scholarly journals Prolonged exposure to stressors suppresses exploratory behavior in zebrafish larvae

2020 ◽  
Vol 223 (22) ◽  
pp. jeb224964
Author(s):  
William A. Haney ◽  
Bushra Moussaoui ◽  
James A. Strother
Keyword(s):  
Dopaminergic Neurons ◽  
Prolonged Exposure ◽  
Area Postrema ◽  
Model Organism ◽  
Neural Correlates ◽  
Neural Pathways ◽  
Zebrafish Larvae ◽  
Induced Changes ◽  
Acute Stressor ◽  
Light Preference

ABSTRACTEnvironmental stressors induce rapid physiological and behavioral shifts in vertebrate animals. However, the neurobiological mechanisms responsible for stress-induced changes in behavior are complex and not well understood. Similar to mammalian vertebrates, zebrafish adults display a preference for dark environments that is associated with predator avoidance, enhanced by stressors, and broadly used in assays for anxiety-like behavior. Although the larvae of zebrafish are a prominent model organism for understanding neural circuits, few studies have examined the effects of stressors on their behavior. This study examines the effects of noxious chemical and electric shock stressors on locomotion and light preference in zebrafish larvae. We found that both stressors elicited similar changes in behavior. Acute exposure induced increased swimming activity, while prolonged exposure depressed activity. Neither stressor produced a consistent shift in light–dark preference, but prolonged exposure to these stressors resulted in a pronounced decrease in exploration of different visual environments. We also examined the effects of exposure to a noxious chemical cue using whole-brain calcium imaging, and identified neural correlates in the area postrema, an area of the hindbrain containing noradrenergic and dopaminergic neurons. Pharmaceutical blockade experiments showed that α-adrenergic receptors contribute to the behavioral response to an acute stressor but are not necessary for the response to a prolonged stressor. These results indicate that zebrafish larvae have complex behavioral responses to stressors comparable to those of adult animals, and also suggest that these responses are mediated by similar neural pathways.

scholarly journals α-Synuclein-induced dysregulation of neuronal activity contributes to murine dopamine neuron vulnerability

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Abeer Dagra ◽  
Douglas R. Miller ◽  
Min Lin ◽  
Adithya Gopinath ◽  
Fatemeh Shaerzadeh ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neuronal Activity ◽  
Dopaminergic Neurons ◽  
Prolonged Exposure ◽  
D2 Receptor ◽  
Neuronal Firing ◽  
Dopamine Neurons ◽  
Loss Of Function ◽  
Therapeutic Implications

AbstractPathophysiological damages and loss of function of dopamine neurons precede their demise and contribute to the early phases of Parkinson’s disease. The presence of aberrant intracellular pathological inclusions of the protein α-synuclein within ventral midbrain dopaminergic neurons is one of the cardinal features of Parkinson’s disease. We employed molecular biology, electrophysiology, and live-cell imaging to investigate how excessive α-synuclein expression alters multiple characteristics of dopaminergic neuronal dynamics and dopamine transmission in cultured dopamine neurons conditionally expressing GCaMP6f. We found that overexpression of α-synuclein in mouse (male and female) dopaminergic neurons altered neuronal firing properties, calcium dynamics, dopamine release, protein expression, and morphology. Moreover, prolonged exposure to the D2 receptor agonist, quinpirole, rescues many of the alterations induced by α-synuclein overexpression. These studies demonstrate that α-synuclein dysregulation of neuronal activity contributes to the vulnerability of dopaminergic neurons and that modulation of D2 receptor activity can ameliorate the pathophysiology. These findings provide mechanistic insights into the insidious changes in dopaminergic neuronal activity and neuronal loss that characterize Parkinson’s disease progression with significant therapeutic implications.

scholarly journals Dissecting neural pathways for forgetting in Drosophila olfactory aversive memory

2015 ◽  
Vol 112 (48) ◽  
pp. E6663-E6672 ◽  
Author(s):  
Yichun Shuai ◽  
Areekul Hirokawa ◽  
Yulian Ai ◽  
Min Zhang ◽  
Wanhe Li ◽  
...  
Keyword(s):  
Reversal Learning ◽  
Dopaminergic Neurons ◽  
Mushroom Body ◽  
Biologically Active ◽  
Molecular Pathways ◽  
Neural Pathways ◽  
Active Process ◽  
Glutamatergic Neurons ◽  
Memory Decay ◽  
Over Time

Recent studies have identified molecular pathways driving forgetting and supported the notion that forgetting is a biologically active process. The circuit mechanisms of forgetting, however, remain largely unknown. Here we report two sets of Drosophila neurons that account for the rapid forgetting of early olfactory aversive memory. We show that inactivating these neurons inhibits memory decay without altering learning, whereas activating them promotes forgetting. These neurons, including a cluster of dopaminergic neurons (PAM-β′1) and a pair of glutamatergic neurons (MBON-γ4>γ1γ2), terminate in distinct subdomains in the mushroom body and represent parallel neural pathways for regulating forgetting. Interestingly, although activity of these neurons is required for memory decay over time, they are not required for acute forgetting during reversal learning. Our results thus not only establish the presence of multiple neural pathways for forgetting in Drosophila but also suggest the existence of diverse circuit mechanisms of forgetting in different contexts.

Autonomic mechanisms underlying area postrema stimulation-induced cardiovascular responses in rats

1991 ◽  
Vol 261 (1) ◽  
pp. R1-R8 ◽  
Author(s):  
A. V. Ferguson ◽  
P. Smith
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Rate Control ◽  
Area Postrema ◽  
Cardiovascular Responses ◽  
Pressure Control ◽  
Blocking Agent ◽  
Adrenergic Blockade ◽  
Neural Pathways ◽  
Heart Rate Control

Experiments were designed to examine the autonomic mechanisms underlying the decreases in blood pressure and heart rate elicited by electrical stimulation in the rat area postrema (AP). Vagotomy was found to significantly reduce the bradycardia observed in response to AP stimulation (control -123.5 +/- 23.5 beats/min; vagotomized -7 +/- 5.4 beats/min; P less than 0.001) but was without significant effect on blood pressure responses. Hexamethonium significantly reduced both heart rate (control -225.5 +/- 11.9 beats/min; hexamethonium -5.5 +/- 2.8 beats/min; P less than 0.001) and depressor (control -35.4 +/- 4.7 mmHg; hexamethonium -6.4 +/- 0.8 mmHg; P less than 0.001) responses to such stimulation, whereas combined alpha- and beta-adrenergic blockade was without effect. The muscarinic blocking agent atropine also abolished both blood pressure (control -22.0 +/- 4.3 mmHg; atropine 2.8 +/- 4.4 mmHg; P less than 0.01) and heart rate (control -187.0 +/- 41.9 beats/min; atropine 8.8 +/- 2.6 beats/min; P less than 0.01) responses to AP stimulation. These data suggest that AP stimulation influences two separate neural pathways eliciting distinct cardiovascular responses. It would appear that activation of one of these pathways results in activation of vagal efferents to the heart and thus bradycardia. A second parallel pathway influenced by AP stimulation apparently elicits depressor response through actions on cholinergic muscarinic receptors.

scholarly journals The Neural Correlates of Crowding-Induced Changes in Appearance

2012 ◽  
Vol 22 (13) ◽  
pp. 1199-1206 ◽  
Author(s):  
Elaine J. Anderson ◽  
Steven C. Dakin ◽  
D. Samuel Schwarzkopf ◽  
Geraint Rees ◽  
John A. Greenwood
Keyword(s):  
Neural Correlates ◽  
Induced Changes

scholarly journals Expression of endocrine genes in zebrafish larvae in response to environmental salinity

2007 ◽  
Vol 193 (3) ◽  
pp. 481-491 ◽  
Author(s):  
Kazuyuki Hoshijima ◽  
Shigehisa Hirose
Keyword(s):  
Model Organism ◽  
Endocrine System ◽  
The Other ◽  
Regulatory Mechanisms ◽  
Transcription Level ◽  
Environmental Salinity ◽  
Larval Stages ◽  
Zebrafish Larvae ◽  
Osmotic Homeostasis ◽  
Comprehensive Study

We tested the capability of the endocrine system in zebrafish to respond to environmental salinity challenges during larval stages. We reveal that the zebrafish larvae have a system in which several endocrine genes, including atrial natriuretic peptide (anp), renin, prolactin, growth hormone ( gh) and parathyroid hormone 1 (pth1), respond at the transcription level to changes in environmental salinity and that the responses are gene specific. Both anp and renin are upregulated in larvae raised in dilute freshwater medium but are downregulated in concentrated medium. On the other hand, expression of prolactin and gh is strongly enhanced in the dilute medium, but shows little or no change under higher salinity conditions. Interestingly, PTH1 expression depends on Ca2+ concentration, as observed in mammals. Thus, taken together with the advantages of a model organism, including accessibility to genetic approaches, we propose that zebrafish larvae are useful for a comprehensive study of the regulatory mechanisms of the endocrine system in ionic and osmotic homeostasis.

scholarly journals Eating less or more – Mindset induced changes in neural correlates of pre-meal planning

Appetite ◽  
2018 ◽  
Vol 125 ◽  
pp. 492-501 ◽  
Author(s):  
Maike A. Hege ◽  
Ralf Veit ◽  
Jan Krumsiek ◽  
Stephanie Kullmann ◽  
Martin Heni ◽  
...  
Keyword(s):  
Neural Correlates ◽  
Meal Planning ◽  
Induced Changes

Nitric oxide regulates energy metabolism and Bcl-2 expression in intestinal epithelial cells

1998 ◽  
Vol 274 (5) ◽  
pp. G797-G801 ◽  
Author(s):  
Manabu Nishikawa ◽  
Kenta Takeda ◽  
Eisuke F. Sato ◽  
Tetso Kuroki ◽  
Masayasu Inoue
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cells ◽  
Prolonged Exposure ◽  
Intestinal Epithelial Cells ◽  
Enteric Bacteria ◽  
Intestinal Lumen ◽  
Intestinal Epithelial ◽  
Mucosal Cells ◽  
Respiration Of Mitochondria ◽  
Induced Changes

Nitric oxide (NO) inhibits the respiration of mitochondria and enteric bacteria, particularly under low O2concentration, and induces apoptosis of various types of cells. To gain insight into the molecular role of NO in the intestine, we examined its effects on the respiration, Ca2+status, and expression of Bcl-2 in cultured intestinal epithelial cells (IEC-6). NO reversibly inhibited the respiration of IEC-6 cells, especially under physiologically low O2concentration. Although NO elevated cytosolic Ca2+as determined by the fura 2 method, the cells were fairly resistant to NO. Kinetic analysis revealed that prolonged exposure to NO elevated the levels of Bcl-2 and suppressed the NO-induced changes in Ca2+status of the cells. Because Bcl-2 possesses antiapoptotic function, toxic NO effects might appear minimally in enterocytes enriched with Bcl-2. Thus NO might effectively exhibit its antibacterial action in anaerobic intestinal lumen without inducing apoptosis of Bcl-2-enriched mucosal cells.

Temporal stability of acute stressor-induced changes in cellular immunity

1995 ◽  
Vol 19 (3) ◽  
pp. 287-290 ◽  
Author(s):  
Paul J. Mills ◽  
Soraya L. Haeri ◽  
Joel E. Dimsdale
Keyword(s):  
Cellular Immunity ◽  
Temporal Stability ◽  
Induced Changes ◽  
Acute Stressor
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