Insulin receptors and insulin action in dissociated brain cells

Masters, Brian A.; Shemer, Joshua; Judkins, Jennifer H.; Clarke, Derrel W.; Roith, Derek Le; Raizada, Mohan K.

doi:10.1016/0006-8993(87)90449-5

Cited by 57 publications

(20 citation statements)

References 33 publications

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“…On the other hand, insulin is found to be able to increase the turnover rate of epinephrine and norepinephrine [214]. The effects of insulin on norepinephrine have been investigated in dissociated brain cells and synaptosomes prepared from the adult rat brain, and it is shown that norepinephrine uptake is inhibited by insulin [215,216]. Similar results are also reported in cell culture studies [217,218].…”

Section: Insulin and Neurotransmissionsupporting

confidence: 71%

“…Based on these observations, and the fact that insulin is able to cross the BBB and the presence of IR in brain areas involved in the control of GnRH secretion including the arcuate nucleus and the median eminence [137,138], it seems that the effects of central insulin on GnRH is due to the direct actions of insulin than indirect action upon glucose availability [134]. However, Bucholtz et al did not rule out the effects of glucose in this process and reported that LH secretion is not wholly dependent on insulin activity and specialized glucodetectors in the hypothalamus can also modulate GnRH secretion in both insulin-dependent and insulin-independent manners [133].…”

Section: Reproductionmentioning

confidence: 99%

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Insulin in the Brain: Sources, Localization and Functions

et al. 2012

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Historically, insulin is best known for its role in peripheral glucose homeostasis, and insulin signaling in the brain has received less attention. Insulin-independent brain glucose uptake has been the main reason for considering the brain as an insulin-insensitive organ. However, recent findings showing a high concentration of insulin in brain extracts, and expression of insulin receptors (IRs) in central nervous system tissues have gathered considerable attention over the sources, localization, and functions of insulin in the brain. This review summarizes the current status of knowledge of the peripheral and central sources of insulin in the brain, site-specific expression of IRs, and also neurophysiological functions of insulin including the regulation of food intake, weight control, reproduction, and cognition and memory formation. This review also considers the neuromodulatory and neurotrophic effects of insulin, resulting in proliferation, differentiation, and neurite outgrowth, introducing insulin as an attractive tool for neuroprotection against apoptosis, oxidative stress, beta amyloid toxicity, and brain ischemia.

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Section: Insulin and Neurotransmissionsupporting

confidence: 71%

Section: Reproductionmentioning

confidence: 99%

Insulin in the Brain: Sources, Localization and Functions

et al. 2012

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“…Consistent with its enriched distribution in adrenergic terminals, insulin is found to promote central catecholaminergic activities by releasing both epinephrine and norepinephrine (20), inhibiting synaptic reuptake of norepinephrine (21), and altering catecholomine kinetics (22). In the hippocampus, insulin is reported to enhance ␣1 adrenergic receptor activity, leading to stimulation of membrane phosphoinositol turnover * The costs of publication of this article were defrayed in part by the payment of page charges.…”

mentioning

confidence: 89%

Brain Insulin Receptors and Spatial Memory

Zhao

Hui

et al. 1999

Journal of Biological Chemistry

482

154

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“…For example, insulin decreases the uptake of NE from sympathetic nerve terminals, reduces NE transporter binding and mRNA synthesis in locus ceruleus, and increases NE release when applied directly to hypothalamic slices [22, 23, 24, 25, 26, 27, 28, 29, 30]. There are also several reports that diabetes modifies NE metabolism.…”

Section: Introductionmentioning

confidence: 99%

Effects of Diabetes and Estradiol on Norepinephrine Release in Female Rat Hypothalamus, Preoptic Area and Cortex

Karkanias

Morales²,

Etgen³

1998

Neuroendocrinology

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These studies determined whether diabetes and estradiol treatment altered norepinephrine (NE) release from hypothalamus, preoptic area (POA), and cortical slices from ovariectomized (OVX) female rats. Animals were sacrificed 12 days after the onset of streptozotocin-induced diabetes and 48 h following vehicle or estradiol injection. Brain slices were preloaded with ³H-NE, and release was evoked twice (S1 and S2) by electrical stimulation. Diabetes increased hypothalamic NE release during S1 regardless of the administration of vehicle or estradiol. Neither estradiol treatment nor diabetes alone affected NE release during S2 in the hypothalamus or POA. Estradiol treatment elevated NE release in the POA during S2 but only in diabetic animals. Moreover, estradiol elevated cortical NE release during S2 regardless of the presence or absence of disease. We also examined whether α₂-adrenoceptor regulation of NE release was influenced by diabetes or hormone treatment. Enhancement of NE release by α₂-adrenoceptor antagonism was evident in all 3 brain regions. However, α₂-adrenoceptor regulation of NE release was unaffected by diabetes and hormone treatment. These findings suggest that diabetes alters NE release in the hypothalamus/POA of female rats. Additionally, this work identifies a novel action of estradiol to enhance stimulated NE release in the cortex of female rats.

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Insulin receptors and insulin action in dissociated brain cells

Cited by 57 publications

References 33 publications

Insulin in the Brain: Sources, Localization and Functions

Insulin in the Brain: Sources, Localization and Functions

Brain Insulin Receptors and Spatial Memory

Effects of Diabetes and Estradiol on Norepinephrine Release in Female Rat Hypothalamus, Preoptic Area and Cortex

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