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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.
Kinetic modeling and statistical optimization of submerged production of anti-Parkinson’s prodrug L-DOPA by Pseudomonas fluorescens
Published in Preparative Biochemistry & Biotechnology, 2022
Ananya Naha, Santosh Kumar Jha, Hare Ram Singh, Muthu Kumar Sampath
Levodopa is an amino acid and a precursor of dopamine. It can easily cross the blood-brain barrier and convert to dopamine by Dopa Carboxylase by a single enzymatic step, thus increasing the store of dopamine in the brain. Unlike dopamine, L-DOPA can be taken orally or intravenously. It is rapidly taken up by dopaminergic neurons and converted to dopamine.[4] The conversion of L-DOPA to dopamine mainly occurs in the periphery as well as in Central Nervous System (CNS) thus facilitating the reuptake of dopamine by the dopamine transporter (DAT) and vesicular monoamine transporter (VMAT). DAT helps to transport dopamine from extracellular to intracellular space, and VMAT reloads dopamine into the vesi hcles. The whole process is energy-dependent and uses Na-K ions for ATP hydrolysis to create a concentration gradient of ions across the presynaptic membrane. This drive opens the transporter and cotransport Na and Cl ions and dopamine from the synaptic cleft. The released K ions in the synaptic cleft help in the equilibration of the ionic gradient across the presynaptic membrane. Metabolism of dopamine by monoamine oxidase (MAO) and catechol-O-methyl transferase (COMT) is one of the effective mechanisms for dopamine inactivation. This includes several pathways like oxidative deamination by MAO, conjugation by glucuronidase or sulfotransferases, and O-methylation by COMT. MAO acts intracellularly and is located at the external membrane of mitochondria, whereas COMT acts extracellularly and is located within the external cell membrane.[5]
Application of molecular imaging technology in neurotoxicology research
Published in Journal of Environmental Science and Health, Part C, 2018
Xuan Zhang, Qi Yin, Marc Berridge, Che Wang
Methylphenidate, another CNS stimulant, is widely used to treat attention deficit disorder and attention deficit hyperactivity disorder (ADHD). It has been proven that treatment with MPH can efficiently alleviate the primary symptoms in approximately 70% of children with ADHD. Methylphenidate may exert its effects through the blockade of the DAT and the NET, and increases monoamine signaling at the synapse.[56–59] Recently, medical use of MPH has been over-used owing to the high prevalence of ADHD, persisting symptoms in adolescents and adults, and over-diagnosis of ADHD. This has raised concerns regarding its long-term side effects and potential toxicity to the CNS.[65–70] To determine whether chronic MPH exposure during development is associated with subsequent long-term cognitive deficits, drug-induced neurochemical changes were explored by monitoring changes in the uptake (binding) of radiotracers (e.g., FDG, glucose metabolism marker; [18F]-AV133, a marker of vesicular monoamine transporter type 2 [VMAT2]; and 4-18F-ADAM, a radioligand for SERT), in specific regions of interest in the nonhuman primate brain.[70–72] According to these microPET/CT studies, gluocose metabolism in the cerebellum was significantly decreased in both the low- and the high-dose MPH groups. Compared to the control group, the SERT levels significantly increased in the high-dose MPH-treated NHPs in frontal cortex, caudate, putamen, thalamus, and midbrain. Monoamine transporter type 2 levels in thalamus, caudate, putamen, temporal lobe of the cortex, and midbrain were decreased in the low-dose MPH-treated NHPs and decreased in the temporal lobe of the cortex and midbrain in the high-dose group.