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Neuroimaging in Nuclear Medicine
Published in Michael Ljungberg, Handbook of Nuclear Medicine and Molecular Imaging for Physicists, 2022
Anne Larsson Strömvall, Susanna Jakobson Mo
Like a key in a keyhole locking up a door, a neurotransmitter fits into special receptors, which in the receiving neuron triggers a specific process leading to action, a nerve impulse. There may be different kinds of receptors for each kind of neurotransmitter. Dopamine, for example, fits several kinds of dopamine receptors, called the D1, D2, D3, D4, and D5 receptors. The strength of the signal that is transmitted between two neurons depends on the amount of neurotransmitter in the synapse and the amount of time the neurotransmitter is allowed to act on the receptors. Therefore, there are specialized proteins or enzymes that degrade or recycle the released neurotransmitter in order to tune the signal. For example, neurotransmitters called monoamines (dopamine, serotonin, and noradrenaline) have their own transporter proteins (monoamine transporter proteins, MAPs) located at the nerve terminals. These reabsorb the neurotransmitter back into the nerve terminal. In this way, MAPs regulate the amount of available neurotransmitter in the synapse and thereby the response is tuned. In addition, some of the released neurotransmitter is recycled and may be re-used the next time. The dopamine transporter (DAT) is a well-known transporter protein, exclusively found on dopamine producing neurons. Apart from the MAPs, monoaminergic neurotransmission is regulated by enzymes called monoamine oxidase (MAO). The MAOs reduce the amount of available monoaminergic neurotransmitters in the synaptic cleft by decomposition.
Voltammetric Detection of Neurotransmitter Release
Published in Richard P. Buck, William E. Hatfield, Mirtha UmañA, Edmond F. Bowden, Biosensor Technology Fundamentals and Applications, 2017
Dopamine was first considered to be a neurotransmitter in the late 1950’s (2,3). Using a fluorescence assay, neuroscientists were able to show that this compound is found in high amounts (50 nmoles/gram) in a region of the brain known as the caudate nucleus. In the 1960’s it was shown that patients with Parkinson’s disease show an almost complete depletion of dopamine in this region. The pathways of dopamine-containing neurons have been mapped in the rat brain making it an ideal species for the further characterization of this system. Dopamine neurons in the caudate nucleus were demonstrated to have the capability to uptake dopamine from the surrounding fluid which can inactivate dopamine neurotransmission. It was further shown that drugs of abuse such as cocaine and amphetamine could inhibit this uptake process, and this cellular action correlates with the behavioral changes induced by these drugs. A correlation also exists between the binding of antipsychotic drugs to dopamine receptors and their efficacy in controlling the symptoms of schizophrenia. Thus, the interest in dopamine neurotransmission is far reaching, as it seems that the proper regulation of this process is required for normal functioning and behavior.
Drugs for Treatment of Neurological and Psychological Conditions
Published in Richard J. Sundberg, The Chemical Century, 2017
Dopamine, too, received attention. In particular, Arvid Carlsson in Sweden demonstrated that reserpine also depleted dopamine levels. The role of the amphetamines stimulants could also be interpreted in terms of their effect on dopamine. Unlike reserpine, chlorpromazine does not deplete dopamine levels. It was shown that, instead, it blocks dopamine receptors. This was first indicated in the 1960s and directly demonstrated in the 1970s. The explicit proposal that dopamine was a major factor in the etiology of schizophrenia was put forward by Jaques M. van Rossum in 1966. At about the same time, it was proposed that the catecholamines played a critical role in depression.7 Other studies showed that serotonin and its receptors also had an important role in mental status. While many details remained to be clarified, it was becoming apparent that the antipsychotic drugs acted through effects on the monoamine neurotransmitters. In the 1970s, it became possible to identify receptors for dopamine and the other monoamines. Dopamine receptors are associated with the “reward” and “motivation” aspects of behavior and dopamine is considered to mediate the connection between experience and response. If this connection is dysfunctional, the response is inappropriate and delusional. Excessive dopamine release and receptor response is associated with psychoses. To the extent that antipsychotic drugs can correct the function of dopamine and the receptors, the patient’s condition is improved.
The effects of Alzheimer's disease related striatal pathologic changes on the fractional amplitude of low-frequency fluctuations
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2020
Dopamine has a dual action on MSNs; it inhibits the (D2-type) MSNs in the indirect pathway and excites (D1-type) MSNs in the direct pathway. Therefore, depending on D1 or D2 type dopamine receptors inclusion, MSNs population is split in two population of roughly equal size. These receptors have different effects on both intrinsic and synaptic ion channels, (Humphries et al. 2009). Dopaminergic modulation of intrinsic ion channels in D1 MSNs is given by where is for simulating the hyperpolarizing effect of D1 activation. ϕ1 is the parameter for specifying the level of dopamine receptor for D1. For D2 MSNs, dopaminergic modulation of intrinsic ion channels is given as
Evaluation of potential health effects associated with occupational and environmental exposure to styrene – an update
Published in Journal of Toxicology and Environmental Health, Part B, 2019
M.I. Banton, J.S. Bus, J.J. Collins, E. Delzell, H.-P. Gelbke, J.E. Kester, M.M. Moore, R. Waites, S.S. Sarang
Zaidi et al. (1985) studied styrene’s effects on some aspects of brain function, after exposure of rats during gestation and lactation by the gavage at only one dose level of 200 mg/kg bw/day. One group was treated throughout gestation and the pups were raised without further treatment either by treated or untreated mothers. Another group was exposed during gestation and lactation up to 2 and 3 weeks and a third group from postnatal day 1 up to 2 or 3 weeks. Animals were sacrificed at the age of 2 or 3 weeks. The number of litters investigated was very small (n = 3 or 4), especially in regard to the non-routine parameters studied. The study concentrated on the measurement of dopamine receptor binding in corpora striata, amphetamine-induced locomotor activity, and apomorphine-induced stereotypy. Dopamine receptor binding was not affected for exposure only during gestation, but was increased by exposure during lactation. The increased binding was due to an increased number of receptors. Amphetamine-induced locomotor activity was increased by combined exposure throughout gestation and lactation. Apomorphine-induced stereotypy was potentiated by styrene exposure. A clear interpretation of the study is limited by the small number of litters.
Oculomotor dynamics in skilled soccer players: The effects of sport expertise and strenuous physical effort
Published in European Journal of Sport Science, 2019
Teresa Zwierko, Wojciech Jedziniak, Beata Florkiewicz, Miłosz Stępiński, Rafał Buryta, Dorota Kostrzewa-Nowak, Robert Nowak, Marek Popowczak, Jarosław Woźniak
Moreover, other previous investigations in healthy individuals undergoing pharmacological intervention on eye movements confirmed a relationship between brain catecholamines and saccadic control. For instance, Glue, White, Wilson, Ball, and Nutt (1991) observed that the administration of clonidine, an α 2-adrenoreceptor agonist that inhibits noradrenaline release, substantially reduced peak velocity, acceleration and deceleration of saccadic eye movements in healthy male volunteers. Conversely, the administration of an α2-adrenoreceptor antagonist (idazoxan), did not increase saccade velocity, acceleration or deceleration above the baseline state. Furthermore, administration of the first-generation antipsychotic chlorpromazine (100 mg), a D2-dopamine receptor antagonist, slowed peak saccade velocity in healthy individuals (Barrett, Bell, Watson, & King, 2004; Green & King, 1998). In relation to our study it is highly likely that the potential perturbations in the synthesis and metabolism of several neurotransmitters as result of maximal intensity exercise may affect some of the specific brain areas involved in saccadic eye movement control, such as the superior colliculus, frontal eye fields, supplementary eye fields, and the paramedian pontine reticular formation (Munoz & Everling, 2004).