scholarly journals On the learning of addictive behavior: Sensation-seeking propensity predicts dopamine turnover in dorsal striatum

2021 ◽  
Author(s):  
Natalie Hong Siu Chang ◽  
Yoshitaka Kumakura ◽  
Arne Møller ◽  
Jakob Linnet ◽  
Dirk Bender ◽  
...  
Keyword(s):  
Caudate Nucleus ◽  
Sensation Seeking ◽  
Dopamine Synthesis ◽  
Dopamine Turnover ◽  
Receptor Density ◽  
Premorbid Personality ◽  
Addictive Disorders ◽  
Dopaminergic Neurotransmission ◽  
Extracellular Dopamine ◽  
Dopamine Oxidation

AbstractWe asked if sensation-seeking is linked to premorbid personality characteristics in patients with addictive disorders, or the characteristics follow the sensation-seeking activity. We interpreted the former as a state associated with normal rates of dopamine synthesis, and the latter as a trait of individuals with abnormally high rates of synthesis. We previously determined dopaminergic receptor density in striatum, and we now tested the hypothesis that an elevated dopaminergic condition with increased extracellular dopamine and receptor density follows increased dopamine synthesis capacity in highly sensation-seeking individuals, as measured by positron emission tomography of 18 men with tracer fluorodopa (FDOPA). We detected a site in left caudate nucleus where the volume of distribution of FDOPA-derived metabolites correlated negatively with FDOPA metabolite turnover, consistent with decreased metabolite breakdown in highly sensation-seeking subjects. High rates of sensation-seeking attenuated the dopamine turnover in association with a low rate of dopamine recycling, low dopamine oxidation, and elevated extracellular dopamine and receptors in caudate nucleus. In contrast, low rates of sensation-seeking were associated with rapid dopamine recycling, rapid dopamine oxidation, low extracellular dopamine, and low receptor density. We conclude that the modulation of dopaminergic neurotransmission associated with sensation-seeking is a state of sensation-seeking, rather than a trait of personality following abnormal regulation of dopaminergic neurotransmission.

Extracellular dopamine and its metabolites increase in the rat's caudate nucleus during treadmill walking

1991 ◽  
Vol 16 ◽  
pp. 116
Author(s):  
Satoshi Hattori ◽  
Qianming Li ◽  
Nobuo Matsui ◽  
Hitoo Nishino
Keyword(s):  
Caudate Nucleus ◽  
Treadmill Walking ◽  
Extracellular Dopamine

scholarly journals Changes of Dopamine Turnover in the Progression of Parkinson's Disease as Measured by Positron Emission Tomography: Their Relation to Disease-Compensatory Mechanisms

2004 ◽  
Vol 24 (8) ◽  
pp. 869-876 ◽  
Author(s):  
Vesna Sossi ◽  
Raúl de la Fuente-Fernández ◽  
James E. Holden ◽  
Michael Schulzer ◽  
Thomas J. Ruth ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Positron Emission Tomography ◽  
Parkinson's Disease ◽  
Emission Tomography ◽  
Dopamine Synthesis ◽  
Dopamine Turnover ◽  
Compensatory Mechanisms ◽  
Clinical Onset ◽  
Positron Emission ◽  
Uptake Rate Constant

An increase in dopamine turnover has been shown to occur early in Parkinson's disease (PD). This study investigated changes of dopamine turnover as a function of PD duration using the effective distribution volume (EDV) for dopamine, determined by positron emission tomography with 6-[18F]-fluoro-L-dopa, and compared them with changes in dopamine synthesis and storage ability, quantified with the fluorodopa uptake rate constant Ki. Six healthy subjects, 9 early PD patients (PD1), and 13 advanced PD patients (PD2) participated in the study. In the caudate, the Ki and EDV for PD1 were not significantly different from the normal values, whereas in the putamen Ki was 63% of normal and EDV was only 35%. Between PD1 and PD2 the decline in EDV was higher than that for Ki (caudate 44% and putamen 46% for EDV vs. 21% and 34%, respectively, for Ki). Turnover was higher in the caudate than the putamen in controls, whereas the PD patients exhibited the reverse pattern. This comparison of changes in Ki and EDV as a function of disease progression indicates that a relatively slower decrease in dopamine synthesis and a relatively faster increase in turnover in early disease likely act as compensatory mechanisms, and that the clinical onset of PD reflects a global failure of dopaminergic compensatory mechanisms.

Perspective food addiction, caloric restriction, and dopaminergic neurotransmission

2013 ◽  
Vol 25 (5) ◽  
pp. 257-267
Author(s):  
Arwen Urrsula Malgorzata Stankowska ◽  
Albert Gjedde
Keyword(s):  
Caloric Restriction ◽  
Sensation Seeking ◽  
Drugs Of Abuse ◽  
Food Addiction ◽  
Eating Behaviour ◽  
Drug Abusers ◽  
Obese People ◽  
Dopaminergic Neurotransmission ◽  
Increased Risk ◽  
Risk Of Relapse

People attempt to change their lifestyle when obesity impairs their quality of life. The attempts often fail when multiple habits must be changed in unison. Here we explore relations among food addiction, the neurobiology of habits, and caloric restriction, when people seek to return to normal eating behaviour, with particular emphasis on the role of dopaminergic neurotransmission.Severely obese individuals have specific neurobiological characteristics in common with drug abusers, including low availability of dopamine receptors in the striatum, impaired neuronal responses to dopamine, and reduced activity in prefrontal regions of the cerebral cortex. The neurobiological characteristics suggest that obese people also have a pathological dependence in common with addicts, in the form of food addiction.Malnutrition and dieting both relate to binge eating, possibly as a compensation for a reduced cognitive reward condition. The combination of caloric restriction and food addiction imparts a high risk of relapse as a result of further reduction of dopaminergic neurotransmission and the subsequent loss of reward. As with drugs of abuse, ingestion of large quantities of sugar in circumstances of uncontrolled eating increases dopamine release in the nucleus accumbens. This and other evidence suggests that abuse of food is a habit learned by means of mechanisms centred in the basal ganglia, with an increased risk of relapse in the presence of associative amplifiers. This risk is predicted by the relationship between dopamine receptor availability in the striatum and sensation-seeking in the form of an inverted U, suggested by recent findings, consistent with two opposite states of hypodopaminergic and hyperdopaminergic neuromodulation.

Pathological gambling: Relation of skin conductance response to dopaminergic neurotransmission and sensation-seeking

2010 ◽  
Vol 20 (11) ◽  
pp. 766-775 ◽  
Author(s):  
Ericka Peterson ◽  
Arne Møller ◽  
Doris J. Doudet ◽  
Christopher J. Bailey ◽  
Kim Vang Hansen ◽  
...  
Keyword(s):  
Pathological Gambling ◽  
Skin Conductance ◽  
Sensation Seeking ◽  
Skin Conductance Response ◽  
Dopaminergic Neurotransmission

Mechanisms of action of clozapine in the treatment of neuroleptic-resistant and neuroleptic-intolerant schizophrenia

1995 ◽  
Vol 10 (S1) ◽  
pp. 39s-46s ◽  
Author(s):  
AY Deutch
Keyword(s):  
Prefrontal Cortex ◽  
Side Effects ◽  
Caudate Nucleus ◽  
Mechanisms Of Action ◽  
Laboratory Animals ◽  
Therapeutic Effects ◽  
Extrapyramidal Side Effects ◽  
Extracellular Dopamine ◽  
Alternative Approaches ◽  
Sites Of Action

SummaryThe mechanisms of action which account for the effectiveness of clozapine as a pharmacotherapy for the treatment of neuroleptic non-responders and neuroleptic intolerant schizophrenic subjects remain elusive. We review recent data concerning the actions of clozapine in laboratory animals, and discuss the likely sites of action of clozapine and the receptors through which clozapine acts. We suggest that actions at dopamine D2 receptors in the caudate nucleus and putamen underlie the extrapyramidal side effects of conventional neuroleptics. In contrast, we propose that clozapine acts in the prefrontal cortex, specifically targeting an as yet unidentified DA receptor of the D2 family, to exert therapeutic actions in neuroleptic non-responders. We suggest that the ability of clozapine to augment extracellular dopamine levels in the prefrontal cortex may represent a key mechanism contributing to the therapeutic effects of this drug, and suggest some alternative approaches which might be expected to result in effects similar to those of clozapine.

Stimulation of dopamine synthesis in caudate nucleus by intrastriatal enkephalins and antagonism by naloxone

Science ◽  
1978 ◽  
Vol 200 (4341) ◽  
pp. 552-554 ◽  
Author(s):  
G Biggio ◽  
M Casu ◽  
M. Corda ◽  
C Di Bello ◽  
G. Gessa
Keyword(s):  
Caudate Nucleus ◽  
Dopamine Synthesis ◽  
Stimulation Of
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