Localization of kainate receptor subunit GluR5-immunoreactive cells in the rat hypothalamus

Eyigor, Ozhan; Minbay, Zehra; Çavuşoğlu, İlkin; Jennes, Lothar

doi:10.1016/j.molbrainres.2005.01.015

Cited by 14 publications

(16 citation statements)

References 34 publications

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“…Thus, kainic acid receptors likely are the predominant subclass of glutamate receptors in the VMH that stimulate the counterregulatory responses. This finding is consistent with previous reports that showed that activation of VMH kainic acid receptors enhances sympathetic drive to endocrine and neuroendocrine systems, helping to raise plasma glucose concentrations (13,26–29). Although the agonists used in the current study are selective for their respective targets, some overlap exists in the selectivity of the AMPA and kainic acid receptor antagonists.…”

Section: Discussionsupporting

confidence: 93%

Impaired Glutamatergic Neurotransmission in the Ventromedial Hypothalamus May Contribute to Defective Counterregulation in Recurrently Hypoglycemic Rats

et al. 2017

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The objectives of this study were to understand the role of glutamatergic neurotransmission in the ventromedial hypothalamus (VMH) in response to hypoglycemia and to elucidate the effects of recurrent hypoglycemia (RH) on this neurotransmitter. We 1) measured changes in interstitial VMH glutamate levels by using microdialysis and biosensors, 2) identified the receptors that mediate glutamate’s stimulatory effects on the counterregulatory responses, 3) quantified glutamate metabolic enzyme levels in the VMH, 4) examined astrocytic glutamate reuptake mechanisms, and 5) used 1H-[13C]-nuclear magnetic resonance (NMR) spectroscopy to evaluate the effects of RH on neuronal glutamate metabolism. We demonstrated that glutamate acts through kainic acid receptors in the VMH to augment counterregulatory responses. Biosensors showed that the normal transient rise in glutamate levels in response to hypoglycemia is absent in RH animals. More importantly, RH reduced extracellular glutamate concentrations partly as a result of decreased glutaminase expression. Decreased glutamate was also associated with reduced astrocytic glutamate transport in the VMH. NMR analysis revealed a decrease in [4-13C]glutamate but unaltered [4-13C]glutamine concentrations in the VMH of RH animals. The data suggest that glutamate release is important for proper activation of the counterregulatory response to hypoglycemia and that impairment of glutamate metabolic and resynthetic pathways with RH may contribute to counterregulatory failure.

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Section: Discussionsupporting

confidence: 93%

Impaired Glutamatergic Neurotransmission in the Ventromedial Hypothalamus May Contribute to Defective Counterregulation in Recurrently Hypoglycemic Rats

et al. 2017

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“…Anatomical evidence suggests that receptors from the n-methyl-d-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), and kainate receptor families, as well as metabotropic receptors, are localized in CRH-containing regions of the PVN (Herman et al, 2000; Scaccianoce et al, 2003; Eyigor et al, 2005; Ziegler et al, 2005). Antagonist studies have demonstrated functional roles for ionotropic (Ziegler and Herman, 2000) and metabotropic (Johnson et al, 2001; Scaccianoce et al, 2003) glutamate receptors in regulation of the HPA axis.…”

Section: Introductionmentioning

confidence: 99%

GluR5-mediated glutamate signaling regulates hypothalamo–pituitary–adrenocortical stress responses at the paraventricular nucleus and median eminence

Evanson

Hooren

Herman

2009

Psychoneuroendocrinology

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SummaryGlutamate is the main excitatory neurotransmitter in the central nervous system, and plays an excitatory role in generation of hypothalamic-pituitary-adrenocortical (HPA) axis responses to stress. The current study assesses the role of kainate-preferring receptors in glutamatergic excitation of the HPA axis. In situ hybridization and immunohistochemical analyses confirmed the existence of the GluR5 kainate subunit in the paraventricular nucleus of the hypothalamus (PVN). Importantly, GluR5 immunoreactivity was enriched in the external lamina of the median eminence, where it is co-localized with corticotropin releasing hormone (CRH). Intra-PVN infusion of LY382884 increased plasma adrenocorticotropin (ACTH), corticosterone and PVN Fos immunoreactivity. Infusions of LY382884 into the median eminence region, on the other hand, reduced restraint induced ACTH release without altering c-Fos expression. Together, these findings provide evidence for glutamate-mediated signaling in control of CRH release at the PVN and median eminence, mediated by way of kainate-preferring receptor complexes.

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“…Early ultrastructural evidence confirmed glutamate immunopositive synaptic vesicles at asymmetric synapses within the PVH (Bartanusz et al, 2004; Decavel and Van den Pol, 1992; Van den Pol, 1990, 1991), suggesting that glutamate may account for as much as 50% of all synapses within the nucleus (Van den Pol, 1991). This report was followed by studies showing glutamate receptor binding and mRNA and protein expression for glutamate receptor subunits in the PVH (Al-Ghoul et al, 1997; Aubry et al, 1996; Eyigor et al, 2001, 2005; Herman et al, 2000; Khan et al, 2000; Kiss et al, 1996; Mateos et al, 1998; Oliver et al, 1996; Petralia and Wenthold, 1996; Sato et al, 1993; Tasker et al, 1998; Van den Pol et al, 1994; Ziegler et al, 2005). In addition to these anatomical data, electrophysiological data from cultured slices have documented functional excitatory responses of PVH neurons to glutamatergic input (Bartanusz et al, 2004; Boudaba et al, 1997; Daftary et al, 1998, 2000; Van den Pol et al, 1990, 1996; Wuarin and Dudek, 1991) and in vivo studies involving glutamate or glutamate receptor antagonist microinjections in the PVH led to stimulation/inhibition of the HPA axis at the level of corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and corticosterone secretion (Cole and Sawchenko, 2002).…”

mentioning

confidence: 96%

Brainstem origins of glutamatergic innervation of the rat hypothalamic paraventricular nucleus

Ziegler

Edwards

Ulrich‐Lai

et al. 2012

J of Comparative Neurology

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Multiple lines of evidence document a role for glutamatergic input to the hypothalamic paraventricular nucleus (PVH) in stress-induced activation of the hypothalamic-pituitary-adrenocortical (HPA) axis. However, the neuro-anatomical origins of the glutamatergic input have yet to be definitively determined. We have previously shown that vesicular glutamate transporter 2 (VGLUT2) is the predominant VGLUT isoform expressed in the basal forebrain and brainstem, including PVH-projecting regions, and that the PVH is preferentially innervated by VGLUT2-immunoreactive terminals/boutons. The present study employed a dual-labeling approach, combining immunolabeling for a retrograde tract tracer, Fluoro-Gold (FG), with in situ hybridization for VGLUT2 mRNA, to map the brainstem and caudal forebrain distribution of glutamatergic PVH-projecting neurons. The present report presents evidence for substantial dual labeling in the periaqueductal gray, caudal portions of the zona incerta and subparafascicular nucleus, and the lateral parabrachial nucleus. The current data also suggest that relatively few PVH-projecting neurons in ascending raphe nuclei, nucleus of the solitary tract, or ventrolateral medulla are VGLUT2 positive. The data reveal multiple brainstem origins of glutamatergic input to PVH that are positioned to play a role in transducing a diverse range of stressful stimuli.

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Localization of kainate receptor subunit GluR5-immunoreactive cells in the rat hypothalamus

Cited by 14 publications

References 34 publications

Impaired Glutamatergic Neurotransmission in the Ventromedial Hypothalamus May Contribute to Defective Counterregulation in Recurrently Hypoglycemic Rats

Impaired Glutamatergic Neurotransmission in the Ventromedial Hypothalamus May Contribute to Defective Counterregulation in Recurrently Hypoglycemic Rats

GluR5-mediated glutamate signaling regulates hypothalamo–pituitary–adrenocortical stress responses at the paraventricular nucleus and median eminence

Brainstem origins of glutamatergic innervation of the rat hypothalamic paraventricular nucleus

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