Can Physical Activity Prevent or Treat Clinical Depression? 1
Henning Budde, Mirko Wegner in The Exercise Effect on Mental Health, 2018
Neurotransmitters are biochemical substances that send signals from one nerve cell to another. Monoamines are a group of neurotransmitters thought to play a critical role in the regulation of emotions and in the treatment of depression (Dunn & Dishman 1991). Long-term voluntary exercise in rats leads to an increased expression of monoamines in the locus coeruleus (LC) and dorsal raphe nucleus (DRN), and these increases are accompanied by a reduction in depressive behaviors (Dishman et al. 1997; Kim, Lim, Baek, Ryu, & Seo 2015). In humans, brain monoamine activity is indirectly estimated from blood and urine, and evidence is mixed as to whether exercise leads to an increase in monoamine metabolites or not (Dunn & Dishman 1991). Exercise also activates the opioid system, and this may account for the “runner’s high” phenomenon (Boecker et al. 2008). Much of the attention has focused on the opioid β-endorphin. Several studies have shown increased β-endorphin levels in blood plasma following high-intensity exercise (Farrell, Gates, Maksud, & Morgan 1982), and these increases correlate with mood improvements (Wildmann, Kruger, Schmole, Niemann, & Matthaei 1986). However, contradictory associations with depressive symptoms question its role in the therapeutic effect of exercise (Darko, Risch, Gillin, & Golshan 1992). As with monoamines, peripheral estimates of β-endorphin may not provide an accurate valuation of central opioidergic activity, but a recent neuroimaging study provided the first evidence that exercise increases the release of opioids in the human brain (Boecker et al. 2008).
Exercise, neurotransmission and neurotrophic factors
Romain Meeusen, Sabine Schaefer, Phillip Tomporowski, Richard Bailey in Physical Activity and Educational Achievement, 2017
Neurotransmitters govern the communication between neurons in different brain regions and neuronal pathways. Generally speaking, nerve cells in the brain are firing all the time, giving a massive ‘background noise’. Probably none of the neurons in the brain are exposed only to excitation, and certainly no nerve cells are affected solely by inhibitory signals. Most brain functions such as learning, memory, cognition, control of movement and other mechanisms need the interaction of neurotransmitters and neuromodulators. In order to establish new memories and to encode, store and retrieve memories, cross-talk between several brain structures such as the hippocampus and interplay between several neurotransmitters and neuromodulators are important (Taylor et al., 2016). Understanding the function of various neurotransmitters and neuromodulators helps in understanding their role during whole-body exercise, fatigue, learning and memory. In this chapter we will describe how different forms of exercise influence neurotransmission and how neurotrophic factors and especially brain-derived neurotrophic factor (BDNF) respond to an exercise stimulus, forming the basis for learning and memory.
The basal ganglia: an overview
Hans O Lüders in Deep Brain Stimulation and Epilepsy, 2020
Several neurotransmitter systems are active in the basal ganglia. Gamma-aminobutyric acid (GABA) and glutamate are the most common neurotransmitters followed by dopamine, acetylcholine, substance P, dynorphin and enkephalins. Dopamine (DA) plays an important role in the regulation of basal ganglia function. There is substantial evidence that release of DA into the striatum via the nigrostriatal pathway facilitates transmission in the direct pathway by activating D1 receptors and inhibits transmission over the indirect pathway via activation of D receptors. In addition, DA may modulate basal ganglia output through its actions at extrastriatal sites. DAergic neurons in the SN also send projections to the STN and the GPi and may affect the release of GABA in the striatoni-gral pathway through somatodendritic release of DA. With the exception of the excitatory (glutamatergic) efferents of the STN, intrinsic and output connections of the basal ganglia are inhibitory (GABAergic) (Figure 2.2).
Treatment of schizophrenia in the 21st Century: beyond the neurotransmitter hypothesis
Published in Expert Review of Neurotherapeutics, 2009
Donald P Rogers, Carroll-Ann W Goldsmith
Over the last six decades, the treatment of schizophrenia has focused primarily on interactions at monoamine neurotransmitter receptor sites, including those for dopamine and serotonin. While first-generation antipsychotics demonstrate antagonism at the dopamine 2 receptor, newer atypical agents involve multiple receptors at various neurotransmitter sites. Despite the advent of these newer agents, the treatment of schizophrenia continues to elude clinicians, perhaps owing to a lack of information about the factors contributing to the development of the disease. While the etiology is complex and not yet fully delineated, we suggest that treating clinicians be willing to look beyond neurotransmitters and entertain other potential factors involved in the pathogenesis of schizophrenia. One such factor that is often overlooked is the possible contribution of autoimmunity to disease development in at least a subset of patients. In this article we make an argument for consideration of immune dysfunction in the development of schizophrenia and suggest future directions for the field.
A diffusion tensor-based finite element model of microdialysis in the deep brain
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2015
Elin Diczfalusy, Mats Andersson, Karin Wårdell
Microdialysis of the basal ganglia was recently used to study neurotransmitter levels in relation to deep brain stimulation. In order to estimate the anatomical origin of the obtained data, the maximum tissue volume of influence (TVImax) for a microdialysis catheter was simulated using the finite element method. This study investigates the impact of brain heterogeneity and anisotropy on the TVImax using diffusion tensor imaging (DTI) to create a second-order tensor model of the basal ganglia. Descriptive statistics showed that the maximum migration distance for neurotransmitters varied by up to 55% (n = 98,444) for DTI-based simulations compared with an isotropic reference model, and the anisotropy differed between different targets in accordance with theory. The size of the TVImax was relevant in relation to the size of the anatomical structures of interest, and local tissue properties should be accounted for when relating microdialysis data to their anatomical targets.
Transmissions of serotonin, dopamine, and glutamate are required for the formation of neurotoxicity from Al
Published in Nanotoxicology, 2013
Yinxia Li, Shunhui Yu, Qiuli Wu, Meng Tang, Dayong Wang
In this study, we investigated genetic mechanisms of neurotransmitters in regulating the formation of adverse effects on locomotion behavior in Al2O3 nanoparticles (NPs)-exposed Caenorhabditis elegans. Al2O3-NPs exposure caused the decrease of locomotion behavior with head thrash and body bend as endpoints. Interestingly, the neurotransmitters of glutamate, serotonin, and dopamine were required for the adverse effects of Al2O3-NPs on locomotion behavior in nematodes. Glutamate transporter EAT-4, serotonin transporter MOD-5, and dopamine transporter DAT-1 might serve as the molecular targets of Al2O3-NPs for neurotoxicity formation. Moreover, the behavioral response of nematodes to Al2O3-NPs exposure was primarily mediated by non-NMDA glutamate receptors GLR-2 and GLR-6, ionotropic serotonin receptor MOD-1, and D1-like dopamine receptor DOP-1. Therefore, Al2O3-NPs exposure influences locomotion behavior of nematodes primarily by impinging on their glutamatergic, serotoninergic, and dopaminergic systems. Our data will shed light on questions surrounding the involvement of neurotransmitters in mediating the adverse behavioral effects from Al2O3-NPs.
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