Intraventricular insulin increases dopamine transporter mRNA in rat VTA/substantia nigra

Figlewicz, Dianne P.; Szot, Patricia; Chavez, Mark; Woods, Stephen C.; Veith, Richard C.

doi:10.1016/0006-8993(94)91698-5

Cited by 158 publications

(94 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Synaptically released dopamine is retro-transported into dopaminergic nerve terminals where it is re-packaged or degraded and this function of the DAT represents the major mechanism whereby dopamine signaling is terminated within the CNS (41). We have demonstrated that ICV insulin increases DAT mRNA (42), and that in vitro insulin reverses the effect of acute, in vivo, food restriction to decrease DA re-uptake (i.e., insulin stimulates DAT function) (10). Subsequent studies in cellular systems have demonstrated that this action of insulin is caused by enhanced recruitment of DATs to the cell membrane and is dependent on insulin-stimulation of the PI3 kinase pathway (43).…”

Section: Cns Sites Of Action For Adiposity Signal Modulation Of Food mentioning

confidence: 88%

Modulation of food reward by adiposity signals

Figlewicz

Naleid

Sipols

2007

Physiology & Behavior

Self Cite

137

123

View full text Add to dashboard Cite

Extensive historical evidence from the drug abuse literature has provided support for the concept that there is functional communication between central nervous system (CNS) circuitries which subserve reward/motivation, and the regulation of energy homeostasis. This concept is substantiated by recent studies that map anatomical pathways, or which demonstrate that hormones and neurotransmitters associated with energy homeostasis regulation can directly modulate reward and motivation behaviors. Studies from our laboratory have focused specifically on the candidate adiposity hormones, insulin and leptin, and show that these hormones can decrease performance in behavioral paradigms that assess the rewarding or motivating properties of food. Additionally we and others have provided evidence that the ventral tegmental area may be one direct target for these effects, and we are currently exploring other potential anatomical targets. Finally, we are beginning to explore the interaction between adiposity signals, chronic maintenance diet of rats, and different types of food rewards to more closely simulate the current food environments of Westernized societies including the U.S. We propose that future studies of food reward should include a more complex environment in the experimental design that takes into account abundance and variety of rewarding foods, psychological stressors, and choices of reward modalities.

show abstract

Section: Cns Sites Of Action For Adiposity Signal Modulation Of Food mentioning

confidence: 88%

Modulation of food reward by adiposity signals

Figlewicz

Naleid

Sipols

2007

Physiology & Behavior

Self Cite

137

123

View full text Add to dashboard Cite

show abstract

“…Central administration of insulin also has been shown to increase DA transporter (DAT) mRNA in the VTA/SNpc [10]. This increase in transporter likely influences DA signaling, since exogenously administered insulin has been shown in vitro to increase DA uptake in striatal tissue [11,12] and human DATtransfected cells [11,13].…”

Section: Introductionmentioning

confidence: 99%

Alterations in blood glucose levels under hyperinsulinemia affect accumbens dopamine

Bello

Hajnal

2006

Physiology & Behavior

View full text Add to dashboard Cite

Dopaminergic systems have been implicated in diabetes and obesity. Notwithstanding, the most basic relationship between dopamine and plasma insulin as well as glucose levels yet remains unknown. The present experiments were designed to investigate the effects of acute hyperinsulinemia on basal dopamine levels in the nucleus accumbens of the rat under chloral hydrate anesthesia using acute microdialysis in combination with the hyperinsulinemic-glycemic clamping procedure. In Experiment 1, each rat was infused with one of three concentrations of insulin (2.4, 4.8, or 9.6 mU/ kg per min) while plasma glucose levels were maintained at euglycemia (∼5.5 mmol/L). Dopamine, dihydroxyphenylacetic acid and homovanillic acid were not significantly different from baseline during either the clamp or post clamp periods for all insulin concentrations. In Experiment 2, rats were infused with the highest concentration of insulin (9.6 mU/kg per min) and plasma glucose levels were maintained at either hypoglycemia (∼3 mmol/L) or hyperglycemia (∼14 mmol/L). Dopamine was elevated at 100 min (+113% above basal levels) and 120 min (+117%) in the hypoglycemic condition and at 120 min (+121%) in the hyperglycemic condition. In the hyperglycemic post clamp period, homovanillic acid was decreased below basal levels (approximately -32%). These results together suggest that short-term blood glucose deviations coupled with acute hyperinsulinemia affect the mesoaccumbens dopamine system.

show abstract

“…As one of the main metabolic changes in diabetes is lack of insulin or/and insulin ineffectiveness and in view of the recent findings of insulin-induced alterations in steady-state DA-T and NA-T mRNA levels in the brain of normal rats (Figlewicz et al, 1993(Figlewicz et al, , 1994, it can be speculated that the changes we observed are related to reduced levels of insulin and/or insulin ineffectiveness in the brain in diabetes. Insulin has a neuromodulatory role in the brain, interacting particularly with catecholaminergic transmission (Baskin et al, 1987;Wozniak et al, 1993).…”

Section: Fig 2 Dark-field and Bright-field Photomi-mentioning

confidence: 55%

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

Petrišić

Augood²,

Bicknell

1997

Journal of Neurochemistry

View full text Add to dashboard Cite

Diabetic animals exhibit altered neurotransmission in brain monoaminergic systems. By means of in situ hybridization, we have investigated the expression of dopamine, noradrenaline, and serotonin transporter (DA-T, NA-T, and 5-HT-T, respectively) mRNAs in the brains of alloxan-and streptozotocin-diabetic rats. The expression of DA-T mANA is decreased in 1-(-11%) and 4-(-17%) week alloxan-diabetic and 4-(-9%) and 8-20%) week streptozotocin-diabetic rats in the ventral medial bundle. The expression of NA-T mRNA is decreased in the locus coeruleus of 8-(-26%) week streptozotocin-diabetic rats, in the noradrenergic Al cell group of 4-(-27%) week alloxan-and 8-(-25%) week streptozotocin-diabetic rats, and in the noradrenergic A2 cell group of 1-(-21%) and 4-(-28%) week alloxan-diabetic and 4-(-27%) and 8-(-25%) week streptozotocin-diabetic animals. The expression of 5-HT-T mRNA in the dorsal raphe nucleus is increased in 1-(+14%) and 4-(+44%) week alloxan-and 4-(+28%) and 8-(-i-44%) week streptozotocin-diabetic rats. The expression of each of the three monoamine transporter genes may be differentially regulated in diabetes and dependent on the duration of diabetes. Altered monoamine transporter gene expression may possibly contribute to the observed dysfunctions in brain monoamine transmission in chronic diabetes.

show abstract

Intraventricular insulin increases dopamine transporter mRNA in rat VTA/substantia nigra

Cited by 158 publications

References 20 publications

Modulation of food reward by adiposity signals

Modulation of food reward by adiposity signals

Alterations in blood glucose levels under hyperinsulinemia affect accumbens dopamine

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

Contact Info

Product

Resources

About