Effect of Long‐Lasting Diabetes Mellitus on Rat and Human Brain Monoamines

Lacković, Zdravko; Šalković, Melita; Kuci, Z; Relja, Maja

doi:10.1111/j.1471-4159.1990.tb13294.x

Cited by 108 publications

(68 citation statements)

References 19 publications

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“…In the post-mortem study, 5-HT concentration was increased in the hypothalamus of diabetic subjects (Lackovic et al, 1990). In addition, a recent positron emission tomography (PET) study, significantly greater 5-HT 1A receptor binding was detected in mesial temporal cortex in type 2 diabetic subjects (Price et al, 2002).…”

Section: Introductionmentioning

confidence: 89%

Diabetes Attenuates the Antidepressant-Like Effect Mediated by the Activation of 5-HT1A Receptor in the Mouse Tail Suspension Test

Miyata

Hirano

Kamei

2003

Neuropsychopharmacol

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Several lines of evidence have indicated that the prevalence of depression in diabetic subjects is higher than that in the general population, however, little information is available on the effects of antidepressants in diabetes. In the present study, the antidepressantlike effect mediated by the activation of 5-HT 1A receptors was examined using the tail suspension test in streptozotocin-induced diabetic mice. Long-lasting increases in 5-HT turnover rates were observed in the diabetic mouse midbrain and frontal cortex, but not in the hippocampus. Duration of immobility was significantly longer in diabetic than in nondiabetic mice in the tail suspension test. The 5-HT 1A receptor agonist ( 7 )-8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) (3-30 mg/kg, i.p.) reduced the duration of immobility in nondiabetic mice, and this effect was completely antagonized by pretreatment with, a selective 5-HT 1A receptor antagonist. In contrast, 8-OH-DPAT (3 mg/kg-3 mg/kg, i.p.) was ineffective in diabetic mice. The selective 5-HT reuptake inhibitor fluoxetine (3-56 mg/kg, i.p.) reduced the duration of immobility in both nondiabetic and diabetic mice. However, fluoxetine was less effective in diabetic mice than in nondiabetic mice. WAY-100635 (30 mg/kg, s.c.) reversed the suppression of the duration of immobility by fluoxetine (30 mg/kg, i.p.) in nondiabetic mice. On the other hand, the anti-immobility effect of fluoxetine (56 mg/kg, i.p.) was not antagonized by WAY-100635 (30 mg/kg, s.c.) in diabetic mice. The selective 5-HT 2 receptor antagonist 6-methyl-1-(1-methylethyl)-ergoline-8b-carboxylic acid 2-hydroxy-1-methylpropyl ester (LY53,857) (30 mg/kg, s.c.) reversed the anti-immobility effect of fluoxetine in both nondiabetic and diabetic mice. Spontaneous locomotor activity in diabetic mice was not different from that in nondiabetic mice. 8-OH-DPAT (30 mg/kg, i.p.), but not fluoxetine, increased the spontaneous locomotor activity in both nondiabetic and diabetic mice. The number of 5-HT 1A receptors in the mouse frontal cortex was unaffected by diabetes. Plasma corticosterone levels in diabetic mice were significantly higher than that in nondiabetic mice. These results suggest that the antidepressant-like effect mediated by 5-HT 1A receptors may be attenuated by diabetes.

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Section: Introductionmentioning

confidence: 89%

Diabetes Attenuates the Antidepressant-Like Effect Mediated by the Activation of 5-HT1A Receptor in the Mouse Tail Suspension Test

Miyata

Hirano

Kamei

2003

Neuropsychopharmacol

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“…Whether hippocampal NE induces voluntary wheel running has not yet been clarified, although genetically or pharmacologically enhanced NE level in brain regions that include the hippocampus increases field locomotor activity in experimental animals (Xu et al, 2000;Cryan et al, 2004;Shishikina et al, 2004;Lahdesmaki et al, 2003;Cases et al, 1995). Given the fact that obese and diabetic animals with low physical activity have less NE in the hippocampus than normal controls (Gallego et al, 2003;Yamato et al, 2004;Lackovic et al, 1990), we hypothesized that hippocampal NE is involved in the initiation of voluntary exercise.…”

Section: Introductionmentioning

confidence: 96%

Monoamine Oxidase A Activity and Norepinephrine Level in Hippocampus Determine Hyperwheel Running in SPORTS Rats

Miyamoto

Harada

Hara

et al. 2006

Neuropsychopharmacol

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An understanding of neurological mechanisms for wheel running by rodents, especially with high exercise activity, would be applicable to a strategy for promotion of exercise motivation in humans. One of several brain regions that are candidates for the regulation of physical exercise is the hippocampus. Here we examined the running activity of Spontaneously-Running-Tokushima-Shikoku (SPORTS) rat, a new animal model for high levels of wheel-running activity, and its relation with the hippocampal norepinephrine (NE) system including the levels of NE, adrenergic receptors, and degradation enzymes for monoamines. In the hippocampus of SPORTS rats, the level of NE in extracellular fluid was augmented, whereas the level in the homogenate of the whole tissue was decreased even for sedentary conditions. Elevated extracellular NE caused downregulation of a 2 -adrenergic receptors in the hippocampus of SPORTS rats. Local administration of a 2 -adrenergic receptor antagonist yohimbine, but not of a 2 -agonist clonidine, into the hippocampus suppressed high running activity in SPORTS rats. The protein expression and the activity levels of monoamine oxidase A (MAOA), a critical enzyme for the degradation of NE, were decreased in the hippocampus of SPORTS rats to increase extracellular NE level. Thus, inhibition of oxidase activity in normal Wistar rats markedly increased wheel-running activity. These results indicate that decreased MAOA activity, elevation of extracellular NE, and a 2 -adrenergic receptors in the hippocampus determine the neural basis of the psychological regulation of exercise behavior in SPORTS rats.

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“…La dopamina también apareció aumentada en el putamen. Los niveles de norepinefrina aumentaron en el palidum y disminuyeron en el núcleo accumbens y en el claustrum (Lackovic et al 1990). …”

Section: Psicopatología De La Diabetesunclassified