Tag: Aldis Weible

Transgenically-targeted increase in the activity of medial entorhinal layer II neurons induces reversible field expansion and remapping of CA1 place cells

Presenter: Jasmine Dickinson

Mentor: Aldis Weible

AM Session Oral Presentation

Panel Name: M1 Genes and Neurons

Location: Oak Room

Time: 11:00am – 12:00pm

The hippocampal formation plays a critical role in memory acquisition and consolidation. Hippocampal pyramidal neurons fire in a location-specific manner. These “place” cells are thought to generate an internal representation of context dependent space. In a mouse model, we induced transgenic expression in layer II medial entorhinal cortex of a modified muscarinic G-protein coupled receptor that selectively binds clozapine-N-oxide. CNO, an otherwise inert metabolite of the antipsychotic clozapine, is a small molecule drug capable of crossing the blood-brain barrier. Binding of CNO to the receptor triggers an intracellular cascade ultimately resulting in the depolarization of the cell, and thus increased firing that lasts for several hours. We analyzed CA1 place fields before and after CNO injection. Many neurons expanded their place fields following grid cell activation, as predicted by models of grid cell to place cell transformations. However, other neurons drastically changed their firing fields (i.e. they “remapped”), while others were unchanged by CNO. All effects reversed twelve hours post injection. These effects underscore the generative nature of the hip- pocampal network, and provide empirical data to distinguish between theoretical models of place field formation.

Gap Detection in Auditory Cortex

Presenter: Ulysses Duckler

Faculty Mentor: Mike Wehr, Aldis Weible

Presentation Type: Poster 92

Primary Research Area: Science

Major: Biochemistry

Funding Source: OURS Summer Research Program

Strong evidence supports that hearing loss and difficulty with speech comprehension in noisy environments for older adults is the result of temporal processing deficits in central auditory structures such as the auditory cortex. There is a general canonical circuit model of layer by layer serial information flow through the auditory cortex from the thalamus, before information is projected back into inferior colliculus neurons. However the specific cortical circuits and cell types which regulate temporal processing though the auditory cortex are still unknown and not linked to behavior. The auditory cortex is necessary for temporal acuity in receiving auditory stimulus. Temporal acuity is necessary for brief noise gap detection and discriminating between similar phonemes, causing speech perception deficits when impaired. In this study, I tested gap detection in mice by measuring their startle response to noise gaps in white noise, gaps which were paired with a startle stimulus in repeated behavioral trials. The presence of the noise gap attenuates startle response to the stimulus, so that measuring the startle response gives a measure of temporal acuity by assessing gap detection behavior. Optogenetics allows for the gaps to be paired with a laser signal that silences auditory cortex neurons and allowed me to see how gap detection is impaired by temporally precise auditory cortex neuron suppression. By probing cortex circuit mechanisms through layer specific optogenetic silencing before and after gap, I found that layer specific silencing of auditory cortex neuron populations in layers four and five suggests behavior in accordance with the canonical model.