Dataset Information

Effects of humans on behaviour of wildlife exceed those of natural predators in a landscape of fear.

ABSTRACT:

Background

Human disturbance can influence wildlife behaviour, which can have implications for wildlife populations. For example, wildlife may be more vigilant near human disturbance, resulting in decreased forage intake and reduced reproductive success. We measured the effects of human activities compared to predator and other environmental factors on the behaviour of elk (Cervus elaphus Linnaeus 1758) in a human-dominated landscape in Alberta, Canada.

Methodology/principal findings

We collected year-round behavioural data of elk across a range of human disturbances. We estimated linear mixed models of elk behaviour and found that human factors (land-use type, traffic and distance from roads) and elk herd size accounted for more than 80% of variability in elk vigilance. Elk decreased their feeding time when closer to roads, and road traffic volumes of at least 1 vehicle every 2 hours induced elk to switch into a more vigilant behavioural mode with a subsequent loss in feeding time. Other environmental factors, thought crucial in shaping vigilance behaviour in elk (natural predators, reproductive status of females), were not important. The highest levels of vigilance were recorded on public lands where hunting and motorized recreational activities were cumulative compared to the national park during summer, which had the lowest levels of vigilance.

Conclusions/significance

In a human-dominated landscape, effects of human disturbance on elk behaviour exceed those of habitat and natural predators. Humans trigger increased vigilance and decreased foraging in elk. However, it is not just the number of people but also the type of human activity that influences elk behaviour (e.g. hiking vs. hunting). Quantifying the actual fitness costs of human disturbance remains a challenge in field studies but should be a primary focus for future researches. Some species are much more likely to be disturbed by humans than by non-human predators: for these species, quantifying human disturbance may be the highest priority for conservation.

SUBMITTER: Ciuti S

PROVIDER: S-EPMC3509092 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:Experimental evidence in humans and non-human animals suggests that the administration of propranolol shortly after the retrieval of an emotional memory can lead to an attenuation of its later expression, a phenomenon known as post-reactivation amnesia. Using more potent amnestic drugs, post-reactivation amnesia has been shown in animals to be reversible by re-administration of the drug prior to memory retention testing. The latter finding suggests that, at least under some circumstances, post-reactivation amnesia may not reflect a disruption of reconsolidation (i.e., a memory storage deficit) but an acquired state-dependency of memory expression (i.e., a memory retrieval deficit that is relieved when the drug state is recreated during testing). We conducted a double-blind, placebo-controlled study to investigate whether the previously established amnestic effects of post-reactivation propranolol administration on memory retention in humans may similarly reflect a retrieval deficit. In four groups of participants, fear memories were first established through differential fear conditioning. One day later, a single presentation of the CS+ without shock was used to reactivate the memory in three of the four groups, followed by the administration of 40 mg Propranolol HCl (Groups PrPl and PrPr) or placebo (Group PlPl). Memory was not reactivated in the fourth group (Group NR). Another 24 h later, Propranolol HCl (Group PrPr) or placebo (Groups PrPl, PlPl, and NR) was again administered, followed by a test of memory retention (extinction testing) and recovery (reinstatement testing). We did not observe any effects of post-reactivation propranolol on memory retention; conditioned responding was similar for all groups at the start of retention testing and similarly sensitive to recovery through reinstatement. We did observe an acute effect of propranolol administration on fear-potentiated startle responding during retention testing in Group PrPr, where participants exhibited attenuated startle responses during extinction testing but similar sensitivity to reinstatement as participants in the other groups. While our findings fail to corroborate previous reports of propranolol-induced post-reactivation amnesia in humans, they do point to acute effects of propranolol administration on extinction performance.