The fly pharyngeal sense organs lie at the transition between external and internal nutrient sensing mechanisms. Here, we investigate the function of pharyngeal sweet gustatory receptor neurons (GRNs), demonstrating that they express a subset of the nine previously identified sweet receptors and respond to stimulation with a panel of sweet compounds. We show that pox-neuro (poxn) mutants lacking taste function in the legs and labial palps have intact pharyngeal sweet taste, which is both necessary and sufficient to drive preferred consumption of sweet compounds by prolonging ingestion. Moreover, flies putatively lacking all sweet taste show little preference for nutritive or non-nutritive sugars in a short-term feeding assay. Together, our data demonstrate that pharyngeal sense organs play an important role in directing sustained consumption of sweet compounds, and suggest that post-ingestive sugar sensing does not effectively drive food choice in a simple short-term feeding paradigm.

Nutrient deprivation can lead to dramatic changes in feeding behavior, including acceptance of foods that are normally rejected. In flies, this behavioral shift depends in part on reciprocal sensitization and desensitization of sweet and bitter taste, respectively. However, the mechanisms for bitter taste modulation remain unclear. Here, we identify a set of octopaminergic/tyraminergic neurons, named OA-VLs, that directly modulate bitter sensory neuron output in response to starvation. OA-VLs are in close proximity to bitter sensory neuron axon terminals and show reduced tonic firing following starvation. We find that octopamine and tyramine potentiate bitter sensory neuron responses, suggesting that starvation-induced reduction in OA-VL activity depotentiates bitter taste. Consistent with this model, artificial silencing of OA-VL activity induces a starvation-like reduction in bitter sensory neuron output. These results demonstrate that OA-VLs mediate a critical step in starvation-dependent bitter taste modulation, allowing flies to dynamically balance the risks associated with bitter food consumption against the threat of severe starvation.

Contrast adaptation is a commonly studied phenomenon in vision, where prolonged exposure to spatial contrast alters perceived stimulus contrast and produces characteristic shifts in the contrast response functions of primary visual cortex neurons in cats and primates. In this study we investigated contrast adaptation in mouse primary visual cortex with two goals in mind. First, we sought to establish a quantitative description of contrast adaptation in an animal model, where genetic tools are more readily applicable to this phenomenon. Second, the orientation specificity of contrast adaptation was studied to comparatively assess the possible role of local cortical networks in contrast adaptation. In cats and primates, predictable differences in visual processing across the cortical surface are thought to be caused by inhomogeneous local network membership that arises from the pinwheel organization of orientation columns. Because mice lack this pinwheel organization, we predicted that local cortical networks would have access to a broad spectrum of orientation signals, and contrast adaptation in mice would not be specific to the recorded cell's preferred orientation. We found that most mouse V1 neurons showed contrast adaptation that was robust regardless of whether the adapting stimulus matched the cell's preferred orientation or was orthogonal to it.

The gross structure of neurons is supported by proteins that compose the cytoskeleton. Neurofilaments are intermediate cytoskeletal proteins that contribute to neuron structure and function, and three neurofilament subunits different in their molecular mass assemble to form heteropolymers that produce a structure-providing intracellular scaffold. The light neurofilament subunit is obligatory and can assemble with either the medium or heavy subunit, indicating some degree of independence between subunits. The presence of the heavy subunit has been shown to be associated with mature cells and is linked to large neurons in the cerebral cortex and thalamus. Spectrin is a membrane-associated actin-binding protein that, like neurofilament, has been linked to neuron shape. In this study of the cat dorsal lateral geniculate nucleus (dLGN) we examined whether labeling for neurofilament subunits and spectrin is linked to neuron size. We found that about one-third of neurons contained a visible amount of labeling for each neurofilament subunit, and the bulk of these labeled cells were large in comparison to the general population of neurons. The distribution of neuron sizes was not different between neurofilament subunits, indicating that neurofilament subunit content is not determined by neuron size. Spectrin labeling was evident in most dLGN neurons, and was not related to the size of neurons. That reactivity for neurofilament was predominant in large cells led us to directly examine the relationship between neurofilament and interneurons. The large majority of neurofilament-positive neurons did not contain GABA, indicating that neurofilament is predominant in projection cells and not in interneurons.

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