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Experimental & Molecular Medicine Apr 2021Body homeostasis is predominantly controlled by hormones secreted by endocrine organs. The central nervous system contains several important endocrine structures,... (Review)
Review
Body homeostasis is predominantly controlled by hormones secreted by endocrine organs. The central nervous system contains several important endocrine structures, including the hypothalamic-pituitary axis. Conventionally, neurohormones released by the hypothalamus and the pituitary gland (hypophysis) have received much attention owing to the unique functions of the end hormones released by their target peripheral organs (e.g., glucocorticoids released by the adrenal glands). Recent advances in mouse genetics have revealed several important metabolic functions of hypothalamic neurohormone-expressing cells, many of which are not readily explained by the action of the corresponding classical downstream hormones. Notably, the newly identified functions are better explained by the action of conventional neurotransmitters (e.g., glutamate and GABA) that constitute a neuronal circuit. In this review, we discuss the regulation of appetite and metabolism by hypothalamic neurohormone-expressing cells, with a focus on the distinct contributions of neurohormones and neurotransmitters released by these neurons.
Topics: Animals; Appetite; Energy Metabolism; Homeostasis; Humans; Hypothalamo-Hypophyseal System; Hypothalamus; Neuroendocrine Cells; Neurons; Neurosecretory Systems; Neurotransmitter Agents; Thyroid Gland
PubMed: 33837263
DOI: 10.1038/s12276-021-00597-9 -
Advances in Experimental Medicine and... 2012Sociability consists of behaviors that bring animals together and those that keep animals apart. Remarkably, while the neural circuitry that regulates these two "faces"... (Review)
Review
Sociability consists of behaviors that bring animals together and those that keep animals apart. Remarkably, while the neural circuitry that regulates these two "faces" of sociability differ from one another, two neurohormones, oxytocin (Oxt) and vasopressin (Avp), have been consistently implicated in the regulation of both. In this chapter the the structure and function of the Oxt and Avp systems, the ways in which affiliative and aggressive behavior are studied and the roles of Oxt and Avp in the regulation of sociability will be briefly reviewed. Finally, work implicating Oxt and Avp in sociability in humans, with a focus on neuropsychiatric disorders will be highlighted.
Topics: Animals; Humans; Mental Disorders; Neurobiology; Neurotransmitter Agents; Social Behavior
PubMed: 22399403
DOI: 10.1007/978-1-4614-1704-0_12 -
Journal of Neurochemistry Jun 2021Reward-seeking is critical for survival. Learning about the relationship between actions and outcomes helps us to make decisions and select behaviours that result in a...
Reward-seeking is critical for survival. Learning about the relationship between actions and outcomes helps us to make decisions and select behaviours that result in a specific outcome. This special issue entitled "The Neurochemistry of Reward-Seeking" addresses this crucial facet of behaviour and brings together a number of key thought-leaders to provide a timely update on the circuitry, chemistry and mechanisms underlying different aspects of reward-seeking. The reviews in this issue canvass unanswered questions in the field and provide a degree of forethought about how we may advance our understanding of reward-seeking by embracing novel technology alongside existing scholarship. This issue also highlights the neurochemical complexity of reward-seeking, and the reader will uncover both distinct and shared circuits and transmitters driving various forms of reward-seeking. Accordingly, we hope that this special issue will provide a valuable resource for the field and trigger future research on this topic.
Topics: Animals; Humans; Neurobiology; Neurochemistry; Neurotransmitter Agents; Reward
PubMed: 33891317
DOI: 10.1111/jnc.15317 -
WormBook : the Online Review of C.... Aug 2005The most abundant synapses in the central nervous system of vertebrates are inhibitory synapses that use the neurotransmitter gamma-aminobutyric acid (GABA). GABA is... (Review)
Review
The most abundant synapses in the central nervous system of vertebrates are inhibitory synapses that use the neurotransmitter gamma-aminobutyric acid (GABA). GABA is also an important neurotransmitter in C. elegans; however, in contrast to vertebrates where GABA acts at synapses of the central nervous system, in nematodes GABA acts primarily at neuromuscular synapses. Specifically, GABA acts to relax the body muscles during locomotion and foraging and to contract the enteric muscles during defecation. The importance of this neurotransmitter for basic motor functions of the worm has facilitated the genetic analysis of proteins required for GABA function. Genetic screens have identified the GABA biosynthetic enzyme, the vesicular transporter, inhibitory and excitatory receptors, and a transcription factor required for the differentiation of GABA cell identity. The plasma membrane transporter and other GABA receptors have been identified by molecular criteria.
Topics: Animals; Nematoda; Neurons; Neurotransmitter Agents; gamma-Aminobutyric Acid
PubMed: 18050397
DOI: 10.1895/wormbook.1.14.1 -
Journal of Alzheimer's Disease : JAD 2017Alzheimer's disease (AD) is a progressive neurodegenerative disease, characterized by the loss of memory, multiple cognitive impairments and changes in the personality... (Review)
Review
Alzheimer's disease (AD) is a progressive neurodegenerative disease, characterized by the loss of memory, multiple cognitive impairments and changes in the personality and behavior. Several decades of intense research have revealed that multiple cellular changes are involved in disease process, including synaptic damage, mitochondrial abnormalities and inflammatory responses, in addition to formation and accumulation of amyloid-β (Aβ) and phosphorylated tau. Although tremendous progress has been made in understanding the impact of neurotransmitters in the progression and pathogenesis of AD, we still do not have a drug molecule associated with neurotransmitter(s) that can delay disease process in elderly individuals and/or restore cognitive functions in AD patients. The purpose of our article is to assess the latest developments in neurotransmitters research using cell and mouse models of AD. We also updated the current status of clinical trials using neurotransmitters' agonists/antagonists in AD.
Topics: Alzheimer Disease; Animals; Humans; Neurotransmitter Agents
PubMed: 28211810
DOI: 10.3233/JAD-161118 -
Brain : a Journal of Neurology May 2018Frontotemporal lobar degeneration causes a spectrum of complex degenerative disorders including frontotemporal dementia, progressive supranuclear palsy and corticobasal... (Review)
Review
Frontotemporal lobar degeneration causes a spectrum of complex degenerative disorders including frontotemporal dementia, progressive supranuclear palsy and corticobasal syndrome, each of which is associated with changes in the principal neurotransmitter systems. We review the evidence for these neurochemical changes and propose that they contribute to symptomatology of frontotemporal lobar degeneration, over and above neuronal loss and atrophy. Despite the development of disease-modifying therapies, aiming to slow neuropathological progression, it remains important to advance symptomatic treatments to reduce the disease burden and improve patients' and carers' quality of life. We propose that targeting the selective deficiencies in neurotransmitter systems, including dopamine, noradrenaline, serotonin, acetylcholine, glutamate and gamma-aminobutyric acid is an important strategy towards this goal. We summarize the current evidence-base for pharmacological treatments and suggest strategies to improve the development of new, effective pharmacological treatments.
Topics: Animals; Frontotemporal Lobar Degeneration; Humans; Neurotransmitter Agents
PubMed: 29373632
DOI: 10.1093/brain/awx327 -
PLoS Genetics Apr 2014
Topics: Cholinergic Neurons; Humans; Neurotransmitter Agents; Transcription Factors; Transcription, Genetic
PubMed: 24762739
DOI: 10.1371/journal.pgen.1004313 -
Journal of Neuroscience Methods Jan 2022Chemical biosensors with the capacity to continuously monitor various neurotransmitter dynamics can be powerful tools to understand complex signaling pathways in the... (Review)
Review
Chemical biosensors with the capacity to continuously monitor various neurotransmitter dynamics can be powerful tools to understand complex signaling pathways in the brain. However, in vivo detection of neurochemicals is challenging for many reasons such as the rapid release and clearance of neurotransmitters in the extracellular space, or the low target analyte concentrations in a sea of interfering biomolecules. Biosensing platforms with adequate spatiotemporal resolution coupled to specific and selective receptors termed aptamers, demonstrate high potential to tackle such challenges. Herein, we review existing literature in this field. We first discuss nanoparticle-based systems, which have a simple in vitro implementation and easily interpretable results. We then examine methods employing near-infrared detection for deeper tissue imaging, hence easier translation to in vivo implementation. We conclude by reviewing live cell imaging of neurotransmitter release via aptamer-modified platforms. For each of these sensors, we discuss the associated challenges for translation to real-time in vivo neurochemical imaging. Realization of in vivo biosensors for neurotransmitters will drive future development of early prevention strategies, treatments, and therapeutics for psychiatric and neurodegenerative diseases.
Topics: Biosensing Techniques; Neurotransmitter Agents
PubMed: 34653500
DOI: 10.1016/j.jneumeth.2021.109386 -
Trends in Neurosciences Mar 2016Action potentials invading the presynaptic terminal trigger discharge of docked synaptic vesicles (SVs) by opening voltage-dependent calcium channels (CaVs) and... (Review)
Review
Action potentials invading the presynaptic terminal trigger discharge of docked synaptic vesicles (SVs) by opening voltage-dependent calcium channels (CaVs) and admitting calcium ions (Ca(2+)), which diffuse to, and activate, SV sensors. At most synapses, SV sensors and CaVs are sufficiently close that release is gated by individual CaV Ca(2+) nanodomains centered on the channel mouth. Other synapses gate SV release with extensive Ca(2+) microdomains summed from many, more distant CaVs. We review the experimental preparations, theories, and methods that provided principles of release nanophysiology and highlight expansion of the field into synaptic diversity and modifications of release gating for specific synaptic demands. Specializations in domain gating may adapt the terminal for roles in development, transmission of rapid impulse frequencies, and modulation of synaptic strength.
Topics: Animals; Neurotransmitter Agents; Synapses; Synaptic Transmission
PubMed: 26896416
DOI: 10.1016/j.tins.2016.01.005 -
Movement Disorders : Official Journal... Jun 2013Symptomatic animal models have clinical features consistent with human disorders and are often used to identify the anatomical and physiological processes involved in... (Review)
Review
Symptomatic animal models have clinical features consistent with human disorders and are often used to identify the anatomical and physiological processes involved in the expression of symptoms and to experimentally demonstrate causality where it would be infeasible in the patient population. Rodent and primate models of dystonia have identified basal ganglia abnormalities, including alterations in striatal GABAergic (ie, transmitting or secreting γ-aminobutyric acid) and dopaminergic transmission. Symptomatic animal models have also established the critical role of the cerebellum in dystonia, particularly abnormal glutamate signaling and aberrant Purkinje cell activity. Further, experiments suggest that the basal ganglia and cerebellum are nodes in an integrated network that is dysfunctional in dystonia. The knowledge gained from experiments in symptomatic animal models may serve as the foundation for the development of novel therapeutic interventions to treat dystonia. © 2013 Movement Disorder Society.
Topics: Animals; Animals, Genetically Modified; Basal Ganglia; Disease Models, Animal; Dystonia; Humans; Neurotransmitter Agents
PubMed: 23893454
DOI: 10.1002/mds.25526