Defects in hair cells disrupt the development of auditory peripheral circuitry.

Deafness is the most common form of sensory impairment in humans and frequently caused by defects in hair cells of the inner ear. Here we demonstrate that in male mice which model recessive non-syndromic deafness (DFNB6), inactivation of Tmie in hair cells disrupts gene expression in the neurons that innervate them. This includes genes regulating axonal pathfinding and synaptogenesis, two processes that are disrupted in the inner ear of the mutant mice.

Molecular signatures define subtypes of auditory afferents with distinct peripheral projection patterns and physiological properties.

Type I spiral ganglion neurons (SGNs) are the auditory afferents that transmit sound information from cochlear inner hair cells (IHCs) to the brainstem. These afferents consist of physiological subtypes that differ in their spontaneous firing rate (SR), activation threshold, and dynamic range and have been described as low, medium, and high SR fibers. Lately, single-cell RNA sequencing experiments have revealed three molecularly defined type I SGN subtypes.

Transgenerational Effects of Prenatal Ethanol Exposure in Prepubescent Mice.

Fetal alcohol spectrum disorders (FASD) represent a leading cause of non-genetic neuropathologies. Recent preclinical evidence from suggests that prenatal ethanol exposure (PrEE), like other environmental exposures, may have a significant, transgenerational impact on the offspring of directly exposed animals, including altered neocortical development at birth and behavior in peri-pubescent mice. How these adverse behavioral outcomes are manifested within the brain at the time of behavioral disruption remains unknown.

Rescue of ethanol-induced FASD-like phenotypes via prenatal co-administration of choline.

Maternal consumption of alcohol during pregnancy can generate a multitude of deficits in the offspring. Fetal Alcohol Spectrum Disorders, or FASD, describe a palette of potentially life-long phenotypes that result from exposure to ethanol during human gestation. There is no cure for FASD and cognitive-behavioral therapies typically have low success rates, especially in severe cases.

Early postnatal gene expression in the developing neocortex of prairie voles (Microtus ochrogaster) is related to parental rearing style.

The earliest and most prevalent sensory experience includes tactile, thermal, and olfactory stimulation delivered to the young via contact with the mother, and in some mammals, the father. Prairie voles (Microtus ochrogaster), like humans, are biparental and serve as a model for understanding the impact of parent/offspring interactions on the developing brain. Prairie voles also exhibit natural variation in the level of tactile stimulation delivered by the parents to the offspring, and this has been well documented and quantified.

The Impact of Paternal Alcohol Consumption on Offspring Brain and Behavioral Development.

Background: Fetal alcohol spectrum disorders (FASD) describe the wide array of long-lasting developmental abnormalities in offspring due to prenatal alcohol (ethanol [EtOH]) exposure via maternal gestational drinking. Although the teratogenic consequences of prenatal EtOH exposure, are apparent, the effects of preconception paternal EtOH exposure (PatEE) are still unclear. Previous research suggests that PatEE can induce molecular changes and abnormal behavior in the offspring.

Prenatal Ethanol Exposure and Neocortical Development: A Transgenerational Model of FASD.

Fetal Alcohol Spectrum Disorders, or FASD, represent a range of adverse developmental conditions caused by prenatal ethanol exposure (PrEE) from maternal consumption of alcohol. PrEE induces neurobiological damage in the developing brain leading to cognitive-perceptual and behavioral deficits in the offspring. Alcohol-mediated alterations to epigenetic function may underlie PrEE-related brain dysfunction, with these changes potentially carried across generations to unexposed offspring.