Effect of Sand and Wood-Shavings Bedding on the Behavior of Broiler Chickens

The purpose of this study was to determine the effect of 2 different bedding types, sand and wood shavings, on the behavior of broiler chickens. In experiment 1, 6 pens were divided down the center and bedded half with sand and half with wood shavings. Male broilers (10/pen) were observed by scan sampling at 5- or 12-min intervals throughout the 6-wk growth period during the morning (between 0800 to 0900 h), afternoon (1200 to 1500 h), and night (2300 to 0600 h). There was a significant behavior x substrate x week interaction during the day (P \u3c 0.0001) and at night (P \u3c 0.0002). Drinking, dustbathing, preening, and sitting increased in frequency on the sand side but decreased on the wood shavings side during the day, as did resting at night. In general, broilers performed a greater proportion of their total behavioral time budget on the sand (P \u3c 0.0001) as they aged. Broilers used the divider between the 2 bedding types to perch; perching behavior peaked during wk 4. In experiment 2, male broilers were housed in 8 pens (50 birds/pen) bedded only in sand or wood shavings. Bedding type had no effect on behavioral time budgets (P = 0.8946), although there were age-related changes in behavior on both bedding types. These results indicate that when given a choice, broilers increasingly performed many of their behaviors on sand, but if only one bedding type was provided they performed those behaviors with similar frequency on sand or wood shavings

Activity-dependent translation dynamically alters the proteome of the perisynaptic astrocyte process

Within eukaryotic cells, translation is regulated independent of transcription, enabling nuanced, localized, and rapid responses to stimuli. Neurons respond transcriptionally and translationally to synaptic activity. Although transcriptional responses are documented in astrocytes, here we test whether astrocytes have programmed translational responses. We show that seizure activity rapidly changes the transcripts on astrocyte ribosomes, some predicted to be downstream of BDNF signaling. In acute slices, we quantify the extent to which cues of neuronal activity activate translation in astrocytes and show that this translational response requires the presence of neurons, indicating that the response is non-cell autonomous. We also show that this induction of new translation extends into the periphery of astrocytes. Finally, synaptic proteomics show that new translation is required for changes that occur in perisynaptic astrocyte protein composition after fear conditioning. Regulation of translation in astrocytes by neuronal activity suggests an additional mechanism by which astrocytes may dynamically modulate nervous system functioning

Supplementary Material for: WNT/β-Catenin Pathway and Epigenetic Mechanisms Regulate the Pitt-Hopkins Syndrome and Schizophrenia Risk Gene TCF4

<p>Genetic variation within the transcription factor <i>TCF4</i> locus can cause the intellectual disability and developmental disorder Pitt-Hopkins syndrome (PTHS), whereas single-nucleotide polymorphisms within noncoding regions are associated with schizophrenia. These genetic findings position TCF4 as a link between transcription and cognition; however, the neurobiology of TCF4 remains poorly understood. Here, we quantitated multiple distinct <i>TCF4</i> transcript levels in human induced pluripotent stem cell-derived neural progenitors and differentiated neurons, and PTHS patient fibroblasts. We identify two classes of pharmacological treatments that regulate <i>TCF4</i> expression: WNT pathway activation and inhibition of class I histone deacetylases. In PTHS fibroblasts, both of these perturbations upregulate a subset of <i>TCF4</i> transcripts. Finally, using chromatin immunoprecipitation sequencing in conjunction with genome-wide transcriptome analysis, we identified TCF4 target genes that may mediate the effect of TCF4 loss on neuroplasticity. Our studies identify new pharmacological assays, tools, and targets for the development of therapeutics for cognitive disorders.</p