Campos, R. C. | Search bioRxiv

bioRxiv2023

Nicotine in adolescence freezes dopamine circuits in an immature state

Nicotine use during adolescence is largely associated with negative long-term outcomes, including addiction to nicotine in adulthood. How nicotine acts on developing neurocircuitry in adolescence remains largely unknown, but may hold the key for informing more effective intervention efforts. We found transient nicotine exposure in early adolescence was sufficient for adult mice to show a marked vulnerability to nicotine. Brain-wide activity mapping showed that these mice had an enhanced response to an acute nicotine injection and widespread disruption of functional connectivity in comparison to controls, particularly within dopaminergic networks. Neurophysiological analysis further revealed that their ventral tegmental area (VTA) dopamine neurons show an immature basal plasticity signature and an adolescent-like imbalance in nicotine-induced activity between nucleus accumbens (NAc) and amygdala (AMG)-projecting pathways, known to respectively produce the reinforcing and anxiogenic effects of nicotine. The anxiogenic effect of nicotine is abolished in adult mice treated with nicotine in adolescence, strongly resembling the normal phenotype of young mice. Together these results suggest that nicotine exposure in adolescence somehow "froze" both their neural circuit and behavioral reaction to nicotine, carrying an adolescent-like vulnerability to the drug into adulthood. Finally, we are able to "thaw" the behavioral response to acute nicotine in adolescent-exposed mice by chemogenetically resetting the balance between the underlying NAc- and AMG-projecting dopamine circuits, restoring a mature anxiety-like response to acute nicotine. Together, our results highlight how diverse dopamine pathways can be impacted by experience in adolescence, and further suggest that the perseverance of a developmental imbalance between dopamine pathways may alter vulnerability profiles for later dopamine-dependent psychopathologies.

neuroscience↗

bioRxiv2020

Disentangling the effects of sampling scale and size on the shape of species abundance distributions

Many authors have tried to explain the shape of the species abundance distribution (SAD). Some of them have suggested that sampling scale is an important factor shaping SADs. These suggestions, however, did not consider the indirect and well-known effect of sample size, which increases as samples are combined to generate SADs at larger scales. Here, we separate the effects of sample size and sampling scale on the shape of the SAD for three groups of organisms (trees, beetles and birds) sampled in the Brazilian Atlantic Forest. We compared the observed SADs at different sampling scales with simulated SADs having the same richness, relative abundances but comparable sample sizes, to show that the main effect shaping SADs is sample size and not sampling scale. The effect of scale was minor and deviations between observed and simulated SADs were present only for beetles. For trees, the match between observed and simulated SADs was improved at all scales when we accounted for conspecific aggregation, which was even more important than the sampling scale effect. We build on these results to propose a conceptual framework where observed SADs are shaped by three main factors, in decreasing order of importance: sample size, conspecific aggregation and beta diversity. Therefore, studies comparing SADs across sites or scales should use sampling and/or statistical approaches capable of disentangling these three effects on the shape of SADs.

ecology↗