Genetically targeted approaches that permit acute and reversible manipulation of neuronal circuit activity have enabled an unprecedented understanding of how discrete neuronal circuits control animal behavior. Zebra finch singing behavior has emerged as an excellent model for studying neuronal circuit mechanisms underlying the generation and learning of behavioral motor sequences. We employed a newly developed, reversible, neuronal silencing system in zebra finches to test the hypothesis that ensembles of neurons in the robust nucleus of the arcopallium (RA) control the acoustic structure of specific song parts, but not the timing nor the order of song elements. Subunits of an ivermectin-gated chloride channel were expressed in a subset of RA neurons, and ligand administration consistently suppressed neuronal excitability. Suppression of activity in a group of RA neurons caused the birds to sing songs with degraded elements, although the order of song elements was unaffected. Furthermore some syllables disappeared in the middle or at the end of song motifs. Thus, our data suggest that generation of specific song parts is controlled by a subset of RA neurons, whereas elements order coordination and timing of whole songs are controlled by a higher premotor area.

Both in rodents and humans, melanocortin-4 receptors (MC4Rs) suppress appetite and prevent obesity. Unfortunately, the underlying neural mechanisms by which MC4Rs regulate food intake are poorly understood. Unraveling these mechanisms may open up avenues for treating obesity. In the present study we have established that MC4Rs on neurons in the paraventricular nucleus of the hypothalamus are both necessary and sufficient for MC4R control of feeding and that these neurons are glutamatergic and not GABAergic and do not express the neuropeptides oxytocin, corticotropin-releasing hormone, prodynorphin, or vasopressin. In addition, we identify downstream projections from these glutamatergic neurons to the lateral parabrachial nucleus, which could mediate the appetite suppressing effects.

Work in animals and humans suggest the existence of a slow–wave sleep (SWS) promoting/EEG synchronizing center in the mammalian lower brainstem. While sleep–active GABAergic neurons in the medullary parafacial zone (PZ) are needed for normal SWS, it remains unclear if these neurons can initiate and maintain SWS or EEG slow wave activity (SWA) in behaving mice. We used genetically targeted activation and optogenetic–based mapping to uncover the downstream circuitry engaged by SWS–promoting PZ neurons, and we show that this circuit uniquely and potently initiates SWS and EEG SWA, regardless of the time of day. PZ neurons monosynaptically innervate and release synaptic GABA onto parabrachial neurons that in turn project to and release synaptic glutamate onto cortically–projecting neurons of the magnocellular basal forebrain; hence a circuit substrate is in place through which GABAergic PZ neurons can potently trigger SWS and modulate the cortical EEG.