scholarly journals Effects of Temperature Acclimation on a Central Neural Circuit and Its Behavioral Output

2008 ◽  
Vol 100 (6) ◽  
pp. 2997-3008 ◽  
Author(s):  
Theresa M. Szabo ◽  
Ted Brookings ◽  
Thomas Preuss ◽  
Donald S. Faber
Keyword(s):  
Neural Circuit ◽  
Escape Behavior ◽  
Input Resistance ◽  
Temperature Acclimation ◽  
M Cell ◽  
Escape Probability ◽  
Single Action ◽  
Vertebrate Brain ◽  
Behavioral Responsiveness ◽  
The Impact

In this study, we address the impact of temperature acclimation on neuronal properties in the Mauthner (M-) system, a brain stem network that initiates the startle-escape behavior in goldfish. The M-cell can be studied at cellular and behavioral levels, since it is uniquely identifiable physiologically within the intact vertebrate brain, and a single action potential in this neuron determines not only whether a startle response will occur but also the direction of the escape. Using animals acclimated to 15°C as a control, 25°C-acclimated fish showed a significant increase in escape probability and a decrease in the ability to discriminate escape directionality. Intracellular recordings demonstrated that M-cells in this population possessed decreased input resistance and reduced strength and duration of inhibitory inputs. In contrast, fish acclimated to 5°C were behaviorally similar to 15°C fish and had increased input resistance, increased strength of inhibitory transmission, and reduced excitatory transmission. We show here that alterations in the balance between excitatory and inhibitory synaptic transmission in the M-cell circuit underlie differences in behavioral responsiveness in acclimated populations. Specifically, during warm acclimation, synaptic inputs are weighted on the side of excitation and fish demonstrate hyperexcitability and reduced left–right discrimination during rapid escapes. In contrast, cold acclimation results in transmission weighted on the side of inhibition and these fish are less excitable and show improved directional discrimination.

scholarly journals Removing a single neuron in a vertebrate brain forever abolishes an essential behavior

2020 ◽  
Vol 117 (6) ◽  
pp. 3254-3260 ◽  
Author(s):  
Alexander Hecker ◽  
Wolfram Schulze ◽  
Jakob Oster ◽  
David O. Richter ◽  
Stefan Schuster
Keyword(s):  
Single Neuron ◽  
Escape Behavior ◽  
Extended Period ◽  
Escape Performance ◽  
M Cell ◽  
Giant Neuron ◽  
Vertebrate Brain ◽  
Vital Functions ◽  
Natural Predator ◽  
Actual Survival

The giant Mauthner (M) cell is the largest neuron known in the vertebrate brain. It has enabled major breakthroughs in neuroscience but its ultimate function remains surprisingly unclear: An actual survival value of M cell-mediated escapes has never been supported experimentally and ablating the cell repeatedly failed to eliminate all rapid escapes, suggesting that escapes can equally well be driven by smaller neurons. Here we applied techniques to simultaneously measure escape performance and the state of the giant M axon over an extended period following ablation of its soma. We discovered that the axon survives remarkably long and remains still fully capable of driving rapid escape behavior. By unilaterally removing one of the two M axons and comparing escapes in the same individual that could or could not recruit an M axon, we show that the giant M axon is essential for rapid escapes and that its loss means that rapid escapes are also lost forever. This allowed us to directly test the survival value of the M cell-mediated escapes and to show that the absence of this giant neuron directly affects survival in encounters with a natural predator. These findings not only offer a surprising solution to an old puzzle but demonstrate that even complex brains can trust vital functions to individual neurons. Our findings suggest that mechanisms must have evolved in parallel with the unique significance of these neurons to keep their axons alive and connected.

Serotonergic modulation of startle-escape plasticity in an African cichlid fish: a single-cell molecular and physiological analysis of a vital neural circuit

2011 ◽  
Vol 106 (1) ◽  
pp. 127-137 ◽  
Author(s):  
K. W. Whitaker ◽  
H. Neumeister ◽  
L. S. Huffman ◽  
C. E. Kidd ◽  
T. Preuss ◽  
...  
Keyword(s):  
Single Cell ◽  
Social Life ◽  
Neural Circuit ◽  
Escape Behavior ◽  
Cichlid Fish ◽  
Receptor Subtype ◽  
M Cells ◽  
M Cell ◽  
Trade Off ◽  
Electrophysiological Properties

Social life affects brain function at all levels, including gene expression, neurochemical balance, and neural circuits. We have previously shown that in the cichlid fish Astatotilapia burtoni brightly colored, socially dominant (DOM) males face a trade-off between reproductive opportunities and increased predation risk. Compared with camouflaged subordinate (SUB) males, DOMs exposed to a loud sound pip display higher startle responsiveness and increased excitability of the Mauthner cell (M-cell) circuit that governs this behavior. Using behavioral tests, intracellular recordings, and single-cell molecular analysis, we show here that serotonin (5-HT) modulates this socially regulated plasticity via the 5-HT receptor subtype 2 (5-HTR2). Specifically, SUBs display increased sensitivity to pharmacological manipulation of 5-HTR2 compared with DOMs in both startle-escape behavior and electrophysiological properties of the M-cell. Immunohistochemistry showed serotonergic varicosities around the M-cells, further suggesting that 5-HT impinges directly onto the startle-escape circuitry. To determine whether the effects of 5-HTR2 are pre- or postsynaptic, and whether other 5-HTR subtypes are involved, we harvested the mRNA from single M-cells via cytoplasmic aspiration and found that 5-HTR subtypes 5A and 6 are expressed in the M-cell. 5-HTR2, however, was absent, suggesting that it affects M-cell excitability through a presynaptic mechanism. These results are consistent with a role for 5-HT in modulating startle plasticity and increase our understanding of the neural and molecular basis of a trade-off between reproduction and predation.

scholarly journals Impact of generalized brain arousal on sexual behavior

2010 ◽  
Vol 107 (5) ◽  
pp. 2265-2270 ◽  
Author(s):  
Zachary M. Weil ◽  
Qiuyu Zhang ◽  
Allison Hornung ◽  
David Blizard ◽  
Donald W. Pfaff
Keyword(s):  
Emotional Reactivity ◽  
Behavioral Arousal ◽  
Sensory Stimuli ◽  
Vertebrate Brain ◽  
Plus Maze ◽  
Initial Activation ◽  
High Level ◽  
Global Brain ◽  
Motivated Behaviors ◽  
The Impact

Although there is an extensive amount known about specific sensory and motor functions of the vertebrate brain, less is understood about the regulation of global brain states. We have recently proposed that a function termed generalized arousal (Ag) serves as the most elemental driving force in the nervous system, responsible for the initial activation of all behavioral responses. An animal with increased generalized CNS arousal is characterized by greater motor activity, increased responsivity to sensory stimuli, and greater emotional lability. Implicit in this theory was the prediction that increases in generalized arousal would augment specific motivated behaviors that depend on arousal. Here, we address the idea directly by testing two lines of mice bred for high or low levels of generalized arousal and assessing their responses in tests of specific forms of behavioral arousal, sex and anxiety/exploration. We report that animals selected for differential generalized arousal exhibit marked increases in sensory, motor, and emotional reactivity in our arousal assay. Furthermore, male mice selected for high levels of generalized arousal were excitable and showed more incomplete mounts before the first intromission (IN), but having achieved that IN, they exhibited far fewer IN before ejaculating, as well as ejaculating much sooner after the first IN, thus indicating a high level of sexual arousal. Additionally, high-arousal animals of both sexes exhibited greater levels of anxiety-like behaviors and reduced exploratory behavior in the elevated plus maze and light-dark box tasks. Taken together, these data illustrate the impact of Ag on motivated behaviors.

Cyclic AMP Mediates Serotonin-Induced Synaptic Enhancement of Lateral Giant Interneuron of the Crayfish

2005 ◽  
Vol 94 (4) ◽  
pp. 2644-2652 ◽  
Author(s):  
Makoto Araki ◽  
Toshiki Nagayama ◽  
Jordanna Sprayberry
Keyword(s):  
Biogenic Amines ◽  
Time Course ◽  
Neural Circuit ◽  
Escape Behavior ◽  
Direct Injection ◽  
Phosphodiesterase Inhibitor ◽  
Sensory Stimulation ◽  
Simultaneous Application ◽  
Camp Analogue ◽  
Repetitive Sensory Stimulation

The lateral giant (LG)-mediated escape behavior of the crayfish habituates readily on repetitive sensory stimulation. Recent studies suggested that the biogenic amines serotonin and octopamine modulate the time course of recovery and/or re-depression of the LG response after habituation. However, little is known of how serotonin and octopamine effect LG habituation and what second-messenger cascades they may activate. To investigate the effect of biogenic amines on LG habituation, serotonin and octopamine were superfused before presenting repetitive sensory stimulation. Serotonin and octopamine increased the number of stimuli needed to habituate the LG response. Their effects were mimicked by mixed application of a cAMP analogue [8-(4-chlorophenylthio)-cAMP (CPT-cAMP)] and a phosphodiesterase inhibitor [3-isobutyl-1-methylxanthine (IBMX)] but not by a cGMP analogue (8-bromoguanosine 3′,5′-cyclic monophosphate). Perfusion of the adenylate cyclase inhibitor (SQ22536) abolished the effect of serotonin but not that of octopamine. To investigate the site of action of each biogenic amines in the neural circuit meditating LG escape, the effect of drugs on directly and indirectly elicited postsynaptic potentials in LG was investigated. Serotonin, octopamine, and a mixture of CPT-cAMP and IBMX increased both the direct and indirect synaptic inputs. Simultaneous application of SQ22536 abolished the effect of serotonin on both inputs but did not block the effect of octopamine. Direct injection of the cAMP analogue (Sp-isomer of adenosine-3′,5′-cyclic monophosphorothioate) into LG increased both the direct and indirect inputs to LG. These results indicate that serotonin mediates an increase in cAMP levels in LG, but octopamine acts independently of cAMP and cGMP.

Interactions between invasive plants and heavy metal stresses: a review

2021 ◽  
Author(s):  
Jian Li ◽  
Zhanrui Leng ◽  
Yueming Wu ◽  
Yizhou Du ◽  
Zhicong Dai ◽  
...  
Keyword(s):  
Invasive Species ◽  
Invasive Plants ◽  
Native Plants ◽  
Escape Behavior ◽  
Negative Influence ◽  
Plant Litter ◽  
Global Changes ◽  
Native Plant ◽  
Anthropogenic Contamination ◽  
The Impact

Abstract Global changes have altered the distribution pattern of the plant communities, including invasive species. Anthropogenic contamination may reduce native plant resistance to the invasive species. Thus, the focus of the current review is on the contaminant biogeochemical behavior among native plants, invasive species and the soil within the plant-soil ecosystem to improve our understanding of the interactions between invasive plants and environmental stressors. Our studies together with synthesis of the literature showed that a) the impacts of invasive species on environmental stress were heterogeneous, b) the size of the impact was variable, and c) the influence types were multidirectional even within the same impact type. However, invasive plants showed self-protective mechanisms when exposed to heavy metals (HMs) and provided either positive or negative influence on the bioavailability and toxicity of HMs. On the other hand, HMs may favor plant invasion due to the widespread higher tolerance of invasive plants to HMS together with the “escape behavior” of native plants when exposed to toxic HM pollution. However, there has been no consensus on whether elemental compositions of invasive plants are different from the natives in the polluted regions. A quantitative research comparing plant, litter and soil contaminant contents between native plants and the invaders in a global context is an indispensable research focus in the future.

scholarly journals Computational Analysis of the Impact of Chronic Stress on Intrinsic and Synaptic Excitability in the Hippocampus

2010 ◽  
Vol 103 (6) ◽  
pp. 3070-3083 ◽  
Author(s):  
Rishikesh Narayanan ◽  
Sumantra Chattarji
Keyword(s):  
Chronic Stress ◽  
Pyramidal Neurons ◽  
Three Dimensional ◽  
Input Resistance ◽  
Synaptic Potentiation ◽  
Synaptic Inputs ◽  
Hippocampal Ca3 ◽  
Ca3 Pyramidal Neurons ◽  
Dendritic Atrophy ◽  
The Impact

Dendritic atrophy and impaired long-term synaptic potentiation (LTP) are hallmarks of chronic stress-induced plasticity in the hippocampus. It has been hypothesized that these disparate structural and physiological correlates of stress lead to hippocampal dysfunction by reducing postsynaptic dendritic surface, thereby adversely affecting the availability of synaptic inputs and suppressing LTP. Here we examine the validity of this framework using biophysical models of hippocampal CA3 pyramidal neurons. To statistically match with the experimentally observed region specificity of stress-induced atrophy, we use an algorithm to systematically prune three-dimensional reconstructions of CA3 pyramidal neurons. Using this algorithm, we build a biophysically realistic computational model to analyze the effects of stress on intrinsic and synaptic excitability. We find that stress-induced atrophy of CA3 dendrites leads to an increase in input resistance, which depends exponentially on the percentage of neuronal atrophy. This increase translates directly into higher spiking frequencies in response to both somatic current injections and synaptic inputs at various locations along the dendritic arbor. Remarkably, we also find that the dendritic regions that manifest atrophy-induced synaptic hyperexcitability are governed by the region specificity of the underlying dendritic atrophy. Coupled with experimentally observed modulation of N-methyl-d-aspartate receptor currents, such hyperexcitability could tilt the balance of plasticity mechanisms in favor of synaptic potentiation over depression. Thus paradoxically, our results suggest that stress may impair hippocampal learning and memory, not by directly inhibiting LTP, but because of stress-induced facilitation of intrinsic and synaptic excitability and the consequent imbalance in bidirectional synaptic plasticity.

Differential Impact of Miniature Synaptic Potentials on the Soma and Dendrites of Pyramidal Neurons In Vivo

1997 ◽  
Vol 78 (3) ◽  
pp. 1735-1739 ◽  
Author(s):  
Denis Paré ◽  
Elen Lebel ◽  
Eric J. Lang
Keyword(s):  
Pyramidal Neurons ◽  
Pyramidal Cells ◽  
Input Resistance ◽  
Differential Impact ◽  
Synaptic Potentials ◽  
Ampa Antagonists ◽  
Intact Brain ◽  
The Impact

Paré, Denis, Elen LeBel, and Eric J. Lang. Differential impact of miniature synaptic potentials on the somata and dendrites of pyramidal neurons in vivo. J. Neurophysiol. 78: 1735–1739, 1997. We studied the impact of transmitter release resistant to tetrodotoxin (TTX) in morphologically identified neocortical pyramidal neurons recorded intracellularly in barbiturate-anesthetized cats. It was observed that TTX-resistant release occurs in pyramidal neurons in vivo and at much higher frequencies than was previously reported in vitro. Further, in agreement with previous findings indicating that GABAergic and glutamatergic synapses are differentially distributed in the somata and dendrites of pyramidal cells, we found that most miniature synaptic potentials were sensitive to γ-aminobutyric acid-A (GABAA) or α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) antagonists in presumed somatic and dendritic impalements, respectively. Pharmacological blockage of spontaneous synaptic events produced large increases in input resistance that were more important in dendritic (≈50%) than somatic (≈10%) impalements. These findings imply that in the intact brain, pyramidal neurons are submitted to an intense spike-independent synaptic bombardment that decreases the space constant of the cells. These results should be taken into account when extrapolating in vitro findings to intact brains.

scholarly journals Kappa-opioid receptor-dependent changes in dopamine and affective behavior occur differentially across the nucleus accumbens shell rostro-caudal axis

2020 ◽  
Author(s):  
Breanne E. Pirino ◽  
Mary B. Spodnick ◽  
Andrew T. Gargiulo ◽  
Genevieve R. Curtis ◽  
Jessica R. Barson ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Opioid Receptor ◽  
Dopamine Release ◽  
Neural Circuit ◽  
Ex Vivo ◽  
Kappa Opioid Receptor ◽  
Affective Behavior ◽  
Kappa Opioid ◽  
Affective Behaviors ◽  
The Impact

ABSTRACTNeural circuit engagement within the nucleus accumbens (NAc) shell is implicated in the regulation of both negative and positive affect. Classically, the dynorphin/kappa opioid receptor (KOR) system in the NAc was believed to promote dysphoric behavior, while dopamine was viewed as interacting with reward behavior, and KOR activation was known to inhibit dopamine release. Recently, however, both the KOR and dopamine systems have, separately, been shown to have differential effects across the rostro-caudal axis of the NAc shell on hedonic responses. Whether or not this is due to interactions between KORs and dopamine, and if it extends to other affective behaviors, remains to be determined. In this study, we examined in rats the relationship between the KOR and dopamine systems in both the rostral and caudal NAc shell using ex vivo fast scan cyclic voltammetry and the impact of KOR activation on affective behavior using approach-avoidance assays. We report here that activation of KORs in the caudal NAc shell significantly inhibits dopamine release, stimulates novelty-induced rearing behavior, increases avoidance behavior, and reduces locomotor activity. In contrast, activation of KORs in the rostral NAc shell inhibits dopamine release to a lesser extent and instead increases approach behavior. Taken together, these results indicate that there is heterogeneity across the rostro-caudal axis of the NAc shell in the effects of KOR stimulation on affective behaviors, and they suggest that this might be due to differences in KOR control over dopamine release.

Application of WetSpa model for assessing land use impacts on floods in the Margecany–Hornad watershed, Slovakia

2006 ◽  
Vol 53 (10) ◽  
pp. 37-45 ◽  
Author(s):  
A. Bahremand ◽  
F. De Smedt ◽  
J. Corluy ◽  
Y.B. Liu ◽  
J. Poórová ◽  
...  
Keyword(s):  
Land Use ◽  
Land Use Changes ◽  
Hydrologic Model ◽  
Land Use Impacts ◽  
M Cell ◽  
Time To Peak ◽  
Wetspa Model ◽  
Spatially Distributed ◽  
The Impact ◽  
Good Agreement

The spatially distributed hydrologic model WetSpa combines elevation, soil and land use data within GIS, to predict flood hydrographs and spatial distribution of hydrologic characteristics in a watershed. The model is applied to the Margecany–Hornad river basin (1,131 km2) in Slovakia. Daily hydrometeorological data from 1991–2000, including precipitation data from nine stations, temperature data from four stations and evaporation data measured at one station are used as input to the model. Three base maps, i.e. DEM, land use and soil type are prepared in GIS form, using 100 × 100 m cell size. Results of the simulations show good agreement between calculated and measured hydrographs. The model predicts the daily/hourly hydrographs with 75–80% accuracy according to the Nash–Sutcliff criteria. For assessing the impact of land use changes on floods, the calibrated model is applied for a reforestation scenario, which considers a 50% increase of forest areas. The model results show that the reforestation scenario decreases the peak discharge by 12%. Investigation of peak discharges from the whole simulation period, shows that the scenario results are reduced by 18% on average, while for small discharges the reduction is even about 34%. The time to peak of the simulated hydrograph of the reforestation scenario is 20 hours longer than for the present land use.

scholarly journals Effects of 7°C environmental temperature acclimation during a 3-week training period

2020 ◽  
Vol 128 (4) ◽  
pp. 768-777
Author(s):  
Robert Shute ◽  
Katherine Marshall ◽  
Megan Opichka ◽  
Halee Schnitzler ◽  
Brent Ruby ◽  
...  
Keyword(s):  
Room Temperature ◽  
Environmental Temperature ◽  
Cellular Signaling ◽  
Temperature Acclimation ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Training Adaptations ◽  
Before And After ◽  
The Impact ◽  
Environmental Temperatures

Cold environmental temperatures during exercise and recovery alter the acute response to cellular signaling and training adaptations. Approximately 3 wk is required for cold temperature acclimation to occur. To determine the impact of cold environmental temperature on training adaptations, fitness measurements, and aerobic performance, two groups of 12 untrained male subjects completed 1 h of cycling in 16 temperature acclimation sessions in either a 7°C or 20°C environmental temperature. Fitness assessments before and after acclimation occurred at standard room temperature. Muscle biopsies were taken from the vastus lateralis muscle before and after training to assess molecular markers related to mitochondrial development. Peroxisome proliferator-activated receptor-γ coactivator 1α ( PGC-1α) mRNA was higher in 7°C than in 20°C in response to acute exercise before training ( P = 0.012) but not after training ( P = 0.813). PGC-1α mRNA was lower after training ( P < 0.001). BNIP3 was lower after training in the 7°C than in the 20°C group ( P = 0.017) but not before training ( P = 0.549). No other differences occurred between temperature groups in VEGF, ERRα, NRF1, NRF2, TFAM, PINK1, Parkin, or BNIP3L mRNAs ( P > 0.05). PGC-1α protein and mtDNA were not different before training, after training, or between temperatures ( P > 0.05). Cycling power increased during the daily training ( P < 0.001) but was not different between temperatures ( P = 0.169). V̇o2peak increased with training ( P < 0.001) but was not different between temperature groups ( P = 0.460). These data indicate that a 3-wk period of acclimation/training in cold environmental temperatures alters PGC-1α gene expression acutely but this difference is not manifested in a greater increase in V̇o2peak and is dissipated as acclimation takes place. NEW & NOTEWORTHY This study examines the adaptive response of cellular signaling during exercise in cold environmental temperatures. We demonstrate that peroxisome proliferator-activated receptor-γ coactivator 1α mRNA is different between cold and room temperature environments before training but after training this difference no longer exists. This initial difference in transcriptional response between temperatures does not lead to differences in performance measures or increases in protein or mitochondria.

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