Education & Certifications

  • Doctor of Philosophy, Stanford University, NEURS-PHD (2014)
  • Bachelor of Science, Stanford University, ENGR-BS (2004)


Journal Articles

  • Controlling brain States. Neuron Bennett, C., Arroyo, S., Hestrin, S. 2014; 83 (2): 260-261


    Neurons in mouse V1 increase their response to visual stimulation during locomotion. In this issue of Neuron, Lee et al. (2014) show that subthreshold optogenetic stimulation of a brainstem locomotion area can mimic the effect of locomotion on sensory processing.

    View details for DOI 10.1016/j.neuron.2014.07.007

    View details for PubMedID 25033175

  • Nicotinic modulation of cortical circuits FRONTIERS IN NEURAL CIRCUITS Arroyo, S., Bennett, C., Hestrin, S. 2014; 8
  • Subthreshold Mechanisms Underlying State-Dependent Modulation of Visual Responses NEURON Bennett, C., Arroyo, S., Hestrin, S. 2013; 80 (2): 350-357


    The processing of sensory information varies widely across behavioral states. However, little is known about how behavioral states modulate the intracellular activity of cortical neurons to effect changes in sensory responses. Here, we performed whole-cell recordings from neurons in upper-layer primary visual cortex of awake mice during locomotion and quiet wakefulness. We found that the signal-to-noise ratio for sensory responses was improved during locomotion by two mechanisms: (1) a decrease in membrane potential variability leading to a reduction in background firing rates and (2) an enhancement in the amplitude and reliability of visually evoked subthreshold responses mediated by an increase in total conductance and a depolarization of the stimulus-evoked reversal potential. Consistent with the enhanced signal-to-noise ratio for visual responses during locomotion, we demonstrate that performance is improved in a visual detection task during this behavioral state.

    View details for DOI 10.1016/j.neuron.2013.08.007

    View details for Web of Science ID 000326196400017

    View details for PubMedID 24139040

  • Mechanisms Generating Dual-Component Nicotinic EPSCs in Cortical Interneurons JOURNAL OF NEUROSCIENCE Bennett, C., Arroyo, S., Berns, D., Hestrin, S. 2012; 32 (48): 17287-17296


    Activation of cortical nicotinic receptors by cholinergic axons from the basal forebrain (BF) significantly impacts cortical function, and the loss of nicotinic receptors is a hallmark of aging and neurodegenerative disease. We have previously shown that stimulation of BF axons generates a fast ?7 and a slow non-?7 receptor-dependent response in cortical interneurons. However, the synaptic mechanisms that underlie this dual-component nicotinic response remain unclear. Here, we report that fast ?7 receptor-mediated EPSCs in the mouse cortex are highly variable and insensitive to perturbations of acetylcholinesterase (AChE), while slow non-?7 receptor-mediated EPSCs are reliable and highly sensitive to AChE activity. Based on these data, we propose that the fast and slow nicotinic responses reflect differences in synaptic structure between cholinergic varicosities activating ?7 and non-?7 classes of nicotinic receptors.

    View details for DOI 10.1523/JNEUROSCI.3565-12.2012

    View details for Web of Science ID 000311794700024

    View details for PubMedID 23197720

  • Prolonged Disynaptic Inhibition in the Cortex Mediated by Slow, Non-alpha 7 Nicotinic Excitation of a Specific Subset of Cortical Interneurons JOURNAL OF NEUROSCIENCE Arroyo, S., Bennett, C., Aziz, D., Brown, S. P., Hestrin, S. 2012; 32 (11): 3859-3864


    Cholinergic activation of nicotinic receptors in the cortex plays a critical role in arousal, attention, and learning. Here we demonstrate that cholinergic axons from the basal forebrain of mice excite a specific subset of cortical interneurons via a remarkably slow, non-?7 nicotinic receptor-mediated conductance. In turn, these inhibitory cells generate a delayed and prolonged wave of disynaptic inhibition in neighboring cortical neurons, altering the spatiotemporal pattern of inhibition in cortical circuits.

    View details for DOI 10.1523/JNEUROSCI.0115-12.2012

    View details for Web of Science ID 000301525900024

    View details for PubMedID 22423106

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