Catecholamines, derived from the amino acid tyrosine, produced by
the adrenal glands, which are found on top of the kidneys. are
epinephrine (adrenaline), norepinephrine (noradrenaline) and dopamine.
The hormone are released into the blood during times of physical or
emotional stress.
Dopamine
9. Dopamine and motivation
Dopamine
(DA) D2 receptors expressed in DA neurons (D2 autoreceptors) exert a
negative feedback regulation that reduces DA neuron firing, DA synthesis
and DA release. According to the mice study by Consejo Nacional de
Investigaciones Científicas y Técnicas, midbrain DA neurons from mice
deficient in D2 autoreceptors (Drd2(loxP/loxP); Dat(+/IRES-cre),
referred to as autoDrd2KO mice) lacked DA-mediated somatodendritic
synaptic responses and inhibition of DA release. AutoDrd2KO mice
displayed elevated DA synthesis and release, hyperlocomotion and
supersensitivity to the psychomotor effects of cocaine. The mice also
exhibited increased place preference for cocaine and enhanced motivation
for food reward. Our results highlight the importance of D2
autoreceptors in the regulation of DA neurotransmission and demonstrate
that D2 autoreceptors are important for normal motor function,
food-seeking behavior, and sensitivity to the locomotor and rewarding
properties of cocaine(9).
10. Dopimine in punishment and reward
In the study of Variations of extracellular dopamine (DA(ext)) levels in prefrontal cortex were assessed by in vivo microdialysis, found
that a benzodiazepine-sensitive activation of mesoprefrontal DA
neurones is induced by exposure to novel stressful surroundings and by
food availability and consumption. The fact that cortical DA(ext) levels
remained unchanged in rats that exerted complete control upon negative
stimuli indicates that an activation of the mesoprefrontal DA system is
not required for punishment-induced behavioural blockade(10).
11. Dopamine and the inhibition of prolactin production
Transcription of the prolactin
gene is dynamically controlled by positive and negative hormone signals
that target the regulatory promoter region. According to the study by
University of Toronto, dopamine D2 receptor activation and inhibition of MAPK (ERK1/2) signaling lead to rapid deacetylation of histones at the genomic prolactin
promoter. Recruitment of specific HDAC/ corepressor complexes may be an
important mechanism for repression of target gene transcription by
Gi/o-coupled receptors(11).
12. Dopamine and sleep behaviour disorder (IRBD)
In a prospective study,
20 patients with IRBD (mean age 70·55 years [SD 6·02]) underwent serial
DAT imaging with
(123)I-2β-carbomethoxy-3β-(4-iodophenyl)-N-(3-fluoropropyl)-nortropane
((123)I-FP-CIT) SPECT at baseline and again after 1·5 years and 3 years;
20 age-matched and sex-matched control participants (69·50 years
[6·77]) underwent imaging at baseline and 3 years, showed that in
patients with sleep behaviour disorder
(IRBD), serial (123)I-FP-CIT SPECT shows decline in striatal tracer
uptake that reflects progressive nigrostriatal dopaminergic dysfunction.
Serial (123)I-FP-CIT SPECT can be used to monitor the progression of
nigrostriatal deficits in patients with IRBD, and could be useful in
studies of potential disease-modifying compounds in these patients(12).
13. Dopamine in depression
According to the study
by New York State Psychiatric Institute, clinical evidence includes
alterations in depressive symptoms with aging (concomitant with possible
changes in dopamine metabolism),
potential dopaminergic involvement in several subtypes of depression,
similarities between some of the symptoms of Parkinson's disease and
those of depression (including psychomotor retardation and diminished
motivation), and potential dopaminergic abnormalities in seasonal mood disorder. The biochemical evidence in patients with depression derives from studies of homovanillic acid, a dopamine metabolite, indicating diminished dopamine turnover(13).
14. Dopamine and Mood disorder
Dysfunction in the monoamine systems of serotonin (5-HT), norepinephrine (NE) and dopamine
(DA) may causally be related to major depressive disorder
(MDD). According to the study by University of Amsterdam, monoamine
depletion studies demonstrate decreased mood in subjects with a family history of MDD and in drug-free patients with MDD in remission, but do not decrease mood
in healthy humans. Although depletion studies usefully investigate the
etiological link of 5-HT and NE with MDD, they fail to demonstrate a
causal relation. They presumably clarify a vulnerability trait to become
depressed. Directions for further investigation of this vulnerability
trait are proposed(14).
15. Dopamine in the regulation of cognition and attention
Dopamine
(DA) acts as a key neurotransmitter in the brain.. In the early stages
of Parkinson's disease (PD), alterations of executive functions also
suggest a role for DA in regulating cognitive functions. Some other
diseases, which can also involve DA dysfunction, such as schizophrenia
or attention deficit hyperactivity
disorder (ADHD) in children, as shown from the ameliorative action of
dopaminergic antagonists and agonists, respectively, also show
alteration of cognitive functions. According to the study by Université
de La Méditerranée, a correlation exists between DA innervation and
expression of cognitive capacities. Altering the dopaminergic
transmission could, therefore, contribute to cognitive impairment(15).
16. Dopamine and working memory
There is accumulating evidence that training working memory
(WM) leads to beneficial effects in tasks that were not
trained. According to the study by Department of Neuroscience and
Stockholm Brain Institute, Karolinska Institutet, variation in the dopamine
transporter gene (DAT1) influences improvements in WM and fluid
intelligence in preschool-age children following cognitive training. Our
results emphasize the importance of the role of dopamine in determining cognitive plasticity(16).
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Sources
(9) http://www.ncbi.nlm.nih.gov/pubmed/21743470
(10) http://www.ncbi.nlm.nih.gov/pubmed/11420078
(11) http://www.ncbi.nlm.nih.gov/pubmed/15731170
(12) http://www.ncbi.nlm.nih.gov/pubmed/21802993
(13) http://www.ncbi.nlm.nih.gov/pubmed/8099801
(14) http://www.ncbi.nlm.nih.gov/pubmed/17389902
(15) http://www.ncbi.nlm.nih.gov/pubmed/12126656
(16) http://www.ncbi.nlm.nih.gov/pubmed/22103304
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