scholarly journals Population variation alters aggression-associated oxytocin and vasopressin expressions in brains of Brandt’s voles in field conditions

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Shuli Huang ◽  
Guoliang Li ◽  
Yongliang Pan ◽  
Jing Liu ◽  
Jidong Zhao ◽  
...  

AbstractDensity-dependent change in aggressive behavior contributes to the population regulation of many small rodents, but the underlying neurological mechanisms have not been examined in field conditions. We hypothesized that crowding stress and aggression-associated oxytocin (OT) and arginine vasopressin (AVP) in specific regions of the brain may be closely related to aggressive behaviors and population changes of small rodents. We analyzed the association of OT and AVP expression, aggressive behavior, and population density of Brandt’s voles in 24 large semi-natural enclosures (0.48 ha each) in Inner Mongolia grassland. We tested the effects of population density on the OT/AVP system and aggressive behavior by experimentally manipulating populations of Brandt’s voles in the grassland enclosures. High density was positively and significantly associated with more aggressive behavior, and increased expression of mRNA and protein of AVP and its receptor, but decreased expression of mRNA and protein of OT and its receptor in specific brain regions of the voles. Our study suggests that changes in OT/AVP expression are likely a result of the increased psychosocial stress that these voles experience during overcrowding, and thus the OT/AVP system can be used as indicators of density-dependent stressors in Brandt’s voles.

2021 ◽  
Author(s):  
Shuli Huang ◽  
Guoliang Li ◽  
Yongliang Pan ◽  
Jing Liu ◽  
Jidong Zhao ◽  
...  

Abstract Density-dependent change in aggressive behavior is essential for regulating the population dynamics of many small rodents, but the underlying neurological mechanisms have not been examined in field conditions. We hypothesized that aggression-associated oxytocin (OT) and vasopressin (AVP) in specific regions of the brain may be closely related to aggressive behaviors and population changes of small rodents. In this study, we analyzed the associations of OT and AVP expression as well as aggressive behavior with population density of Brandt’s voles in 24 large semi-natural enclosures (0.48 ha for each enclosure) in Inner Mongolia grassland. Then we tested the effects of population density on the OT/AVP system and aggressive behavior in experimentally manipulated populations of Brandt’s voles in the semi-natural enclosures. High density was positively and significantly associated with more aggressive behavior, and increased expression of mRNA and protein of AVP and its receptor, but decreased expression of mRNA and protein of OT and its receptor in specific brain regions of the voles. Our study suggests that OT/AVP systems are important in regulating the density-dependent population dynamics via aggressive behavior of small rodents, and they can be used as indicators of population variation or density-dependent stressors.


Author(s):  
Alita Pinter

A variety of hypotheses has been proposed to explain multiannual fluctuations in population density ("cycles") of small rodents (for reviews see Finerty 1980, Taitt and Krebs 1985). Doubtless, such cycles - known since antiquity (Elton 1942) - result from an interaction of a multitude of factors. However, the inability of extant hypotheses, alone or in combination, to explain the causality of cycles rests in no small measure with the fact that long-term studies of the phenomenon are notoriously uncommon.


2013 ◽  
Vol 77 (7) ◽  
pp. 1401-1408 ◽  
Author(s):  
Robin N. Donohue ◽  
David G. Hewitt ◽  
Timothy E. Fulbright ◽  
Charles A. Deyoung ◽  
Andrea R. Litt ◽  
...  

Author(s):  
Michael J. Fogarty ◽  
Jeremy S. Collie

The observation that no population can grow indefinitely and that most populations persist on ecological timescales implies that mechanisms of population regulation exist. Feedback mechanisms include competition for limited resources, cannibalism, and predation rates that vary with density. Density dependence occurs when per capita birth or death rates depend on population density. Density dependence is compensatory when the population growth rate decreases with population density and depensatory when it increases. The logistic model incorporates density dependence as a simple linear function. A population exhibiting logistic growth will reach a stable population size. Non-linear density-dependent terms can give rise to multiple equilibria. With discrete time models or time delays in density-dependent regulation, the approach to equilibrium may not be smooth—complex dynamical behavior is possible. Density-dependent feedback processes can compensate, up to a point, for natural and anthropogenic disturbances; beyond this point a population will collapse.


2004 ◽  
Vol 55 (3) ◽  
pp. 664-674 ◽  
Author(s):  
Matthew R. Johnson ◽  
Clemente I. Montero ◽  
Shannon B. Conners ◽  
Keith R. Shockley ◽  
Stephanie L. Bridger ◽  
...  

1990 ◽  
Vol 330 (1257) ◽  
pp. 235-251 ◽  

Over the years, there has been much discussion about the relative importance of environmental and biological factors in regulating natural populations. Often it is thought that environmental factors are associated with stochastic fluctuations in population density, and biological ones with deterministic regulation. We revisit these ideas in the light of recent work on chaos and nonlinear systems. We show that completely deterministic regulatory factors can lead to apparently random fluctuations in population density, and we then develop a new method (that can be applied to limited data sets) to make practical distinctions between apparently noisy dynamics produced by low-dimensional chaos and population variation that in fact derives from random (high-dimensional)noise, such as environmental stochasticity or sampling error. To show its practical use, the method is first applied to models where the dynamics are known. We then apply the method to several sets of real data, including newly analysed data on the incidence of measles in the United Kingdom. Here the additional problems of secular trends and spatial effects are explored. In particular, we find that on a city-by-city scale measles exhibits low-dimensional chaos (as has previously been found for measles in New York City), whereas on a larger, country-wide scale the dynamics appear as a noisy two-year cycle. In addition to shedding light on the basic dynamics of some nonlinear biological systems, this work dramatizes how the scale on which data is collected and analysed can affect the conclusions drawn.


1990 ◽  
Vol 47 (9) ◽  
pp. 1724-1737 ◽  
Author(s):  
James W. A. Grant ◽  
Donald L. Kramer

We examined the old, but untested hypothesis that territory size limits the maximum population density of salmonids in streams. We used published data to derive an interspecific regression of territory size (m2) on fork length (cm) (log10 territory size = 2.61 log10 length—2.83, r2 = 0.87, n = 23). Growth and mortality trajectories of salmonid cohorts from eight experimental studies were compared to the maximum-density regression, the inverse of the territory–size regression. In shallow habitats, such as riffles and raceways, the cohort trajectories followed the maximum density regression quite closely and were consistent with the territory–size hypothesis. In addition, natural densities in eight other studies did not exceed the predicted maximum density and tended to fail within the 95% C.L. of the maximum-density regression. Data from shallow habitats, therefore, provide strong support for the territory–size hypothesis. A linear logistic response model showed that the probability of observing density-dependent growth, mortality, or emigration increased significantly with increasing values of an index of habitat saturation, developed from the territory–size regression. Our results suggest that the territory–size regression has practical value for predicting the maximum densities of stream-dwelling salmonids in shallow habitats and the occurrence of density-dependent population responses.


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