptin Receptor Immunoreactivity in Chemically Defined Target Neurons of the Hypothalamus

et al. 1998

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The adipose tissue-derived hormone leptin regulates body weight homeostasis by decreasing food intake and increasing energy expenditure. The weight-reducing action of leptin is thought to be mediated primarily by signal transduction through the leptin receptor (LR) in the hypothalamus. We have used immunohistochemistry to localize LR-immunoreactive (LR-IR) cells in the rat brain using an antiserum against a portion of the intracellular domain of LR that is common to all LR isoforms. The antiserum recognized the short and long isoforms of LR in transfected hematopoietic BaF3 cells. To examine the chemical nature of target cells for leptin, direct double-labeling immunofluorescence histochemistry was applied. The results show extensive distribution of LR-like immunoreactivity (LR-LI) in the brain with positively stained cells present, e.g., in the choroid plexus, cerebral cortex, hippocampus, thalamus, and hypothalamus. In the hypothalamus, strongly LR-IR neurons were present in the supraoptic nucleus (SON) and paraventricular nucleus (PVN), periventricular nucleus, arcuate nucleus, and lateral hypothalamus. Weaker LR-IR neurons were also demonstrated in the lateral and medial preoptic nuclei, suprachiasmatic nucleus, ventromedial and dorsomedial nuclei, and tuberomammillary nucleus. Confocal laser scanning microscopy showed LR-LI in the periphery of individual cells. In magnocellular neurons of the SON and PVN, LR-LI was demonstrated in vasopressin-and oxytocin-containing neurons. In parvocellular neurons of the PVN, LR-LI was demonstrated in many corticotropin-releasing hormone-containing neurons. LR-IR neurons were mainly seen in the ventromedial aspect of the arcuate nucleus, where LR-LI co-localized with neuropeptide Y. In the ventrolateral part of the arcuate nucleus, LR-LI was present in many large adrenocorticotropic hormone-IR proopiomelanocortin-containing neurons and in a few galanin-, neurotensin-, and growth hormone-releasing hormonecontaining neurons. In the dorsomedial arcuate nucleus, few tyrosine hydroxylase (dopamine)-containing neurons were seen to have LR-LI. Melanin-concentrating hormone-containing neurons in the lateral hypothalamus had LR-LI. Based on the immunohistochemical results, possible interactions of leptin with brain mechanisms are discussed.

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Section: Discussionmentioning

confidence: 96%

Leptin Receptor Immunoreactivity in Chemically Defined Target Neurons of the Hypothalamus

et al. 1998

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“…These species-based differences were further highlighted by a comparative study of the chemical neuroanatomy of the mouse DR nucleus with a focus on serotoninergic neurons (Everitt et al, 1986;Meister and Hökfelt, 1988). Despite evidence for the presence of several neuropeptides (including galanin and CRF) in nerve terminal networks close to DR serotonin neurons, indicative of direct or indirect influences on them, a relatively low number of coexisting transmitters was detected in mouse serotonin neurons compared with observations in the rat (e.g., Holets et al, 1988;Xu and Hökfelt, 1997;Larm et al, 2003).…”

Section: Galanin Family Peptide and Galanin Receptor Distributionsmentioning

confidence: 98%

“…b Saar et al (2002). c Bartfai et al (2004 Galanin Family Peptides and Receptors species, including rat (Skofitsch and Jacobowitz, 1985b;Everitt et al, 1986;Ryan and Gundlach, 1996), mouse (Cheung et al, 2001;Perez et al, 2001;Lein et al, 2007;see Allen Brain Institute [www.brain-map.org]), primate (Kordower et al, 1992), and human (Gentleman et al, 1989;Garcia-Falgueras et al, 2011), where it coexists with a complex, species-dependent array of classic neurotransmitters (Melander et al, 1986d;see Merchenthaler et al, 1993b, andJacobowitz et al, 2004, for review) and other peptides (see below). On a relative quantitative scale, GAL mRNA is highly abundant in the hypothalamic and brain stem areas of the rat (Ryan and Gundlach, 1996;Jacobowitz et al, 2004) and mouse (Cheung et al, 2001), with very high levels in the preoptic-, periventricular-, and dorsomedial-hypothalamic nuclei, bed nucleus of the stria terminalis (BNST), medial and lateral amygdala, LC, and nucleus of the solitary tract.…”

Section: Galanin Family Peptide and Galanin Receptor Distributionsmentioning

confidence: 99%

“…There are many other cases of galanin coexistence with a classic transmitter in the CNS and peripheral nervous system (PNS), for example, in GABAergic and dopaminergic neurons in the hypothalamic arcuate nucleus (ARC) (Everitt et al, 1986;Meister and Hökfelt, 1988), in GABAergic neurons in the spinal cord (Skofitsch and Jacobowitz, 1985a;Tuchscherer and Seybold, 1989;Klein et al, 1990;Carlton and Coggeshall, 1996), in cholinergic motor neurons (Lindh et al, 1989;Schreiber et al, 1994;Zhang et al, 1994), in glutamatergic DRG neurons (Skofitsch and Jacobowitz, 1985a;Tuchscherer and Seybold, 1989;Klein et al, 1990;Carlton and Coggeshall, 1996), and in noradrenergic sympathetic neurons (Lindh et al, 1989;Schreiber et al, 1994;Zhang et al, 1994), again with differing levels of cross-species fidelity.…”

Section: Galanin Family Peptide and Galanin Receptor Distributionsmentioning

confidence: 99%

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Physiology, Signaling, and Pharmacology of Galanin Peptides and Receptors: Three Decades of Emerging Diversity

et al. 2014

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“…This area contains tuberoinfundibular dopaminergic neurons, which are believed to be the source of PRL-regulating dopamine. In addition, galanin, growth hormonereleasing factor-like immunoreactivity, gamma-aminobutyric acid and somatostatin -hormones and peptides involved in the regulation of the anterior pituitary -are all present in the arcuate nucleus (8,9).…”

Section: Introductionmentioning

confidence: 99%

Paradoxical GH response to TRH during status epilepticus in man

Lindbom¹,

Al²,

Tomson³

1999

European Journal of Endocrinology

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Information on GH in relation to epilepsy is sparse, and to our knowledge there is no information on GH levels during status epilepticus in man. We studied GH in serum in six patients during status epilepticus, and in a control group of six seizure-free patients with epilepsy, before and after injection of TRH. The baseline GH values before TRH administration were within the normal range in all patients. After injection of TRH all patients with status epilepticus showed a paradoxical peak-shaped increase of GH to at least twice their baseline levels within 45 min after the injection (median basal GH value 1.5 mU/l and median peak GH value 6.5 mU/l, mean increase 330%). No uniform reaction to TRH was observed in the control group (median basal GH value 2.7 mU/l and median of the highest value within 45 min 5.2 mU/l). A paradoxical peak reaction of GH to TRH was significantly more frequent in the status epilepticus group compared with the control group (P = 0.008, Fisher exact probability test). TRH is not considered a GH-releasing hormone in humans during normal conditions, but a paradoxical response of GH to TRH, similar to that observed during status epilepticus, has been reported in various other pathological conditions, such as acromegaly, liver cirrhosis, mental depression and hypothyroidism. Our results of GH release after TRH administration in patients with status epilepticus suggest an altered regulation of GH as a result of the long-standing epileptic activity.

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The hypothalamic arcuate nucleus-median eminence complex: Immunohistochemistry of transmitters, peptides and DARPP-32 with special reference to coexistence in dopamine neurons

Cited by 101 publications

References 187 publications

Leptin Receptor Immunoreactivity in Chemically Defined Target Neurons of the Hypothalamus

Leptin Receptor Immunoreactivity in Chemically Defined Target Neurons of the Hypothalamus

Physiology, Signaling, and Pharmacology of Galanin Peptides and Receptors: Three Decades of Emerging Diversity

Paradoxical GH response to TRH during status epilepticus in man

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