Insulin-Like Growth Factor-1 Inhibits Adult Supraoptic Neurons via Complementary Modulation of Mechanoreceptors and Glycine Receptors

Ster, Jeanne; Colomer, Claude; Monzo, C.; Duvoid-Guillou, Anne; Moos, Françoise; Alonso, Gérard; Hussy, Nicolas

doi:10.1523/jneurosci.4053-04.2005

Cited by 20 publications

(9 citation statements)

References 51 publications

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“…A variety of downstream second-messenger systems use phosphatidylinositol (3,4,5) triphosphate, including mitogenactivated protein kinase and stress-induced protein kinase. Growth factors and insulin may share similar actions on GlyRs because the activation of insulin-like-growth factor-1 (IGF-1) receptor rapidly (within seconds) increases the potency of taurine for GlyRs; however, the actions of IGF-1 were independent of PI3 kinase pathways because they are insensitive to wortmannin (Ster et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Insulin Increases the Potency of Glycine at Ionotropic Glycine Receptors

Caraiscos

Bonin²,

Newell³

et al. 2007

Mol Pharmacol

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The mechanisms by which insulin modulates neuronal plasticity and pain processes remain poorly understood. Here we report that insulin rapidly increases the function of glycine receptors in murine spinal neurons and recombinant human glycine receptors expressed in human embryonic kidney cells. Whole-cell patch-clamp recordings showed that insulin reversibly enhanced current evoked by exogenous glycine and increased the amplitude of spontaneous glycinergic miniature inhibitory postsynaptic currents recorded in cultured spinal neurons. Insulin (1 M) also shifted the glycine concentration-response plot to the left and reduced the glycine EC 50 value from 52 to 31 M. Currents evoked by a submaximal concentration of glycine were increased to approximately 140% of control. The glycine receptor ␣ subunit was sufficient for the enhancement by insulin because currents from recombinant homomeric ␣ 1 receptors and heteromeric ␣ 1 ␤ receptors were both increased. Insulin acted at the insulin receptor via pathways dependent on tyrosine kinase and phosphatidylinositol 3 kinase because the insulin effect was eliminated by the insulin receptor antagonist, hydroxy-2-naphthalenylmethylphosphonic acid trisacetoxymethyl ester, the tyrosine kinase inhibitor lavendustin A, and the phosphatidylinositol 3 kinase antagonist wortmannin. Together, these results show that insulin has a novel regulatory action on the potency of glycine for ionotropic glycine receptors.

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Section: Discussionmentioning

confidence: 99%

Insulin Increases the Potency of Glycine at Ionotropic Glycine Receptors

Caraiscos

Bonin²,

Newell³

et al. 2007

Mol Pharmacol

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“…Other neurotransmitters are modulated by IGF-1 in addition to GABA [28]. These include acetylcholine [29], which is a well-known determinant of cognition, and glycine [30].…”

Section: Potential Mechanisms By Which Hormonal Dysregulation Affectsmentioning

confidence: 99%

Stress hormones, sleep deprivation and cognition in older adults

et al. 2013

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“…OXT stimulates taurine efflux from cultured pituicytes[71] and taurine inhibits SON neuronal activity[72], likely via extrasynaptic glycine receptors[73]. Because hypotonicity-evoked taurine release is causally related to GFAP expression[74], the changes in GFAP expression that occur during suckling might first reduce and then increase taurine release.…”

Section: Role Of Gfap Plasticity In Dynamic Astrocyte-oxt Neuronal Inmentioning

confidence: 99%

Chronic vs. Acute Interactions between Supraoptic Oxytocin Neurons and Astrocytes during Lactation: Role of Glial Fibrillary Acidic Protein Plasticity

Wang

Hamilton

2009

The Scientific World JOURNAL

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In this article, we review studies of astrocytic-neuronal interactions and their effects on the activity of oxytocin (OXT) neurons within the magnocellular hypothalamo-neurohypophysial system. Previous work over several decades has shown that withdrawal of astrocyte processes increases OXT neuron excitability in the hypothalamic supraoptic nucleus (SON) during lactation. However, chronically disabling astrocyte withdrawal does not significantly affect the functioning of OXT neurons during suckling. Nevertheless, acute changes in a cytoskeletal element of astrocytes, glial fibrillary acidic protein (GFAP), occur in concert with changes in OXT neuronal activity during suckling. Here, we compare these changes in GFAP and related proteins with chronic changes that persist throughout lactation. During lactation, a decrease in GFAP levels accompanies retraction of astrocyte processes surrounding OXT neurons in the SON, resulting from high extracellular levels of OXT. During the initial stage of suckling, acute increases in OXT levels further strengthen this GFAP reduction and facilitate the retraction of astrocyte processes. This change, in turn, facilitates burst discharges of OXT neurons and leads to a transient increase in excitatory neurochemicals. This transient neurochemical surge acts to reverse GFAP expression and results in postburst inhibition of OXT neurons. The acute changes in astrocyte GFAP levels seen during suckling likely recur periodically, accompanied by rhythmic changes in glutamate metabolism, water transport, gliotransmitter release, and spatial relationships between astrocytes and OXT neurons. In the neurohypophysis, astrocyte retraction and reversal with accompanying GFAP plasticity also likely occur during lactation and suckling, which facilitates OXT release coordinated with its action in the SON. These studies of the dynamic interactions that occur between astrocytes and OXT neurons mediated by GFAP extend our understanding of astrocyte functions within the central nervous system.

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Insulin-Like Growth Factor-1 Inhibits Adult Supraoptic Neurons via Complementary Modulation of Mechanoreceptors and Glycine Receptors

Cited by 20 publications

References 51 publications

Insulin Increases the Potency of Glycine at Ionotropic Glycine Receptors

Insulin Increases the Potency of Glycine at Ionotropic Glycine Receptors

Stress hormones, sleep deprivation and cognition in older adults

Chronic vs. Acute Interactions between Supraoptic Oxytocin Neurons and Astrocytes during Lactation: Role of Glial Fibrillary Acidic Protein Plasticity

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