Cerebellar interneurons control fear memory consolidation via learning-induced HCN plasticity.

While synaptic plasticity is considered the basis of learning and memory, modifications of the intrinsic excitability of neurons can amplify the output of neuronal circuits and consequently change behavior. However, the mechanisms that underlie learning-induced changes in intrinsic excitability during memory formation are poorly understood. In the cerebellum, we find that silencing molecular layer interneurons completely abolishes fear memory, revealing their critical role in memory consolidation.

Adolescent alcohol exposure produces sex differences in negative affect-like behavior and group I mGluR BNST plasticity.

Adolescent alcohol exposure increases the risk of developing alcohol use disorders (AUDs), yet the mechanisms responsible for this vulnerability remain largely unknown. One potential target for alcohol-induced changes is the circuitry that modulates negative affect and stress, two sexually dependent drivers of alcohol relapse. The bed nucleus of the stria terminalis (BNST) is a sexually dimorphic region that critically regulates negative affective- and stress-induced relapse.

Regulation of NMDA Receptor Plasticity in the BNST Following Adolescent Alcohol Exposure.

Persistent alterations in synaptic plasticity and neurotransmission are thought to underlie the heightened risk of adolescent-onset drinkers to develop alcohol use disorders in adulthood. The bed nucleus of the stria terminalis (BNST) is a compelling region to study the consequences of early alcohol, as it is innervated by cortical structures which undergo continued maturation during adolescence and is critically involved in stress and negative affect-associated relapse. In adult mice, chronic ethanol induces long-term changes in GluN2B-containing NMDA receptors (NMDARs) of the BNST.

Activation of metabotropic glutamate receptors regulates ribosomes of cochlear nucleus neurons.

The brain stem auditory system of the chick is an advantageous model for examining changes that occur as a result of deafness. Elimination of acoustic input through cochlear ablation results in the eventual death of approximately 30% of neurons in the chick cochlear nucleus, nucleus magnocellularis (NM). One early change following deafness is an alteration in NM ribosomes, evidenced both by a decrease in protein synthesis and reduction in antigenicity for Y10B, a monoclonal antibody that recognizes a ribosomal epitope.

In vivo analysis of the role of metabotropic glutamate receptors in the afferent regulation of chick cochlear nucleus neurons.

Cochlea removal results in the death of approximately 20-30% of neurons in the chick nucleus magnocellularis (NM). One early event in NM neuronal degradation is the disruption of their ribosomes. This can be visualized in the first few hours following cochlea removal using Y10B, an antibody that recognizes ribosomal RNA.