Monoamine Transporter Gene Expression in the Central Nervous System in Diabetes Mellitus

Petrišić, Melita Šalković; Augood, Sarah J.; Bicknell, R.J.

doi:10.1046/j.1471-4159.1997.68062435.x

Cited by 37 publications

(10 citation statements)

References 32 publications

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“…The comparatively greater effect of diabetes on serotonin-induced vasoconstriction is interesting in view of evidence linking enhanced serotonergic activity, both at serotonin receptors and the serotonin transporter, to pulmonary hypertension [ 26 , 27 ]. Serum serotonin concentrations are elevated in diabetics [ 28 ] and there is evidence for up regulation of the serotonin transporter in platelets [ 29 ] and brain [ 30 ]. These effects may well contribute to the increased prevalence of pulmonary hypertension in diabetics, because over expression of the serotonin transporter in mice causes pulmonary hypertension [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of streptozotocin-induced diabetes on the pharmacology of rat conduit and resistance intrapulmonary arteries

Gurney

Howarth

2009

Cardiovasc Diabetol

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Section: Discussionmentioning

confidence: 99%

Effects of streptozotocin-induced diabetes on the pharmacology of rat conduit and resistance intrapulmonary arteries

Gurney

Howarth

2009

Cardiovasc Diabetol

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“…WAN are sensitive to various metabolic perturbances, responding either by changes in activity or in measures of injury. Metabolic challenges, e.g., glucose or oxygen dyshomeostasis, influence WAN activity (Figlewicz et al, 1996, Petrisic et al, 1997). Prominent age-related changes in WAN include loss of dendrites, axonopathy, reduction in neurotransmitter synthesis enzymes and, in select populations, lipofuscin accumulation and cell loss (Mann, 1983, Ishida et al, 2001, Zecca et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

SIRT1 Regulation of Wakefulness and Senescence-Like Phenotype in Wake Neurons

Panossian¹,

Fenik²,

Zhu³

et al. 2011

J. Neurosci.

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Wakeneuronsinthebasalforebrainandbrainstemprovidecriticalinputstooptimizealertnessandattention.Theseneurons,however,evidence heightened vulnerability to a diverse array of metabolic challenges, including aging. SIRT1 is an nicotinamide adenine dinucleotide responsive deacetylase serving diverse adaptive responses to metabolic challenges, yet this metabolic rheostat may be downregulated under conditions of significant oxidative stress. We hypothesized that SIRT1 might serve as a critical neuroprotectant for wake neurons in young animals but that this protectant would be lost upon aging, rendering the neurons more vulnerable to metabolic insults. In this collection of studies, we first established the presence of nuclear SIRT1 in wake neurons throughout the forebrain and brainstem. Supporting functional and behavioral roles forSIRT1inwake-activeneurons,transgenicwholeanimal,andconditionallossofbrainSIRT1intheadultmouseimpartselectiveimpairments in wakefulness, without disrupting non-rapid eye movement or rapid eye movement sleep. Populations of wake neurons, including the orexinergic, locus ceruleus, mesopontine cholinergic, and dopaminergic wake neurons, evidence loss of dendrites and neurotransmitter synthesis enzymes and develop accelerated accumulation of lipofuscin, consistent with a senescence-like phenotype in wake neurons. Normal aging results in a progressive loss of SIRT1 in wake-active neurons, temporally coinciding with lipofuscin accumulation. SIRT1 is a critical agesensitive neuroprotectant for wake neurons, and its deficiency results in impaired wakefulness.

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“…Additionally, i.c.v. STZ caused impairment of passive avoidance behaviour, and both working and reference memory (Mayer et al 1990;Blokland and Jolles 1993;Lannert and Hoyer 1998;Prickaerts et al 1999), most probably as a result of cholinergic deafferentiation (Hellweg et al 1992) and changes in monoaminergic neurotransmission (Lackovic and Salkovic 1990;Ding et al 1992;Salkovic et al 1995;Petrisic et al 1997;Sharma and Gupta 2001;Salkovic-Petrisic and Lackovic 2003). Various experimental and methodological approaches used by different investigators have clearly shown that i.c.v.…”

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confidence: 99%

Alzheimer‐like changes in protein kinase B and glycogen synthase kinase‐3 in rat frontal cortex and hippocampus after damage to the insulin signalling pathway

Šalković‐Petrišić

Tribl

Schmidt

et al. 2006

Journal of Neurochemistry

195

136

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The insulin-resistant brain state is related to late-onset sporadic Alzheimer's disease, and alterations in the insulin receptor (IR) and its downstream phosphatidylinositol-3 kinase signalling pathway have been found in human brain. These findings have not been confirmed in an experimental model related to sporadic Alzheimer's disease, for example rats showing a neuronal IR deficit subsequent to intracerebroventricular (i.c.v.) treatment with streptozotocin (STZ). In this study, western blot analysis performed 1 month after i.c.v. injection of STZ showed an increase of 63% in the level of phosphorylated glycogen synthase kinase-3a/b (pGSK-3a/b) protein in the rat hippocampus, whereas the levels of the unphosphorylated form (GSK-3a/b) and protein kinase B (Akt/ PKB) remained unchanged. Three months after STZ treatment, pGSK-3a/b and Akt/PKB levels tended to decrease (by 8 and 9% respectively). The changes were region specific, as a different pattern was found in frontal cortex. Structural alterations were also found, characterized by b-amyloid peptide-like aggregates in brain capillaries of rats treated with STZ. Similar neurochemical changes and cognitive deficits were recorded in rats treated with i.c.v. 5-thio-D-glucose, a blocker of glucose transporter (GLUT)2, a transporter that is probably involved in brain glucose sensing. The IR signalling cascade alteration and its consequences in rats treated with STZ are similar to those found in humans with sporadic Alzheimer's disease, and our results suggest a role for GLUT2 in Alzheimer's pathophysiology. Keywords: Alzheimer's disease; glucose transporter 2; glycogen synthase kinase-3, hippocampus, protein kinase B, streptozotocin. Research into the brain insulin system has intensified in the past decade, particularly regarding its pathophysiology. There is a growing interest in determining the role of neuronal insulin and its receptor in the brain, and particularly in Alzheimer's disease. Recent data indicate that brain insulin deficiency and the insulin-resistant brain state are related to late-onset sporadic Alzheimer's disease (Fulop et al. 2003;Hoyer 2004;De la Monte and Wands 2005;Hoyer and Frölich 2005). The late-onset type of Alzheimer's disease is associated with glucose utilization abnormalities all over the cerebral cortex, and particularly in structures with both high glucose demands and high insulin sensitivity (Henneberg and Hoyer 1995). Neuronal glucose metabolism is under the regulation of neuronal insulin, and abnormalities in brain glucose metabolism found in Alzheimer's disease have been suggested to be induced at the level of insulin signal transduction (Hoyer 2002;Hoyer and Frölich 2005).

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Monoamine Transporter Gene Expression in the Central Nervous System in Diabetes Mellitus

Cited by 37 publications

References 32 publications

Effects of streptozotocin-induced diabetes on the pharmacology of rat conduit and resistance intrapulmonary arteries

Effects of streptozotocin-induced diabetes on the pharmacology of rat conduit and resistance intrapulmonary arteries

SIRT1 Regulation of Wakefulness and Senescence-Like Phenotype in Wake Neurons

Alzheimer‐like changes in protein kinase B and glycogen synthase kinase‐3 in rat frontal cortex and hippocampus after damage to the insulin signalling pathway

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