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Schneider, N. A.

Publications and source records attributed to Schneider, N. A..

4 recordsLinked to original sources

A cortical output channel for perceptual categorization

Perceptual categorization allows the brain to transform diverse sensory inputs into discrete representations that support flexible behavior [1-7]. Auditory cortex (ACtx) has been implicated in this process [8-14], but the cell-type-specific circuits that implement category learning remain unknown. We trained head-fixed mice to categorize the temporal rate of amplitude-modulated noise while performing longitudinal two-photon imaging of layer (L)5 extratelencephalic (L5 ET) neurons alongside comparison populations of L2/3 and L5 intratelencephalic (L5 IT) neurons. With learning, L5 ET neurons underwent pronounced tuning modifications and developed robust, categorical responses, whereas L2/3 and L5 IT neurons did not. This categorical code was task engagement-dependent: it was present during behavior and absent during passive listening in the same neurons on the same day, indicating context-gated expression. Using a generalized linear model to dissociate stimulusfrom choice-related signals, we confirmed that categorical selectivity in L5 ET neurons reflected sensory encoding rather than motor confounds. All three populations carried choice signals, but these were strongest in L5 ET neurons, suggesting a role in linking sensory categorization to action selection. These findings identify a projection-specific, deep-layer cortical output channel in which L5 ET neurons acquire categorical representations and selectively propagate behaviorally relevant signals to downstream targets.

neuroscience↗

Cell-type-specific plasticity in synaptic, intrinsic, and sound response properties of deep-layer auditory cortical neurons after noise trauma

Peripheral trauma, such as noise-induced hearing loss (NIHL), triggers compensatory plasticity in the auditory cortex (ACtx) to maintain auditory function. While cortical plasticity in superficial cortical layers has been relatively well studied, the plasticity mechanisms governing deep-layer excitatory projection neurons remain less understood. Here, we investigated the plasticity of layer (L)5 extratelencephalic (ETs) and L6 corticothalamic neurons (CTs) following NIHL. Using a combination of in vitro slice electrophysiology, optogenetics, and in vivo two-photon imaging in a mouse model of NIHL, we characterized changes in evoked thalamocortical (TC) synaptic input strength, intrinsic excitability, and sound response properties. We found that TC input was initially equivalent between ETs and CTs, then shifted to CT-dominant one day after noise exposure. This shift renormalized to equivalent seven days after noise exposure and was associated with a transient increase in both the quantal size (q) in TC[->]CT synapses and intrinsic CT suprathreshold excitability. ETs maintained stable intrinsic properties and showed minor changes in their TC input. In vivo imaging revealed that CTs displayed a persistent elevation in sound intensity thresholds, whereas ETs transiently shifted their best frequency representation and reduced their responsiveness to high-frequency tones one day after NIHL, followed by recovery at seven days. Together, our findings highlight cell-type-specific plasticity mechanisms in deep-layer cortical neurons, enhance our understanding of cortical adaptation to peripheral damage, and highlight targets for developing therapeutic strategies to mitigate hearing loss and related disorders such as tinnitus and hyperacusis. Short AbstractPeripheral damage drives auditory cortex (ACtx) plasticity, but the underlying synaptic and cellular mechanisms remain poorly understood. We used a combination of in vitro slice electrophysiology, optogenetics, and in vivo two-photon imaging to investigate layer 5 extratelencephalic (ET) and layer 6 corticothalamic (CT) neuronal plasticity in mice, following noise-induced hearing loss (NIHL). Thalamocortical (TC) input was initially balanced between CTs and ETs but shifted to CT-dominant one day post-NIHL and then normalized by day seven. This transient shift was accompanied by increased quantal size and suprathreshold excitability in CTs, with minimal changes in ETs. In vivo, CTs exhibited persistent elevation in sound intensity thresholds, while ETs showed a transient shift in frequency tuning and reduced high-frequency responsiveness that recovered within a week. These findings reveal distinct, cell-type-specific plasticity mechanisms in deep-layer ACtx neurons following peripheral damage and highlight potential targets for treating hearing loss-related disorders such as tinnitus and hyperacusis.

neuroscience↗

Vocalization categorization behavior explained by a feature-based auditory categorization model

Vocal animals produce multiple categories of calls with high between- and within-subject variability, over which listeners must generalize to accomplish call categorization. The behavioral strategies and neural mechanisms that support this ability to generalize are largely unexplored. We previously proposed a theoretical model that accomplished call categorization by detecting features of intermediate complexity that best contrasted each call category from all other categories. We further demonstrated that some neural responses in the primary auditory cortex were consistent with such a model. Here, we asked whether a feature-based model could predict call categorization behavior. We trained both the model and guinea pigs on call categorization tasks using natural calls. We then tested categorization by the model and guinea pigs using temporally and spectrally altered calls. Both the model and guinea pigs were surprisingly resilient to temporal manipulations, but sensitive to moderate frequency shifts. Critically, model performance quantitatively matched guinea pig behavior to a remarkable degree. By adopting different model training strategies and examining features that contributed to solving specific tasks, we could gain insight into possible strategies used by animals to categorize calls. Our results validate a model that uses the detection of intermediate-complexity contrastive features to accomplish call categorization.

neuroscience↗

Impact of acute visual experience on development of LGN receptive fields in the ferret

Selectivity for direction of motion is a key feature of primary visual cortical neurons. Visual experience is required for direction selectivity in carnivore and primate visual cortex, but the circuit mechanisms of its formation remain incompletely understood. Here we examined how developing lateral geniculate nucleus (LGN) neurons may contribute to cortical direction selectivity. Using in vivo electrophysiology techniques, we examined LGN receptive field properties of visually naive female ferrets before and after exposure to 6 hours of motion stimuli in order to assess the effect of acute visual experience on LGN cell development. We found that acute experience with motion stimuli did not significantly affect the weak orientation or direction selectivity of LGN neurons. In addition, we found that neither latency nor sustainedness or transience of LGN neurons significantly changed with acute experience. These results suggest that the direction selectivity that emerges in cortex after acute experience is computed in cortex and cannot be explained by changes in LGN cells. Significance StatementThe development of typical neural circuitry requires experience-independent and experience-dependent factors. In the visual cortex of carnivores and primates, selectivity for motion arises as a result of experience, but we do not understand whether the major brain area that sits between the retina and the visual cortex - the lateral geniculate nucleus of the thalamus - also participates. Here we found that lateral geniculate neurons do not exhibit changes as a result of several hours of visual experience with moving stimuli, at a time when visual cortical neurons undergo a rapid change. We conclude that lateral geniculate neurons do not participate in this plasticity, and that changes in cortex are likely responsible for the development of direction selectivity in carnivores and primates.

neuroscience↗