-
1.
Urinary Dopamine Excretion Rate Decreases during Acute Dietary Protein Deprivation and Is Associated with Increased Plasma Pancreatic Polypeptide Concentration.
Basolo, A, Hollstein, T, Walter, M, Krakoff, J, Piaggi, P
Nutrients. 2021;(4)
Abstract
Background: Dopamine, a key neurotransmitter in the autonomic nervous system participating in the homeostatic balance between sympathetic and parasympathetic divisions, is involved in food intake regulation. Objective: We investigated whether dopamine is altered by acute fasting or overfeeding diets with varying macronutrient content. Design: Ninety-nine healthy subjects underwent 24-h dietary interventions including eucaloric feeding, fasting, and five different overfeeding diets in a crossover design. Overfeeding diets (200% of eucaloric requirements) included one diet with 3%-protein (low-protein high-fat overfeeding-LPF: 46%-fat), three diets with 20%-protein, and a diet with 30%-protein (44%-fat). Urine was collected for 24 h and urinary dopamine concentration was quantified by high-performance liquid chromatography. Plasma pancreatic polypeptide (PP) concentration, an indirect marker of parasympathetic activity, was measured prior to and after each diet after an overnight fast. Results: During 24-h of fasting, dopamine decreased on average by ~14% compared to eucaloric conditions, whereas PP increased by two-fold (both p < 0.001). Lower dopamine during 24-h fasting correlated with increased PP (r = -0.40, p < 0.001). Similarly, on average urinary dopamine decreased during LPF by 14% (p < 0.001) and lower dopamine correlated with increased PP (r = -0.31, p = 0.01). No changes in dopamine and PP concentrations were observed during other overfeeding diets (all p > 0.05). Conclusions: Dopamine concentrations decrease during short-term fasting and overfeeding with a low-protein diet. As both dietary conditions have in common protein deficit, the correlation between dopamine and PP suggests a compensatory mechanism underlying the shift from sympathetic to parasympathetic drive during dietary protein deprivation.
-
2.
Evolution of Hemodynamic and Functional Human Kidney Graft Dose Response to Dopamine Using an Implantable Doppler Device.
Bataille, A, Payen, D, Villiers, S, Chazalet, JJ, Jacob, L
Experimental and clinical transplantation : official journal of the Middle East Society for Organ Transplantation. 2016;(2):176-83
Abstract
OBJECTIVES The relation between dopamine infusion and renal hemodynamics and function has not been studied in renal allografts during early recovery. We analyzed the dose response of dopamine infusion on renal blood flow and function in human kidney transplant recipients at reperfusion and during early graft recovery. MATERIALS AND METHODS Phasic and mean renal blood flow was measured by the pulsed Doppler technique using implantable Doppler microprobes in contact with the graft artery. Systemic and renal parameters were recorded on dopamine infusion (0, 3, 5, and 10 μg·kg⁻¹·min⁻¹) immediately after transplant (day 0) in 13 patients and at day 6 in 7/13 patients with early graft recovery. Results are expressed as median and interquartile range between the 25th and 75th percentiles. RESULTS At day 0, 3 μg·kg⁻¹·min⁻¹) dopamine did not increase mean renal blood flow over baseline (580 mL/min [219-663 mL/min] vs 542 mL/min [207-686 mL/min]; P = .84). There was an absence of effect with higher dopamine doses, whereas cardiac output, heart rate, and systolic and mean arterial pressure were significantly increased. Urinary sodium excretion, creatinine clearance, and urine output increased dose dependently, with a positive correlation between the increase in urine output and mean arterial pressure (r = 0.48, P < .001). At day 6, 3 μg·kg⁻¹·min⁻¹ dopamine increased mean renal blood flow over baseline (318 mL/min [234-897 mL/min] vs 191 mL/min [173-706 mL/min]; P = .016), with no further increase at higher doses. CONCLUSIONS Immediately after transplant, kidney grafts with ischemic-reperfusion injury are fully dilated and do not respond to dopamine. The specific renal effects observed are due to systemic hemodynamic status. Vascular responsiveness to a "renal dopamine dose" returns on graft recovery.
-
3.
BMI modulates calorie-dependent dopamine changes in accumbens from glucose intake.
Wang, GJ, Tomasi, D, Convit, A, Logan, J, Wong, CT, Shumay, E, Fowler, JS, Volkow, ND
PloS one. 2014;(7):e101585
Abstract
OBJECTIVE Dopamine mediates the rewarding effects of food that can lead to overeating and obesity, which then trigger metabolic neuroadaptations that further perpetuate excessive food consumption. We tested the hypothesis that the dopamine response to calorie intake (independent of palatability) in striatal brain regions is attenuated with increases in weight. METHOD We used positron emission tomography with [11C]raclopride to measure dopamine changes triggered by calorie intake by contrasting the effects of an artificial sweetener (sucralose) devoid of calories to that of glucose to assess their association with body mass index (BMI) in nineteen healthy participants (BMI range 21-35). RESULTS Neither the measured blood glucose concentrations prior to the sucralose and the glucose challenge days, nor the glucose concentrations following the glucose challenge vary as a function of BMI. In contrast the dopamine changes in ventral striatum (assessed as changes in non-displaceable binding potential of [11C]raclopride) triggered by calorie intake (contrast glucose - sucralose) were significantly correlated with BMI (r = 0.68) indicating opposite responses in lean than in obese individuals. Specifically whereas in normal weight individuals (BMI <25) consumption of calories was associated with increases in dopamine in the ventral striatum in obese individuals it was associated with decreases in dopamine. CONCLUSION These findings show reduced dopamine release in ventral striatum with calorie consumption in obese subjects, which might contribute to their excessive food intake to compensate for the deficit between the expected and the actual response to food consumption.
-
4.
Acute dopamine depletion with branched chain amino acids decreases auditory top-down event-related potentials in healthy subjects.
Neuhaus, AH, Goldberg, TE, Hassoun, Y, Bates, JA, Nassauer, KW, Sevy, S, Opgen-Rhein, C, Malhotra, AK
Schizophrenia research. 2009;(1-3):167-73
-
-
Free full text
-
Abstract
Cerebral dopamine homeostasis has been implicated in a wide range of cognitive processes and is of great pathophysiological importance in schizophrenia. A novel approach to study cognitive effects of dopamine is to deplete its cerebral levels with branched chain amino acids (BCAAs) that acutely lower dopamine precursor amino acid availability. Here, we studied the effects of acute dopamine depletion on early and late attentive cortical processing. Auditory event-related potential (ERP) components N2 and P3 were investigated using high-density electroencephalography in 22 healthy male subjects after receiving BCAAs or placebo in a randomized, double-blind, placebo-controlled crossover design. Total free serum prolactin was also determined as a surrogate marker of cerebral dopamine depletion. Acute dopamine depletion increased free plasma prolactin and significantly reduced prefrontal ERP components N2 and P3. Subcomponent analysis of N2 revealed a significant attenuation of early attentive N2b over prefrontal scalp sites. As a proof of concept, these results strongly suggest that BCAAs are acting on basic information processing. Dopaminergic neurotransmission seems to be involved in auditory top-down processing as indexed by prefrontal N2 and P3 reductions during dopamine depletion. In healthy subjects, intact early cortical top-down processing can be acutely dysregulated by ingestion of BCAAs. We discuss the potential impact of these findings on schizophrenia research.
-
5.
The subjective and cognitive effects of acute phenylalanine and tyrosine depletion in patients recovered from depression.
Roiser, JP, McLean, A, Ogilvie, AD, Blackwell, AD, Bamber, DJ, Goodyer, I, Jones, PB, Sahakian, BJ
Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. 2005;(4):775-85
-
-
Free full text
-
Abstract
Although there is evidence for the involvement of dopamine (DA) in unipolar depression, no published study has yet used the technique of acute phenylalanine and tyrosine depletion (APTD), a dietary intervention that selectively lowers DA synthesis, in order to investigate the role of DA in mood disturbance. Tyrosine and phenylalanine depleted and placebo amino acid drinks were administered to 20 patients recovered from depression in a double-blind, placebo-controlled, crossover design. Measures included subjective effects, Hamilton Depression Rating Scale scores, and a comprehensive battery of well-validated computerized cognitive tests. APTD induced a substantial reduction in the ratio of plasma tyrosine and phenylalanine to large neutral amino acids. However, relapse of depressive symptoms was not seen. Although performance on most cognitive tests was unaffected, there was a selective effect on decision-making, with APTD causing participants to bet significantly less. In conclusion, These results suggest a specific role for the involvement of DA in reward/punishment processing in humans. While APTD did not induce relapse in any participant, it did cause patients recovered from depression to show lowered sensitivity to reward in a gambling game. It is hypothesized that tests involving reward/punishment processing are preferentially affected by DA depletion, and that a more complete account of depression is likely to result from considering the roles played by serotonin, noradrenaline, and DA in mediating the various cognitive and clinical symptoms, including anhedonia.
-
6.
Hemodynamics and renal function during administration of low-dose dopamine in severely ill patients.
Pereira, CN, Machado, FR, Guimarães, HP, Senna, AP, do Amaral, JL
Sao Paulo medical journal = Revista paulista de medicina. 2004;(4):141-6
Abstract
CONTEXT Although a large number of studies have been performed regarding the renal and hemodynamic effects of the infusion of low-dose dopamine (LDD) in severely ill patients, there is still controversy on this subject. OBJECTIVE To evaluate the effects of dopamine (2 microg/kg/min) on systemic hemodynamics (lowest mean arterial pressure, MAP, highest heart rate, HR, central venous pressure, CVP), creatinine clearance (CLcr), diuresis and fractional sodium excretion (FENa+). TYPE OF STUDY A non-randomized, open, prospective clinical trial. SETTING An intensive care unit in a tertiary university hospital. PARTICIPANTS 22 patients with hemodynamic stability admitted to the intensive care unit. PROCEDURES Patients were submitted to three two-hour periods: without dopamine (P1), with dopamine (P2) and without dopamine (P3). MAIN MEASUREMENTS The above mentioned variables were measured during each period. CLcr was assessed based upon the formula U x V/P, where U is urinary creatinine (mg/dl), V is diuresis in ml/min and P is serum creatinine (mg/dl). FENa+ was calculated based upon the formula: urinary sodium (mEq/l) x P/plasma sodium (mEq/l) x U) x 100. Results were presented as mean and standard deviation. The Student t test was used and results were considered significant if p was less than 0.05. RESULTS Twelve patients (seven males and five females) were included, with a mean age of 55.45 years. There was no significant variation in MAP, HR, CVP, CLcr or FENa+ with a dopamine dose of 2 microg/kg/min. On the other hand, diuresis significantly increased during P2, from 225.4 to 333.9 ml. CONCLUSION Infusion of 2 microg/kg/min of dopamine for 2 hours increases diuresis. At the doses studied, dopamine does not induce significant alterations in MAP, HR, CVP, CLcr and FENa+.
-
7.
Serotonin transporters in the midbrain of Parkinson's disease patients: a study with 123I-beta-CIT SPECT.
Kim, SE, Choi, JY, Choe, YS, Choi, Y, Lee, WY
Journal of nuclear medicine : official publication, Society of Nuclear Medicine. 2003;(6):870-6
Abstract
UNLABELLED In Parkinson's disease (PD), both neuropathologic and biochemical studies suggest that serotonin (5-hydroxytryptamine [5-HT]) neurons are affected by the disease process. The integrity of 5-HT transporters was assessed in PD patients with SPECT using 2beta-carbomethoxy-3beta-(4-(123)I-iodophenyl)tropane ((123)I-beta-CIT), which binds with high affinity to both dopamine (DA) and 5-HT transporters. METHODS Forty-five PD patients at relatively early stages (mean Hoehn-Yahr stage, 2.0 +/- 0.7; range, 1-3) and 7 age-matched healthy control subjects had 15 scans over a 24-h period after injection of (123)I-beta-CIT using a 3-head SPECT system. In the midbrain, the 5-HT transporter parameter k(3)/k(4) was estimated by 3 noninvasive methods: pseudoequilibrium ratio (R(PE)) method, area ratio (R(A)) method, and a modified graphic method that derives the ratio of ligand distribution volumes (R(V)). Striatal V(3)", the DA transporter parameter that is equivalent to k(3)/k(4), was measured using the images acquired at 24 h after tracer injection. All measures were derived using the cerebellum as the reference region. RESULTS In control subjects, the (123)I-beta-CIT activity in the midbrain reached a peak at 91 +/- 21 min after injection and then washed out at a slow rate (1.1%/h +/- 0.5%/h). The peak specific uptake in the midbrain occurred at 315 +/- 46 min. In PD patients, the temporal patterns of the midbrain and cerebellar activity were not significantly different from those in control subjects. None of midbrain R(PE), R(A), and R(V) was significantly different between control subjects and PD patients, whereas striatal V(3)" was bilaterally reduced in all patients, being 32% lower than that of the control subjects (P = 0.002). In PD patients, none of the midbrain outcome measures was significantly correlated with either striatal V(3)" or motor or nonmotor symptom ratings, including the Hoehn-Yahr stage and the Unified Parkinson's Disease Rating Scale scores. When the studies of 7 PD patients with depression were analyzed separately, none of the midbrain outcome measures in these patients either was different significantly from control values or correlated with the Hamilton Depression Rating Scale score. CONCLUSION These results suggest that DA and 5-HT transporters are differentially affected in PD, and 5-HT transporters in the midbrain region may not be affected in relatively early stages of PD. Alternatively, 5-HT transporters in the remaining neurons may be upregulated, thus raising the midbrain 5-HT transporter density to almost normal levels.
-
8.
Modulation of amphetamine-induced striatal dopamine release by ketamine in humans: implications for schizophrenia.
Kegeles, LS, Abi-Dargham, A, Zea-Ponce, Y, Rodenhiser-Hill, J, Mann, JJ, Van Heertum, RL, Cooper, TB, Carlsson, A, Laruelle, M
Biological psychiatry. 2000;(7):627-40
Abstract
BACKGROUND Recent brain imaging studies have indicated that schizophrenia is associated with increased amphetamine-induced dopamine release in the striatum. It has long been hypothesized that dysregulation of subcortical dopamine systems in schizophrenia might result from a failure of the prefrontal cortex (PFC) to adequately control subcortical dopaminergic function. The activity of midbrain dopaminergic neurons is regulated, in part, by glutamatergic projections from the PFC acting via glutamatergic N-methyl-D-aspartate (NMDA) receptors. The goal of this study was to test the hypothesis that a pharmacologically induced disruption of NMDA transmission leads to an increase in amphetamine-induced dopamine release in humans. METHODS In eight healthy volunteers, we compared striatal amphetamine-induced (0.25 mg/kg) dopamine release under control conditions and under sustained disruption of NMDA transmission induced by infusion of the noncompetitive NMDA antagonist ketamine (0.2 mg/kg intravenous bolus followed by 0.4 mg/kg/hour intravenous infusion for 4 hours). Amphetamine-induced dopamine release was determined with single photon emission computed tomography, as the reduction in the binding potential (BP) of the radiolabeled D(2) receptor antagonist [(123)I]IBZM. RESULTS Ketamine significantly enhanced the amphetamine-induced decrease in [(123)I]IBZM BP, from -5.5% +/- 3.5% under control conditions to -12. 8% +/- 8.8% under ketamine pretreatment (repeated-measures analysis of variance, p =.023). CONCLUSIONS The increase in amphetamine-induced dopamine release induced by ketamine (greater than twofold) was comparable in magnitude to the exaggerated response seen in patients with schizophrenia. These data are consistent with the hypothesis that the alteration of dopamine release revealed by amphetamine challenge in schizophrenia results from a disruption of glutamatergic neuronal systems regulating dopaminergic cell activity.