Changes in the central dopaminergic systems in the streptozotocin-induced diabetic rats

Lim, Dae‐Kwang; Lee, K M; Ho, Ing K.

doi:10.1007/bf02979114

Cited by 27 publications

(21 citation statements)

References 35 publications

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“…Also, STZ-treated animals exhibit a decrease in basal and nicotine-evoked dopamine release in the NAc. A similar decrease in dopamine release has also been demonstrated in the dorsal striatum of STZ-treated rats (Lim et al, 1994;Murzi et al, 1996;Owens et al, 2005;Saller, 1984;Williams et al, 2007). Several mechanisms may contribute to a hypodopaminergic state in the NAc of diabetic rats.…”

Section: Interaction Between Insulin and Dopamine Systemssupporting

confidence: 54%

Enhanced vulnerability to tobacco use in persons with diabetes: A behavioral and neurobiological framework

O’Dell

Nazarian

2016

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Section: Interaction Between Insulin and Dopamine Systemssupporting

confidence: 54%

Enhanced vulnerability to tobacco use in persons with diabetes: A behavioral and neurobiological framework

O’Dell

Nazarian

2016

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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“…Moreover, drug [alloxan or streptozotocin (STZ)]-induced hypoinsulinemia can alter [increase (Lozovsky et al, 1981;Trulson and Himmel, 1983;Serri et al, 1985) or decrease (Rowland et al, 1985)] the density of striatal D2 receptors and impair D2 receptorcoupled signal transduction (Abbracchio et al, 1989). Finally, hypoinsulinemic rats showed decreased synthesis (Kono and Takada, 1994), uptake (Owens et al, 2005), and turnover (Kwok and Juorio, 1986;Lim et al, 1994) of DA in the striatum. Thus, it is clear that changes in plasma insulin and glucose can have profound effects on DA neurotransmission.…”

Section: Introductionmentioning

confidence: 99%

Insulin Replacement Restores the Behavioral Effects of Quinpirole and Raclopride in Streptozotocin-Treated Rats

Sevak

Koek²,

Galli

2006

J Pharmacol Exp Ther

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Streptozotocin (STZ)-induced diabetes can modulate dopamine (DA) neurotransmission and thereby modify the behavioral effects of drugs acting on DA systems. Insulin replacement, and in some conditions repeated treatment with amphetamine, can partially restore sensitivity of STZ-treated rats to dopaminergic drugs. The present study sought to characterize the role of insulin and amphetamine in modulating the behavioral effects of drugs that selectively act on D2/D3 receptors. In control rats, quinpirole and quinelorane produced yawning, whereas raclopride and ␥-hydroxybutyric acid (GHB) produced catalepsy. Raclopride antagonized quinpirole-and quinelorane-induced yawning with similar potency. STZ treatment increased blood glucose concentration, decreased body weight, and markedly reduced sensitivity to quinpirole-induced yawning, quinelorane-induced yawning as well as to raclopride-induced catalepsy, while enhancing sensitivity to GHB-induced catalepsy. Repeated treatment with amphetamine partially restored sensitivity of STZ-treated rats to amphetamine-stimulated locomotion and also produced conditioned place preference, without affecting blood glucose and body weight changes. However, amphetamine treatment did not restore sensitivity to the behavioral effects of quinpirole, raclopride, or GHB, suggesting differential regulation of dopamine transporter activity and sensitivity of D2 receptors in hypoinsulinemic rats. Insulin replacement in STZ-treated rats normalized blood glucose and body weight changes and fully restored sensitivity to quinpirole-induced yawning, as well as to raclopride-induced catalepsy, while reducing sensitivity to GHB-induced catalepsy. Overall, these data indicate that changes in insulin status markedly affect sensitivity to the behavioral effects of dopaminergic drugs. The results underscore the importance of insulin in modulating DA neurotransmission; these effects might be especially relevant to understanding the co-morbidity of eating disorders and substance abuse.Several drugs of abuse (e.g., amphetamine and cocaine) and some drugs that are used in the clinic (e.g., haloperidol and bromocriptine) are thought to act predominantly on dopamine (DA) systems. Activity at DA D2 receptors can modulate DA neurotransmission by affecting DA synthesis, release, uptake, or neuronal activity (Zahniser and Doolen, 2001). Importantly, insulin has been shown to regulate DA signaling in the brain (Figlewicz et al., 1994(Figlewicz et al., , 1996. Insulin can cross the blood-brain barrier and act on receptors (i.e., insulin receptors, insulin-like growth factor-1 receptors) that are densely concentrated in the basal ganglia, a region richly expressing D2/D3 receptors and DA transporters (DATs) (Ciliax et al., 1995;Larson and Ariano, 1995;Schulingkamp et al., 2000;Figlewicz et al., 2003). The proximity of insulin and DA systems seems to have functional consequences. For example, rats with decreased circulating insulin showed decreased coupling of DA D2 receptors to G i/o proteins (Abbracchio et a...

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“…Previous studies have shown that STZtreated rats display a profound suppression of dopamine release and D1 receptors in the NAcc [62]. Also, STZ-treated rats display a suppression of dopamine release in the dorsal striatum [90][91][92][93][94]. Based on the finding that STZ-treated rats display a general suppression of dopamine transmission, one might predict that hypoinsulinemic rats would display a larger decrease in NAcc dopamine levels during nicotine withdrawal.…”

Section: Mechanisms Of Nicotine Withdrawal In Vulnerable Populationsmentioning

confidence: 86%

Insight into the Potential Factors That Promote Tobacco Use in Vulnerable Populations

et al. 2016

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It is presently unclear why certain populations are more vulnerable to tobacco use and less responsive to smoking cessation interventions. This review considers the contribution of nicotine reward and withdrawal in populations that appear to be more susceptible to tobacco use. Our focus is on populations that have been modeled in rodents including, adolescents, females, and persons with metabolic disorders, such as diabetes. A common feature across these rodent models is heightened nicotine reward, suggesting that vulnerable populations may experience strong rewarding effects of nicotine that promote tobacco use. One distinguishing factor among these rodent models of at-risk populations is with regard to the magnitude of nicotine withdrawal, which is lower during adolescence. These groups also differ with regard to expression of the physical signs versus affective states produced by withdrawal, suggesting that these distinct facets of withdrawal differentially contribute to tobacco use in vulnerable populations. Thus, we may need to apply different diagnostic criteria and/or specialized treatments that target the unique factors that promote tobacco use in different vulnerable populations.

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Changes in the central dopaminergic systems in the streptozotocin-induced diabetic rats

Cited by 27 publications

References 35 publications

Enhanced vulnerability to tobacco use in persons with diabetes: A behavioral and neurobiological framework

Enhanced vulnerability to tobacco use in persons with diabetes: A behavioral and neurobiological framework

Insulin Replacement Restores the Behavioral Effects of Quinpirole and Raclopride in Streptozotocin-Treated Rats

Insight into the Potential Factors That Promote Tobacco Use in Vulnerable Populations

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