Monday, February 26th, 2024

Time	Event
11:31a	PRENATAL STRESS MODIFIES SPATIAL COGNITION IN MICE: EFFECTS OF AGE AND SEX. Prenatal stress is linked with neuropathology of the cortical-hippocampal circuit, due to abnormal brain development that leads to long term neurological deficits in offspring, in both rodents and in humans with psychiatric disorders. Conflicting reports exist of the effects of prenatal stress in C57BL/6J mice, which is an inbred strain that is the most frequently used for neurobehavioral research. We now present comprehensive analyses of the effects of prenatal stress on spatial cognition and related behaviors in this inbred strain, in males and females at young adult and aged adult stages. The prenatal stress exposure was conducted by exposing pregnant mice to restraint stress three times daily from day 7 to day 18 of gestation. We tested the effects of prenatal stress on cognitive behavior using a battery of behavioral assays including the open-field test, the light-dark box, Morris water maze spatial acquisition and spatial reversal testing, in addition to assays of social interaction and social memory. We compared the behavioral phenotype of male and female offspring in young adult (10-20 weeks) and older adult ages (60-70 weeks). Data reveal that male but not female mice had reduced body weight throughout the lifespan after exposure to prenatal stress. Young prenatally stressed adult females showed greater organization of tracking behavior in spatial acquisition tests than other groups. Prenatal stress improved reversal learning in aged females relative to non-stressed aged females. We detected decreased extinction of the spatial acquisition memory in prenatally stressed young adult mice of both sexes. Overall results indicate that prenatal stress may protect females from detrimental effects of age on function of the hippocampus. Our data support the finding that C57BL/6J are a relatively resilient strain of mouse that may be useful for investigating the differences between resilience and susceptibility to stress. Genomic differences between the C57BL/6J strain relative to Swiss Webster strain, which is more susceptible to prenatal stress are discussed. Future studies of prenatal stress in the C57BL/6J mouse strain should focus on the identification of molecular pathways that underlie resilience to prenatal stress, to identify novel targets for drug development. (Comment on this)
11:31a	Predictive coding for natural vocal signals in the songbird auditory forebrain Predictive coding posits that incoming sensory signals are compared to an internal generative model with resulting error signals carried in the responses of single neurons. Empirical support for predictive coding in individual neurons, particularly in the auditory system and for natural stimuli, has proven difficult to observe. Here, we developed a neural network that uses current sensory context to predict future spectral-temporal features in a natural communication signal, birdsong. Using this model, we represent the waveform of any birdsong as either a set of weighted "latent" predictive features evolving in time, or a corresponding error representation that reflects the difference between the predicted and actual song. We then recorded responses of single neurons in caudomedial nidopallium (NCM), caudal mesopallium (CMM) and Field L, analogs of mammalian auditory cortex, in anesthetized European starlings listening to conspecific songs, and computed the linear/non-linear receptive fields for each neuron fit separately to the spectro-temporal, predictive, and error representations of song. Comparisons between the quality of each receptive field model reveal that NCM spiking responses are best modeled by the predictive spectrotemporal features of song, while CMM and Field L responses capture both predictive and error features. Neural activity is selective for carrying information explicitly about prediction and prediction errors, and their preferences vary across the auditory forebrain. We conclude that this provides strong support for the notion that individual neurons in songbirds encode information related to multiple stimulus representations guided by predictive coding simultaneously. (Comment on this)
9:47p	Sleep pressure accumulates in a voltage-gated lipid peroxidation memory Voltage-gated potassium (KV) channels contain cytoplasmic {beta}-subunits whose aldo-keto reductase activity is required for the homeostatic regulation of sleep. Here we show that Hyperkinetic, the {beta}-subunit of the KV1 channel Shaker in Drosophila, forms a dynamic lipid peroxidation memory. Information is stored in the oxidation state of Hyperkinetics nicotinamide adenine dinucleotide phosphate (NADPH) cofactor, which changes when lipid-derived carbonyls, such as 4-oxo-2-nonenal or an endogenous analog generated by illuminating a membrane-bound photosensitizer, abstract an electron pair. NADP+ remains locked in the active site of KV{beta} until membrane depolarization permits its release and replacement with NADPH. Sleep-inducing neurons use this voltage-gated oxidoreductase cycle to encode their recent lipid peroxidation history in the collective binary states of their KV{beta}-subunits; this biochemical memory influences--and is erased by--spike discharges driving sleep. The presence of a lipid peroxidation sensor at the core of homeostatic sleep control suggests that sleep protects neuronal membranes against oxidative damage. Indeed, brain phospholipids are depleted of vulnerable polyunsaturated fatty acyl chains after enforced waking, and slowing the removal of their carbonylic breakdown products increases the demand for sleep. (Comment on this)

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