Neurobiology and Changing Ecosystems: Mechanisms Underlying Responses to Human-Generated Environmental Impacts.

Human generated environmental change profoundly affects organisms that reside across diverse ecosystems. Although nervous systems evolved to flexibly sense, respond, and adapt to environmental change, it is unclear whether the rapid rate of environmental change outpaces the adaptive capacity of complex nervous systems. Here, we explore neural systems mediating responses to, or impacted by, changing environments, such as those induced by global heating, sensory pollution, and changing habitation zones. We focus on rising temperature and accelerated changes in environments that impact sensory experience as examples of perturbations that directly or indirectly impact neural function, respectively. We also explore a mechanism involved in cross-species interactions that arises from changing habitation zones. We demonstrate that anthropogenic influences on neurons, circuits, and behaviors are widespread across taxa and require further scientific investigation to understand principles underlying neural resilience to accelerating environmental change.SIGNIFICANCE STATEMENT Neural systems evolved over hundreds of millions of years to allow organisms to sense and respond to their environments - to be receptive and responsive, yet flexible. Recent rapid, human-generated environmental changes are testing the limits of the adaptive capacity of neural systems. This presents an opportunity and an urgency to understand how neurobiological processes, including molecular, cellular, and circuit-level mechanisms, are vulnerable or resilient to changing environmental conditions. We showcase examples that range from molecular to circuit to behavioral levels of analysis across several model species, framing a broad neuroscientific approach to explore topics of neural adaptation, plasticity, and resilience. We believe this emerging scientific area is of great societal and scientific importance and will provide a unique opportunity to reexamine our understanding of neural adaptation and the mechanisms underlying neural resilience.

Dissociating reward sensitivity and negative urgency effects on impulsivity in the five-choice serial reaction time task.

Negative urgency describes the tendency for rash and impulsive behaviour during negative emotional states and has been linked to a number of psychiatric disorders. However, there has been limited research on negative urgency as an explanatory mechanism for impulsivity in experimental animals. Such research has important implications for elucidating the neurobiology of negative urgency and thereby the development of future therapeutic interventions. In this study, we investigated the effects of negative urgency using a partial reinforcement schedule to increase the frequency of non-rewarded (i.e. frustrative) trials in the five-choice serial reaction time task, a widely used task to assess visual attention and impulsivity. Using a Markov chain model to analyse trial-by-trial outcomes we found that premature (i.e. impulsive) responses in the five-choice serial reaction time task were more likely to occur after a non-rewarded trial, and mostly after a previous premature trial. However, contrary to the frustration hypothesis of negative urgency, increasing the probability of reinforcement (p(R)) from p(R) = 0.5 to p(R) = 1 increased the number of premature responses in each session. Micro and macro levels of analyses revealed that impulsivity in the five-choice serial reaction time task is governed by at least two processes, one dependent on the overall level of reinforcement hypothesised to determine the state of behavioural activation, the second dependent on trial-by-trial outcomes consistent with negative urgency effects. These processes may depend on distinct neurobiological mechanisms and have relevance for neuropsychiatric disorders that implicate impulsive behaviours dependent on positive and negative affective states.