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Vogler, N. W.

Publications and source records attributed to Vogler, N. W..

2 recordsLinked to original sources

Mechanisms of synaptic zinc plasticity at mouse dorsal cochlear nucleus glutamatergic synapses

In many excitatory synapses, synaptic zinc is co-released with glutamate to modulate neurotransmission. Synaptic zinc modulates the responsiveness of auditory cortex to sound, and synaptic zinc levels and signaling are modulated by sensory experience, termed zinc plasticity. The mechanisms underlying zinc plasticity remain unknown. We discovered that high- and low-frequency electrical stimulation of dorsal cochlear nucleus synapses reduces and increases synaptic zinc signaling, respectively. This bidirectional zinc plasticity is evidenced by changes in zinc inhibition of AMPA and NMDA receptor activity. Increases and decreases in zinc signaling require activation of Group 1 metabotropic glutamate receptors (mGluRs). Activation of Group 1 mGluRs with a higher agonist concentration increases presynaptic zinc levels and postsynaptic zinc signaling, whereas activation with a lower concentration reduces zinc levels and signaling. Sound-induced zinc plasticity also requires Group 1 mGluRs. Our results reveal the mechanisms underlying synaptic zinc plasticity, elicited by either synaptic activity or sound experience.

neuroscience

Opposing spatial gradients of inhibition and neural activity in mouse olfactory cortex

The spatial representation of stimuli in primary sensory cortices is a convenient scaffold for elucidating the circuit mechanisms underlying sensory processing. In contrast, the anterior piriform cortex (APC) lacks topology for odor identity and appears homogenous in terms of afferent and intracortical excitatory circuitry. Here, we show that an increasing rostral-caudal (RC) gradient of inhibition onto pyramidal cells is commensurate with a decrease in active neurons along the RC axis following exploration of a novel odor environment. This inhibitory gradient is supported by somatostatin interneurons that provide an opposing, rostrally-biased, gradient of inhibition to interneurons. Optogenetic or chemogenetic modulation of somatostatin cells neutralizes the inhibitory gradient onto pyramidal cells. This suggests a novel circuit mechanism whereby opposing spatial gradients of inhibition and disinhibition regulate neural activity along the RC-axis. These findings challenge our current understanding of the spatial profiles of neural circuits and odor processing within APC.

neuroscience