China
Africa
Explore chapters and articles related to this topic
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.
Drugs of Abuse and Addiction
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Shalini Mani, Chahat Kubba, Aarushi Singh
Addictive drugs such as cocaine, AMPH (class III drugs) hinder the monoamine transporters of the neurons mainly which are present in the ventral tegmental area (VTA) and blocks the dopamine uptake by them leading to extracellular accumulation of dopamine as illustrated in Figure 20.1. These elevated dopamine concentrations may lead to anterior pituitary hypoplasia, inability to lactate owing to the reduced hypothalamic content of growth hormone-releasing hormone (Amara and Sonders, 1998).
Vitamin C in Neurological Function and Neurodegenerative Disease
Published in Qi Chen, Margreet C.M. Vissers, Vitamin C, 2020
Shilpy Dixit, David C. Consoli, Krista C. Paffenroth, Jordyn M. Wilcox, Fiona E. Harrison
Dopamine itself is considered cytotoxic, and the elevated levels of dopamine found in the SNpc can contribute to oxidative stress vulnerability. It is believed that dopamine oxidation by monoamine oxidase or transition metals exerts the toxic effects on cells. Increased mitochondrial oxidative stress leads to an accumulation of oxidized dopamine in a dose-dependent manner in human-derived dopaminergic-neurons lacking either one or both copies of DJ-1, a chaperone protein believed to mediate cellular oxidant defenses [208]. Selective dopaminergic synaptic terminal loss is observed when dopamine is injected into rat striatum and the amount of loss is in correlation with the amount of oxidized dopamine product [209,210]. Further, PD symptomology and progressive cell loss in the SNpc are observed in mice that cannot package dopamine into vesicles due to deficient expression of the vesicular monoamine transporter type 2 [211–213]. Further, the role of vitamin C in epigenetic modification and, in particular, in the differentiation of dopaminergic neurons through TET-mediated epigenesis [30,214] supports the necessity for vitamin C in the formation and maintenance of the dopaminergic cell population. A clear role for vitamin C in stem cell differentiation and preservation is also a critical consideration if stem cells are ever developed into a safe therapy for PD as has been proposed [216].
Neuroprotective effect of standardized extracts of three Lactuca sativa Linn. varieties against 3-NP induced Huntington’s disease like symptoms in rats
Published in Nutritional Neuroscience, 2022
Jai Malik, Supreet Kaur, Maninder Karan, Sunayna Choudhary
Synthetic drugs, such as, selective serotonin reuptake inhibitors (SSRIs), vesicular monoamine transporter 2 inhibitor, antipsychotics and anticonvulsants are used for symptomatic treatment HD patients which are associated with various side-effects.16 Apart from these synthetic drugs, a number of herbal drugs and bioactive phytocompounds have shown beneficial effects against HD.17,18 To evaluate various test drugs and to understand the pathophysiology of HD, chemical and genetic experimental models are being used. 3-Nitropropionic acid (3-NP) is the most widely used chemical agents that produce HD like symptoms in rodents, and also help in evaluating the efficacy of various test compounds against HD. It is a mycotoxin produced by various members of the genus Astragalus Linn. (Leguminosae) and Arthrinium Sacc. (Apiosporaceae) fungi. 3-NP disrupts electron transport chain in mitochondria and increase oxidative stress to show its toxic effect.19
Cannabis-like activity of Zornia latifolia Sm. detected in vitro on rat cortical neurons: major role of the flavone syzalterin
Published in Drug and Chemical Toxicology, 2022
Susanna Alloisio, Marco Clericuzio, Mario Nobile, Annalisa Salis, Gianluca Damonte, Claudia Canali, Ana Paula Fortuna-Perez, Laura Cornara, Bruno Burlando
Apigenin belongs to the flavone class and is found in several plants, such as Hypericum perforatum L., Matricaria chamomilla L., Melissa officinalis L., and different thyme, citrus and onion species (Nabavi et al. 2015). In the nervous system, apigenin readily crosses the blood-brain barrier and has not demonstrated toxicity at high doses (Venigalla et al. 2015). In particular, it has been shown to act as a monoamine transporter activator, one of the few compounds demonstrated to possess this property (Zhao et al. 2010). Moreover, apigenin is a weak ligand for central benzodiazepine receptors in vitro and exerts slight anxiolytic and sedative effects in an animal model (Viola et al. 1995). It has also effects on adenosine receptors (Jacobson et al. 2002) and at micromolar concentrations has been found to reduce NMDA-evoked currents (Losi et al. 2004). Moreover, like different other flavonoids, apigenin has nanomolar affinity for the opioid receptors (Kd = 410 nM, 970 nM, and 410 nM for the μ-, δ-, and κ-opioid receptors, respectively), acting as a nonselective antagonist (Zbidah et al. 2012). In a pathological model, exposure to apigenin reduced the hyper-excitable phenotype observed in sporadic Alzheimer’s disease neurons, significantly reducing the frequency of spontaneous Ca2+ signaling, while also preventing amyloid beta deposition and tau phosphorylation (Balez et al. 2016).
Methamphetamine Use and Antipsychotic-related Extrapyramidal Side-effects in Patients with Psychotic Disorders
Published in Journal of Dual Diagnosis, 2020
Henk S. Temmingh, Wim van den Brink, Fleur Howells, Goodman Sibeko, Dan J. Stein
Various studies point to potential mechanisms behind increased EPSE in patients on APs who use MA. In animal models of MA administration, potential mechanisms behind striatal dopamine depletion and terminal and synaptic axonal structural abnormalities may include MA interference with the dopamine transporter (DAT) and the vesicular monoamine transporter (VMAT-2) which may lead to intracytoplasmic DA release and consequent superoxide free-radical formation, oxidative stress and cellular damage. Other mechanisms of neuronal damage may include hyperthermia, glutamate release and excitotoxicity and microglial mediated inflammatory immune reactions (Jan et al., 2012). Human neuroimaging studies (positron emission tomography [PET]) have also demonstrated lower DAT and D2 receptor availability in the putamen, with even lower levels in the caudate (Volkow et al., 2001). Interestingly, postmortem studies have shown lower DA levels in the putamen of idiopathic Parkinson patients compared to chronic MA users (compared to much higher levels in normal controls), leading to the theory that MA does not result in more overt parkinsonism in humans (as opposed animals) as it affects the (cognitive) caudate region quantitatively more than the (motor) putamen (Moszczynska et al., 2004). One could speculate that APs attenuate already low putamen dopaminergic transmission in MA users to an even lower level, across a threshold, thus contributing to manifest parkinsonian motor symptom formation.