scholarly journals Dietary yeast influences ethanol sedation in Drosophila via serotonergic neuron function

2019 ◽  
Vol 25 (4) ◽  
Author(s):  
Rebecca E. Schmitt ◽  
Monica R. Messick ◽  
Brandon C. Shell ◽  
Ellyn K. Dunbar ◽  
Huai‐Fang Fang ◽  
...  
Keyword(s):  
Serotonergic Neuron ◽  
Neuron Function

scholarly journals Insect Behavioral Change and the Potential Contributions of Neuroinflammation—A Call for Future Research

Genes ◽  
2021 ◽  
Vol 12 (4) ◽  
pp. 465
Author(s):  
Colleen A. Mangold ◽  
David P. Hughes
Keyword(s):  
Behavioral Change ◽  
Potential Role ◽  
Insect Behavior ◽  
Future Research ◽  
Cell Physiology ◽  
Behavioral Manipulation ◽  
Neuroimmune Communication ◽  
And Function ◽  
Neuron Function ◽  
Insect Innate Immunity

Many organisms are able to elicit behavioral change in other organisms. Examples include different microbes (e.g., viruses and fungi), parasites (e.g., hairworms and trematodes), and parasitoid wasps. In most cases, the mechanisms underlying host behavioral change remain relatively unclear. There is a growing body of literature linking alterations in immune signaling with neuron health, communication, and function; however, there is a paucity of data detailing the effects of altered neuroimmune signaling on insect neuron function and how glial cells may contribute toward neuron dysregulation. It is important to consider the potential impacts of altered neuroimmune communication on host behavior and reflect on its potential role as an important tool in the “neuro-engineer” toolkit. In this review, we examine what is known about the relationships between the insect immune and nervous systems. We highlight organisms that are able to influence insect behavior and discuss possible mechanisms of behavioral manipulation, including potentially dysregulated neuroimmune communication. We close by identifying opportunities for integrating research in insect innate immunity, glial cell physiology, and neurobiology in the investigation of behavioral manipulation.

Sprouting and functional regeneration of an identified serotonergic neuron following axotomy

1985 ◽  
Vol 16 (2) ◽  
pp. 137-151 ◽  
Author(s):  
A. Don Murphy ◽  
David L. Barker ◽  
Jeanne F. Loring ◽  
S. B. Kater
Keyword(s):  
Serotonergic Neuron ◽  
Functional Regeneration

Development of an identified serotonergic neuron in the antennal lobe of the moth and effects of reduction in serotonin during construction of olfactory glomeruli

1995 ◽  
Vol 28 (2) ◽  
pp. 248-267 ◽  
Author(s):  
Lynne A. Oland ◽  
Sheila R. Kirschenbaum ◽  
Wendy M. Pott ◽  
Alison R. Mercer ◽  
Leslie P. Tolbert
Keyword(s):  
Antennal Lobe ◽  
Serotonergic Neuron ◽  
Olfactory Glomeruli

scholarly journals Luqin-like RYamide peptides regulate food-evoked responses in C. elegans

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Hayao Ohno ◽  
Morikatsu Yoshida ◽  
Takahiro Sato ◽  
Johji Kato ◽  
Mikiya Miyazato ◽  
...  
Keyword(s):  
Critical Role ◽  
Egg Laying ◽  
Serotonergic Neuron ◽  
Pacemaker Neurons ◽  
C Elegans ◽  
Peptide Signaling ◽  
Multiple Organs ◽  
Locomotory Behavior ◽  
Control Food ◽  
And Control

Peptide signaling controls many processes involving coordinated actions of multiple organs, such as hormone-mediated appetite regulation. However, the extent to which the mode of action of peptide signaling is conserved in different animals is largely unknown, because many peptides and receptors remain orphan and many undiscovered peptides still exist. Here, we identify two novel Caenorhabditis elegans neuropeptides, LURY-1-1 and LURY-1-2, as endogenous ligands for the neuropeptide receptor-22 (NPR-22). Both peptides derive from the same precursor that is orthologous to invertebrate luqin/arginine-tyrosine-NH2 (RYamide) proneuropeptides. LURY-1 peptides are secreted from two classes of pharyngeal neurons and control food-related processes: feeding, lifespan, egg-laying, and locomotory behavior. We propose that LURY-1 peptides transmit food signals to NPR-22 expressed in feeding pacemaker neurons and a serotonergic neuron. Our results identified a critical role for luqin-like RYamides in feeding-related processes and suggested that peptide-mediated negative feedback is important for satiety regulation in C. elegans.

scholarly journals Omega-3 Hastens and Omega-6 Delays the Progression of Neuropathology in a Murine Model of Familial ALS

2017 ◽  
Vol 11 (1) ◽  
pp. 84-91 ◽  
Author(s):  
Edward F. Boumil ◽  
Rishel Brenna Vohnoutka ◽  
Yuguan Liu ◽  
Sangmook Lee ◽  
Thomas B Shea
Keyword(s):  
Quality Of Life ◽  
Motor Neuron ◽  
Motor Function ◽  
Motor Neurons ◽  
Omega 3 ◽  
Self Medication ◽  
Familial Als ◽  
Neuron Function ◽  
The Impact

Background: Amyotrophic lateral sclerosis (ALS) is a progressive disease of motor neurons that has no cure or effective treatment. Any approach that could sustain minor motor function during terminal stages would improve quality of life. Objective: We examined the impact of omega-3 (Ω-3) and Ω-6, on motor neuron function in mice expressing mutant human superoxide dismutase-1 (SOD-1), which dominantly confers familial ALS and induces a similar sequence of motor neuron decline and eventual death when expressed in mice. Method: Mice received standard diets supplemented with equivalent amounts of Ω-3 and Ω-6 or a 10x increase in Ω-6 with no change in Ω-3 commencing at 4 weeks of age. Motor function and biochemical/histological parameters were assayed by standard methodologies. Results: Supplementation with equivalent Ω-3 and Ω-6 hastened motor neuron pathology and death, while 10x Ω-6 with no change in Ω-3 significantly delayed motor neuron pathology, including preservation of minor motor neuron function during the terminal stage. Conclusion: In the absence of a cure or treatment, affected individuals may resort to popular nutritional supplements such as Ω-3 as a form of “self-medication”. However, our findings and those of other laboratories indicate that such an approach could be harmful. Our findings suggest that a critical balance of Ω-6 and Ω-3 may temporarily preserve motor neuron function during the terminal stages of ALS, which could provide a substantial improvement in quality of life for affected individuals and their caregivers.

scholarly journals Dementia and diabetes mellitus

2008 ◽  
Vol 136 (3-4) ◽  
pp. 170-175 ◽  
Author(s):  
Dragan Pavlovic ◽  
Aleksandra Pavlovic
Keyword(s):  
Diabetes Mellitus ◽  
Cognitive Decline ◽  
Tau Protein ◽  
Brain Inflammation ◽  
Pathogenic Factor ◽  
Insulin Degrading Enzyme ◽  
Slowing Down ◽  
Synapse Plasticity ◽  
Dementia Prevention ◽  
Neuron Function

Dementia and Diabetes mellitus (DM) are major health problems nowadays. DM leads to a significant cognitive decline and increases the risk of dementia, mostly Alzheimer's Disease (AD) and vascular dementia (VaD) by 50-100% and 100-150%, respectively. Amyloid beta (Abeta), the main pathogenic factor in AD development, is eliminated by advanced glycation end products (AGEs) and degraded by insulin degrading enzyme (IDE) for which it competes with insulin. Insulin stimulates secretion of Abeta and promotes brain inflammation. DM I and II cause slowing down of mental speed, lowering of mental flexibility and DM II learning and memory disturbances. DM acts both directly by hyperglycaemia and hyperinsulinaemia and by the blood vessel changes. Hyperglycaemia changes synapse plasticity and leads to cognitive decline. AGEs disrupt the neuron function and bonding to Abeta increases its aggregability. Glycation of tau protein promotes production of neurofibrillary tangles (NFT), the main intracellular pathogenic factor in AD. AGE2 in DM causes pathological angiogenesis and apoptosis of neurons. AGE receptor (RAGE) is also the specific Abeta receptor with which it produces reactive oxygen species that has, as a result, disruption of mitochondrial function and reduction of neuronal energy resources. Insulinoresistance is linked with the dysexecutive syndrome, and hyperinsulinaemia increases the risk of AD especially by enhancing phosphorylation of tau protein and formation of NFT. Application of insulin showed improvement of memory, behaviour and affect in AD patients. Good glycoregulation emerged as an important factor in dementia prevention, and a better insight in relations of DM and brain function will lead to new potential dementia therapies. .

scholarly journals Brain–Computer Interfacing Using Functional Near-Infrared Spectroscopy (fNIRS)

Biosensors ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 389
Author(s):  
Kogulan Paulmurugan ◽  
Vimalan Vijayaragavan ◽  
Sayantan Ghosh ◽  
Parasuraman Padmanabhan ◽  
Balázs Gulyás
Keyword(s):  
Infrared Spectroscopy ◽  
Near Infrared Spectroscopy ◽  
Brain Function ◽  
Near Infrared ◽  
Functional Near Infrared Spectroscopy ◽  
Non Invasive ◽  
Neuron Function ◽  
Brain Computer Interfacing ◽  
The Brain ◽  
Computer Interfacing

Functional Near-Infrared Spectroscopy (fNIRS) is a wearable optical spectroscopy system originally developed for continuous and non-invasive monitoring of brain function by measuring blood oxygen concentration. Recent advancements in brain–computer interfacing allow us to control the neuron function of the brain by combining it with fNIRS to regulate cognitive function. In this review manuscript, we provide information regarding current advancement in fNIRS and how it provides advantages in developing brain–computer interfacing to enable neuron function. We also briefly discuss about how we can use this technology for further applications.

Sign in / Sign up

Export Citation Format

Share Document