Biology subjects

Cary, B. A.

Publications and source records attributed to Cary, B. A..

5 recordsLinked to original sources

bioRxiv2025

Rapid prey capture learning drives a slow resetting of network activity in rodent binocular visual cortex

Neurons within primary visual cortex (V1) possess stable firing rate set points to which they faithfully return when perturbed by passive sensory manipulations. Chronic recordings in vivo suggest that these set points are present early in postnatal development and are stable through adulthood, raising the possibility that once they are established, they are largely immutable. Here we challenge this idea, using an ethological, vision-dependent prey capture learning paradigm in juvenile (critical period) rats. Juvenile rats rapidly (in one day) became proficient at catching crickets. This learning was impaired when V1 was inactivated, and was accompanied by an increase in the number of binocular V1 (V1b) neurons with firing reliably tied to specific behavioral epochs during hunts, indicating that hunting drives rapid functional plasticity within V1b. Remarkably, this rapid learning set in motion a slow, state-dependent increase in V1b firing, that began after learning was complete and persisted for days. This upward firing rate plasticity was gradual, occurred selectively during wake states, and in L2/3 was driven by a TNF-dependent increase in excitatory synapses and excitatory synaptic charge onto pyramidal neurons - all features of homeostatic forms of plasticity within V1. Finally, TNF inhibition administered after learning was complete diminished this increase in excitability and impaired the retention of hunting skills. Taken together, these data suggest that naturalistic learning in juvenile animals co-opts homeostatic forms of plasticity to reset firing rate setpoints within V1b, in a process that facilitates skill consolidation.

neuroscience↗

bioRxiv2025

Prey capture learning drives critical period-specific plasticity in mouse binocular visual cortex

Critical periods are developmental windows of high experience-dependent plasticity essential for the correct refinement of neuronal circuitry and function. While the consequences for the visual system of sensory deprivation during the critical period have been well-characterized, far less is known about the effects of enhanced sensory experience. Here, we use prey capture learning to assess structural and functional plasticity mediating visual learning in the primary visual cortex of critical period mice. We show that prey capture learning improves temporal frequency discrimination and drives a profound remodeling of visual circuitry through an increase in excitatory connectivity and spine turnover. This global and persistent rewiring is not observed in adult hunters and is mediated by TNF-dependent mechanisms. Our findings demonstrate that enhanced visual experience in a naturalistic paradigm during the critical period can drive structural plasticity to improve visual function, and promotes a long-lasting increase in spine dynamics that could enhance subsequent plasticity.

neuroscience↗

bioRxiv2020

Ciliary neuropeptidergic signaling dynamically regulates excitatory synapses in postnatal neocortical pyramidal neurons

Primary cilia are compartmentalized sensory organelles present on the majority of neurons in the mammalian brain throughout adulthood. Recent evidence suggests that cilia regulate multiple aspects of neuronal development, including the maintenance of neuronal connectivity. However, whether ciliary signals can dynamically modulate postnatal circuit excitability is unknown. Here we show that acute cell-autonomous knockdown of ciliary signaling rapidly strengthens glutamatergic inputs onto cultured neocortical pyramidal neurons, and increases spontaneous firing. This increased excitability occurs without changes to passive neuronal properties or intrinsic excitability. Further, the neuropeptide receptor somatostatin receptor 3 (SSTR3) is localized nearly exclusively to excitatory neuron cilia both in vivo and in culture, and pharmacological manipulation of SSTR3 signaling bidirectionally modulates excitatory synaptic inputs onto these neurons. Our results indicate that ciliary neuropeptidergic signaling dynamically modulates excitatory synapses, and suggest that defects in this regulation may underlie a subset of behavioral and cognitive disorders associated with ciliopathies.

neuroscience↗

bioRxiv2019

Stability of cortical synapses across sleep and wake

Sleep is important for brain plasticity, but its exact function remains mysterious. An influential but controversial idea is that a crucial function of sleep is to drive widespread downscaling of excitatory synaptic strengths. Here we used real-time sleep classification, ex vivo measurements of postsynaptic strength, and in vivo optogenetic monitoring of thalamocortical synaptic efficacy to ask whether sleep and wake states can constitutively drive changes in synaptic strength within the neocortex of juvenile rats. We found that miniature EPSC amplitudes onto L4 and L2/3 pyramidal neurons were stable across sleep and wake dense epochs in both primary visual (V1) and prefrontal cortex (PFC). Further, chronic monitoring of thalamocortical synaptic efficacy in V1 of freely behaving animals revealed stable responses across even prolonged periods of natural sleep and wake. Together these data demonstrate that neocortical synaptic strengths are remarkably stable across sleep and wake states, and provide strong evidence against the view that sleep drives widespread synaptic downscaling at neocortical synapses.

neuroscience↗

bioRxiv2018

Sensory Deprivation Independently Regulates Neocortical Feedforward and Feedback Excitation-Inhibition Ratio

Brief (2-3d) monocular deprivation (MD) during the critical period induces a profound loss of responsiveness within layer 4 of primary visual cortex (V1). This has largely been ascribed to long-term depression (LTD) at thalamocortical synapses onto pyramidal neurons, while a contribution from intracortical inhibition has been controversial. Here we used optogenetics to probe feedforward thalamocortical and feedback intracortical excitation-inhibition (E-I) ratios following brief MD. While thalamocortical inputs onto pyramidal neurons were depressed, there was stronger depression onto PV+ interneurons, which shifted the thalamocortical-evoked E-I ratio toward excitation. In contrast, feedback intracortical E-I ratio was shifted toward inhibition, and a computational model of layer 4 demonstrated that these opposing shifts produced an overall suppression of layer 4 excitability. Thus, feedforward and feedback E-I ratios onto the same postsynaptic target can be independently regulated by visual experience, and enhanced feedback inhibition is the primary driving force behind loss of visual responsiveness.

neuroscience↗