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The comparative approach is a powerful way to explore the relationship between brain structure and cognitive function. Thus far, the field has been dominated by the assumption that a bigger brain somehow means better cognition. Correlations between differences in brain size or neuron number between species and differences in specific cognitive abilities exist, but these correlations are very noisy. Extreme differences exist between clades in the relationship between either brain size or neuron number and specific cognitive abilities. This means that correlations become weaker, not stronger, as the taxonomic diversity of sampled groups increases. Cognition is the outcome of neural networks. Here we propose that considering plausible neural network models will advance our understanding of the complex relationships between neuron number and different aspects of cognition. Computational modelling of networks suggests that adding pathways, or layers, or changing patterns of connectivity in a network can all have different specific consequences for cognition. Consequently, models of computational architecture can help us hypothesise how and why differences in neuron number might be related to differences in cognition. As methods in connectomics continue to improve and more structural information on animal brains becomes available, we are learning more about natural network structures in brains, and we can develop more biologically plausible models of cognitive architecture. Natural animal diversity then becomes a powerful resource to both test the assumptions of these models and explore hypotheses for how neural network structure and network size might delimit cognitive function. [ABSTRACT FROM AUTHOR]

While drug addiction is a uniquely human problem, most research examining the biological mechanisms of the transition from substance use to addiction is conducted with vertebrate animal models. Many other fields of neuroscience have greatly benefitted from contributions from simple and manipulable invertebrate model systems. However, the potential of invertebrate research has yet to be fully capitalised on in the field of addiction neuroscience. This may be because of the complexity of addiction and the clinical imperative of addiction research. We argue that the homocentric diagnostic criteria of addiction are no more a hindrance to the use of invertebrate models than they are to vertebrate models. We highlight the strengths of the diversity of different invertebrate model systems in terms of neuroanatomy and molecular machinery, and stress that working with a range of different models will aid in understanding addiction and not be a disadvantage. Finally, we discuss the specific advantages of utilising invertebrate animals for addiction research and highlight key areas in which invertebrates are suited for making unique and meaningful contributions to this field. © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Efficient division of labor is one of the main reasons for the success of the social insects. In honey bees the division of labor is principally achieved by workers changing tasks as they age. Typically, young adult bees perform a series of tasks within the colony before ultimately making the transition to foraging outside the hive for resources. This lifelong behavioral development is a well-characterized example of naturally occurring behavioral plasticity, but its neural bases are not well understood. Two techniques were used to assess the role of biogenic amines in the transition from in-hive work to foraging, which is the most dramatic and obvious transition in honey bee behavioral development. First, associations between amines and tasks were determined by measuring the levels of amines in dissected regions of individual bee brains using HPLC analysis. Second, colonies were orally treated with biogenic amines and effects on the onset of foraging were observed. Octopamine concentration in the antennal lobes of the bee brain was most reliably associated with task: high in foragers and low in nurses regardless of age. In contrast, octopamine in the mushroom bodies, a neighboring neuropil, was associated with age and not behavior, indicating independent modulation of octopamine in these two brain regions. Treating colonies with octopamine resulted in an earlier onset of foraging in young bees. In addition, octopamine levels were not elevated by non-foraging flight, but were already high on return from the first successful foraging trip and subsequently remained high, showing no further change with foraging experience. This observation suggests that octopamine becomes elevated in the antennal lobes in anticipation of foraging and is involved in the release and maintenance of the foraging state. Foraging itself, however, does not modulate octopamine levels. Behaviorally related changes in octopamine are modulated by juvenile hormone, which has also been implicated in the control of honey bee division of labor. Treatment with the juvenile hormone analog methoprene elevated octopamine and octopamine treatment ‘rescued’ the delay in behavioral development caused by experimentally depleting juvenile hormone in bees. Although the pathways linking juvenile hormone and octopamine are presently unknown, it is clear that octopamine acts ‘downstream’ of juvenile hormone to influence behavior and that juvenile hormone modulates brain octopamine levels. A working hypothesis is that octopamine acts as an activator of foraging by modulating responsiveness to foraging-related stimuli. This is supported by the finding that octopamine treatment increased the response of bees to brood pheromone, a stimulator of foraging activity. Establishing a role for octopamine in honey bee behavioral development is a first step in understanding the neural bases of this example of naturally occurring, socially mediated, behavioral plasticity. The next level of analysis will be to determine precisely where and how octopamine acts in the nervous system to coordinate this complex social behavior.Copyright © 2003 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]