title: Intraspecific competition and coordination in the evolution of lateralization.
abstract: Recent studies have revealed a variety of left-right asymmetries among vertebrates and invertebrates. In many species, left- and right-lateralized individuals coexist, but in unequal numbers ('population-level' lateralization). It has been argued that brain lateralization increases individual efficiency (e.g. avoiding unnecessary duplication of neural circuitry and reducing interference between functions), thus counteracting the ecological disadvantages of lateral biases in behaviour (making individual behaviour more predictable to other organisms). However, individual efficiency does not require a definite proportion of left- and right-lateralized individuals. Thus, such arguments do not explain population-level lateralization. We have previously shown that, in the context of prey-predator interactions, population-level lateralization can arise as an evolutionarily stable strategy when individually asymmetrical organisms must coordinate their behaviour with that of other asymmetrical organisms. Here, we extend our model showing that populations consisting of left- and right-lateralized individuals in unequal numbers can be evolutionarily stable, based solely on strategic factors arising from the balance between antagonistic (competitive) and synergistic (cooperative) interactions.
authors.affiliation: Department of Psychology, University of Bologna, Bologna, Italy.
authors.forename: Stefano
authors.initials: S
authors.lastname: Ghirlanda
authors.forename: Elisa
authors.initials: E
authors.lastname: Frasnelli
authors.forename: Giorgio
authors.initials: G
authors.lastname: Vallortigara
mesh_terms: D000818:Animals; D001519:Behavior / Q000502:physiology*; D001522:Behavior, Animal / Q000502:physiology; D001921:Brain / Q000502:physiology*; D007839:Functional Laterality / Q000502:physiology*; D006801:Humans; D007448:Invertebrates / Q000502:physiology; D008959:Models, Neurological; D013045:Species Specificity; D014714:Vertebrates / Q000502:physiology