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Freedom 515 - Colorado

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Physiology Of Behavior PORTABLE

PSY 340 - Physiology of Behavior(3 units)Prerequisites: PSY 100 , PSY 220 , PSY 241 .An in-depth examination of central nervous system (CNS) components that create our behavioral capabilities. Topics include major structural and functional features of the neuron and of selected systems representative of the sensory, integrative, and motor capabilities of the CNS.Both grading options.

Physiology of behavior

Neural circuits are constantly monitored and supported by the surrounding microglial cells, using finely tuned mechanisms which include both direct contact and release of soluble factors. These bidirectional interactions are not only triggered by pathological conditions as a S.O.S. response to noxious stimuli, but they rather represent an established repertoire of dynamic communication for ensuring continuous immune surveillance and homeostasis in the healthy brain. In addition, recent studies are revealing key tasks for microglial interactions with neurons during normal physiological conditions, especially in regulating the maturation of neural circuits and shaping their connectivity in an activity- and experience-dependent manner. Chemokines, a family of soluble and membrane-bound cytokines, play an essential role in mediating neuron-microglia crosstalk in the developing and mature brain. As part of this special issue on Cytokines as players of neuronal plasticity and sensitivity to environment in healthy and pathological brain, our review focuses on the fractalkine signaling pathway, involving the ligand CX3CL1 which is mainly expressed by neurons, and its receptor CX3CR1 that is exclusively found on microglia within the healthy brain. An extensive literature largely based on transgenic mouse models has revealed that fractalkine signaling plays a critical role in regulating a broad spectrum of microglial properties during normal physiological conditions, especially their migration and dynamic surveillance of the brain parenchyma, in addition to influencing the survival of developing neurons, the maturation, activity and plasticity of developing and mature synapses, the brain functional connectivity, adult hippocampal neurogenesis, as well as learning and memory, and the behavioral outcome.

Studies of neuropeptide and peptide hormone signaling are coming of age in Drosophila due to rapid developments in molecular genetics approaches that overcome the difficulties caused by the small size of the fly. In addition we have genome-wide information on genes involved in peptide signaling, and growing pools of peptidomics data. A large number of different neuropeptides has been identified in a huge variety of neuron types in different parts of the Drosophila nervous system and cells in other locations. This review addresses questions related to peptidergic signaling in the Drosophila nervous system, especially how peptides regulate physiology and behavior during development and in the mature fly. We first summarize novel findings on neuropeptide precursor genes, processed bioactive peptides and their cognate receptors. Thereafter we provide an overview of the physiological and behavioral roles of peptide signaling in Drosophila. These roles include regulation of development, growth, feeding, metabolism, reproduction, homeostasis, and longevity, as well as neuromodulation in learning and memory, olfaction and locomotor control. The substrate of this signaling is the peptide products of about 42 precursor genes expressed in different combinations in a variety of neuronal circuits or that act as circulating hormones. Approximately 45 G-protein-coupled peptide receptors are known in Drosophila and for most of these the ligands have been identified. Functions of some peptides are better understood than others, and much work remains to reveal the spectrum of roles neuropeptides and peptide hormones play in the daily life of a fly.

Longitudinal study of 2 cohorts of children selected in the second or third year of life to be extremely cautious and shy (inhibited) or fearless and outgoing (uninhibited) to unfamiliar events revealed preservation of these 2 behavioral qualities through the sixth year of life. Additionally, more of the inhibited children showed signs of activation in 1 or more of the physiological circuits that usually respond to novelty and challenge, namely, the hypothalamic-pituitary-adrenal axis, the reticular activating system, and the sympathetic arm of the autonomic nervous system. It is suggested that the threshold of responsivity in limbic and hypothalamic structures to unfamiliarity and challenge is tonically lower for inhibited than for uninhibited children.

Behavior and physiology are orchestrated by neuropeptides acting as central neuromodulators and circulating hormones. An outstanding question is how these neuropeptides function to coordinate complex and competing behaviors. In Drosophila, the neuropeptide leucokinin (LK) modulates diverse functions, but mechanisms underlying these complex interactions remain poorly understood. As a first step towards understanding these mechanisms, we delineated LK circuitry that governs various aspects of post-feeding physiology and behavior. We found that impaired LK signaling in Lk and Lk receptor (Lkr) mutants affects diverse but coordinated processes, including regulation of stress, water homeostasis, feeding, locomotor activity, and metabolic rate. Next, we sought to define the populations of LK neurons that contribute to the different aspects of this physiology. We find that the calcium activity in abdominal ganglia LK neurons (ABLKs), but not in the two sets of brain neurons, increases specifically following water consumption, suggesting that ABLKs regulate water homeostasis and its associated physiology. To identify targets of LK peptide, we mapped the distribution of Lkr expression, mined a brain single-cell transcriptome dataset for genes coexpressed with Lkr, and identified synaptic partners of LK neurons. Lkr expression in the brain insulin-producing cells (IPCs), gut, renal tubules and chemosensory cells, correlates well with regulatory roles detected in the Lk and Lkr mutants. Furthermore, these mutants and flies with targeted knockdown of Lkr in IPCs displayed altered expression of insulin-like peptides (DILPs) and transcripts in IPCs and increased starvation resistance. Thus, some effects of LK signaling appear to occur via DILP action. Collectively, our data suggest that the three sets of LK neurons have different targets, but modulate the establishment of post-prandial homeostasis by regulating distinct physiological processes and behaviors such as diuresis, metabolism, organismal activity and insulin signaling. These findings provide a platform for investigating feeding-related neuroendocrine regulation of vital behavior and physiology.

Animals ranging from jellyfish to humans use multiple neuropeptides to orchestrate various aspects of behavior and physiology. A major question in biology is how animals are able to coordinate complex and competing behaviors to ensure maintenance of a stable internal environment. To address this, we delineated the functions of the neuronal pathways using the neuropeptide leucokinin (LK) in the fruit fly Drosophila melanogaster. We discovered that mutant flies lacking LK signaling exhibit defects in diverse but coordinated processes, including regulation of stress, water balance, gut function, activity, and metabolic rate. We also attribute these functions to different subsets of neurons that produce LK. Lastly, we show that this neuropeptide interacts with insulin signaling to affect stress tolerance and metabolism. This is of broad interest since stress, obesity and ensuing metabolic disorders, such as heart disease and diabetes, are immense problems in society. Our work provides a foundation for further investigation of neuroendocrine regulation of vital behavior and physiology associated with feeding.

Citation: Zandawala M, Yurgel ME, Texada MJ, Liao S, Rewitz KF, Keene AC, et al. (2018) Modulation of Drosophila post-feeding physiology and behavior by the neuropeptide leucokinin. PLoS Genet 14(11): e1007767.

To determine the role of LK signaling in adult post-feeding physiology and behavior, we generated novel Lk and Lkr mutant flies. By testing these mutants in various feeding-related physiological and behavioral assays, we demonstrate that LK signaling regulates water homeostasis and associated stress, feeding, locomotor activity, and metabolic rate. Based on these data, we propose that the homeostatic roles of LK can be linked to the regulation of post-feeding physiology and behavior. The abdominal ganglion LK neurons (ABLKs), but not the two sets in the brain, display increased calcium-signaling activity in response to rehydration (drinking) following desiccation. Next, to reveal novel targets of LK peptide, we mapped the distribution of Lkr expression. Using two independent Lkr-GAL4 lines to drive expression of GFP, we show that Lkr is expressed in various peripheral tissues, including the gut, Malpighian tubules and chemosensory cells, which comports well with the functions suggested by the mutant analysis. In addition, the expression of the Lkr in the insulin-producing cells (IPCs) and the phenotypes seen after targeted receptor knockdown in these cells indicate interaction between LK and insulin signaling. Thus, the three different populations of LK neurons use LK to modulate post-prandial physiology by acting on different targets in the CNS, as well as cells of the renal tubules and intestine.

To investigate the role of Lk signaling in modulation of feeding-associated physiology and behavior, we utilized CRISPR-Cas9 gene editing to generate GAL4 knock-in mutants for Lk and Lkr (Fig 1A). First, we tested the efficiency of the Lk and Lkr mutants by quantitative real-time PCR (qPCR) and immunolabeling. In qPCR experiments, we found an 80% reduction of Lk expression, whereas Lkr mRNA was reduced by about 60% (Fig 1C), confirming the efficacy of these gene-edited mutants for Lk and Lkr (residual expression presumably reflects some level of transcriptional read-through of the inserted GAL4 cassette). In the homozygous Lk mutants, LK immunolabeling is completely abolished in all cells of the CNS (Fig 1B and 1D), establishing that Lk mutants do not produce a functional peptide. To verify that signaling by LKR is disrupted in Lkr mutants, we measured LK peptide levels by immunolabeling. The rationale for this was that we predicted that Lkr mutant flies would compensate for the diminished receptor expression, for instance in MTs, by increasing production of the peptide in neurosecretory cells to maintain homeostasis. Indeed, LK immunolabeling was elevated in the abdominal LK neurons (ABLKs) (Fig 2A and 2B), and the cell bodies of these neurons were also enlarged (Fig 2C), probably due to the increased peptide production [see [22]]. Interestingly, LK immunolabeling in the lateral horn LK (LHLK) neurons of the brain does not change in Lkr mutant flies (Fig 2D and 2E), suggesting these neurons are not subjected to autoregulatory feedback. Thus, LK levels are differentially regulated in neurons of the brain versus those of the abdominal ganglion, and there appears to be feedback between receptor and peptide expression in abdominal ABLK neurons of Lkr mutant flies. A possible explanation for this is that the ABLKs are neurosecretory cells that target peripheral tissues such as MTs with hormonal LK (see [10]) and periphery-to-CNS feedback may be critical for homeostatic regulation. 041b061a72


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