China
Africa
Explore chapters and articles related to this topic
Pharmacotherapy of Neurochemical Imbalances
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Rupali Patil, Aman Upaganlawar, Suvarna Ingale
After the execution of the action, neurotransmitter is inactivated by different mechanisms such as diffusion out of synaptic cleft, inactivation or disintegration by specific enzymes, engulfment by astrocytes (macrophages) and reuptake into the axon terminal. Many neurotransmitters are actively taken back (reuptake) into the nerve terminals with the help of membrane proteins known as neurotransmitter transporters and repacked into new synaptic vesicles for further actions (Muller and Nistico, 1989; Edwards, 2007).
Use of PET to Study Addiction in Humans
Published in Edythe D. London, Imaging Drug Action in the Brain, 2017
Nora D. Volkow, Joanna S. Fowler
These measure processes that relate to neurotransmission. Tracers have been developed to measure postsynaptic neurotransmitter receptor concentration (Wagner et al., 1983; Farde et al., 1985; Arnett et al., 1986; Dewey et al., 1990; Halldin et al., 1986; Frost et al., 1985; Pappata et al., 1988; Wong et al., 1987), neurotransmitter transporters at the presynaptic terminal (Aquilonius et al., 1987; Kilbourn et al., 1988; Fowler et al., 1989b), neurotransmitter synthesis (Diksic et al., 1990; Firnau et al., 1986; DeJesus et al., 1989; Gildersleeve et al., 1989), and neurotransmitter degrading enzymes (Fowler et al., 1987) (Figure 1). Neurochemical PET studies can be performed either with no intervention (Wagner et al., 1983) or after pretreatment with specific pharmacological agents (Wong et al., 1986a, 1986b).
Lipid Raft Alteration and Functional Impairment in Aged Neuronal Membranes
Published in Shamim I. Ahmad, Aging: Exploring a Complex Phenomenon, 2017
Julie Colin, Lynn Gregory-Pauron, Frances T. Yen, Thierry Oster, Catherine Malaplate-Armand
On the basis of their capacity to provide the proper environment to segregate functional groups of proteins, rafts are considered as key players in many cellular processes including endocytosis and signal transduction, being involved in particular in the endocytosis of the interleukin-2, high-affinity IgE, and insulin receptors [139]. The role of rafts in exocytosis has also been extensively reported. For example, the concentration of certain SNARE complex proteins [140] was reported to be up to 25 times higher in rafts [111]. Furthermore, rafts are thought to play an important role in synaptic signaling, as demonstrated by the enrichment of synaptic proteins, such as the synaptosomal-associated protein (SNAP) [141] and the postsynaptic density (PSD) in rafts of rat forebrain synaptic membranes and pheochromocytoma PC12 cells [142]. Cerebral and, in particular, neuronal function can also be affected due to raft-dependent neurotransmitter transporter activity and trafficking, as is the case for choline and serotonin in cells stably expressing the respective transporters [143,144]. Through lateral segregation of membrane-associated proteins, rafts also play a role in the regulation of protein–protein interactions. On the one hand, clustering of proteins within rafts statistically favors their interaction. On the other hand, inclusion of a particular protein within rafts prevents its interaction with proteins located outside of rafts or in distinct subpopulations of rafts. This latter situation results in the inhibition of the signaling complex assembly and subsequent activation of cascade events [145,146].
Cortical astroglia undergo transcriptomic dysregulation in the G93A SOD1 ALS mouse model
Published in Journal of Neurogenetics, 2018
Sean J. Miller, Jenna C. Glatzer, Yi-chun Hsieh, Jeffrey D. Rothstein
Astroglia are essential for maintaining nervous system homeostasis (Zhang & Barres, 2010). They are a tremendously diverse glial cell type that performs a vast array of functions, including and not limited to: neurotransmitter recycling, ion homeostasis, neuronal spine formation and elimination, immune-modulation, neurotrophin release, and maintenance of the blood–brain barrier (Miller & Rothstein, 2016). Astroglia in different anatomical regions exhibit highly different molecular profiles. Importantly, these molecular profiles also have been shown to change dramatically in neurological disease (Miller, Zhang, Glatzer, & Rothstein, 2016). In motor neuron diseases such as amyotrophic lateral sclerosis (ALS), astroglia downregulate essential ion, and neurotransmitter transporters such as the synaptically localized glutamate-transporter I, Glt1, and potassium ion channel, Kcnj10 (Kaiser et al., 2006; Rothstein, Van Kammen, Levey, Martin, & Kuncl, 1995). The downregulation of these key membrane proteins is apparent in areas of motor neuron death, such as the lower motor neurons in the spinal cord and the upper motor neurons in the cortex.
Protective effects of thymoquinone on D-galactose and aluminum chloride induced neurotoxicity in rats: biochemical, histological and behavioral changes
Published in Neurological Research, 2018
Yasmin S. Abulfadl, Nabila .N. El-Maraghy, Amany Ali. Eissa Ahmed, Shahira Nofal, Osama A. Badary
It has been recently reported that nitrosylation of vesicular acetylcholine transporter (VAChT), a neurotransmitter transporter which is responsible for loading ACh in neurons, may be associated with dysfunctional acetylcholinergic neurotransmission in AD [59]. In another study, nitrosylation of this transporter inhibits the vesicular uptake of acetylcholine in an animal model for AD [60,61]. According to these studies and in addition to our results, we suggest that TQ may prevent VAChT nitrosylation by scavenging NO and preventing it from attacking -SH of cysteine residues of VACht thereby making ACh available for secretion. TQ could therefore effectively enhance the induced cognitive impairment in our AD model. This suggestion is similar to that in a recent study [62] which stated that forebrain-specific deletion of VAChT has severe deficits in cognitive performance. Moreover, treatment with TQ (20 mg/kg, orally) succeeded to restore the brain content of BDNF. The protected level of this factor is likely to improve the synaptic efficacy and in turn improve cognition.
Two novel forms of ERG oscillation in Drosophila: age and activity dependence
Published in Journal of Neurogenetics, 2018
Atsushi Ueda, Scott Woods, Ian McElree, Tristan C. D. G. O’Harrow, Casey Inman, Savantha Thenuwara, Muhammad Aftab, Atulya Iyengar
Comparisons between ERG waveforms from WT flies and those of rosA mutants, which display RP oscillations and a loss of transients (Gavin et al., 2007), can provide clues on how activity-dependent oscillations evoked by repetitive light flashes arise. The putative Na+/Cl− solute transporter encoded by rosA gene product, along with other neurotransmitter transporters such as carT (Chaturvedi, Luan, Guo, & Li, 2016; Xu et al., 2015), may play an important role in shuttling histamine and related metabolites across the plasma membranes as well as in influencing the ionic composition of intracellular and local extracellular spaces (Burg et al., 1996; Huang & Stern, 2002). The ERG oscillations in rosA mutants differ from activity-dependent oscillations in WT flies in their location within the ERG waveform and in oscillation frequency (Figure 4). In contrast to light-on or light-off oscillations in WT flies which are associated with the ERG transients, ERG oscillations in rosA appear during the RP component, gradually growing in amplitude and ceasing immediately after the light flash ends. Additionally, the frequency of RP oscillations in rosA was generally lower than the light-on or light-off oscillations in WT flies.