Neural plasticity, the ability of neurons to change their properties in response to experiences, underpins the nervous system's capacity to form memories and actuate behaviors. How different plasticity mechanisms act together in vivo and at a cellular level to transform sensory information into behavior is not well understood. We show that in Caenorhabditis elegans two plasticity mechanisms-sensory adaptation and presynaptic plasticity-act within a single cell to encode thermosensory information and actuate a temperature preference memory. Sensory adaptation adjusts the temperature range of the sensory neuron (called AFD) to optimize detection of temperature fluctuations associated with migration. Presynaptic plasticity in AFD is regulated by the conserved kinase nPKCε and transforms thermosensory information into a behavioral preference. Bypassing AFD presynaptic plasticity predictably changes learned behavioral preferences without affecting sensory responses. Our findings indicate that two distinct neuroplasticity mechanisms function together through a single-cell logic system to enact thermotactic behavior. VIDEO ABSTRACT.

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Sleep, a state of quiescence associated with growth and restorative processes, is conserved across species. Invertebrates including the nematode Caenorhabditis elegans exhibit sleep-like states during development, satiety, and stress. Here, we describe behavior and neural activity during sleep and awake states in adult C. elegans hermaphrodites using new microfluidic methods. We observed effects of fluid flow, oxygen, feeding, odors, and genetic perturbations on long-term sleep behavior over 12 h. We developed a closed-loop sleep detection system to automatically deliver chemical stimuli to assess sleep-dependent changes to evoked neural responses in individual animals. Sleep increased the arousal threshold to aversive stimulation, yet the associated sensory neuron and first-layer interneuron responses were unchanged. This localizes adult sleep-dependent neuromodulation within interneurons presynaptic to the premotor interneurons, rather than afferent sensory circuits. However, sleep prolonged responses in appetitive chemosensory neurons, suggesting that sleep modulates responsiveness specifically across sensory systems rather than broadly damping global circuit activity. SIGNIFICANCE STATEMENT Much is known about molecular mechanisms that facilitate sleep control. However, it is unclear how these pathways modulate neural circuit-level sensory processing or how misregulation of neural activity contributes to sleep disorders. The nematode Caenorhabditis elegans provides the ability to study neural circuitry with single-neuron resolution, and recent studies examined sleep states between developmental stages and when stressed. Here, we examine an additional form of spontaneous sleep in adult C. elegans at the behavioral and neural activity levels. Using a closed-loop system, we show that delayed behavioral responses to aversive chemical stimulation during sleep arise from sleep-dependent sensorimotor modulation localized presynaptic to the premotor circuit, rather than early sensory circuits.

OBJECTIVECavernous internal carotid artery (ICA) aneurysms are frequently diagnosed incidentally and the benign natural history of these lesions is well known, but there is limited information assessing the risk of growth in untreated patients. The authors sought to assess and analyze risk factors in patients with cavernous ICA aneurysms and compare them to those of patients with intracranial berry aneurysms in other locations.METHODSData from consecutive patients who were diagnosed with a cavernous ICA aneurysm were retrospectively reviewed. The authors evaluated patients for the incidence of cavernous ICA aneurysm growth and rupture. In addition, the authors analyzed risk factors for cavernous ICA aneurysm growth and compared them to risk factors in a population of patients diagnosed with intracranial berry aneurysms in locations other than the cavernous ICA during the same period.RESULTSIn 194 patients with 208 cavernous ICA aneurysms, the authors found a high risk of aneurysm growth (19.2% per patient-year) in patients with large/giant aneurysms. Size was significantly associated with higher risk of growth. Compared to patients with intracranial berry aneurysms in other locations, patients with cavernous ICA aneurysms were significantly more likely to be female and have a lower incidence of hypertension.CONCLUSIONSAneurysms of the cavernous ICA are benign lesions with a negligible risk of rupture but a definite risk of growth. Aneurysm size was found to be associated with aneurysm growth, which can be associated with new onset of symptoms. Serial follow-up imaging of a cavernous ICA aneurysm might be indicated to monitor for asymptomatic growth, especially in patients with larger lesions.

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Sleep, a state of quiescence associated with growth and restorative processes, is conserved across species. Invertebrates including the nematode Caenorhabditis elegans exhibit sleep-like states during development and periods of satiety and stress.Here we describe two methods to study behavior and associated neural activity during sleep and awake states in adult C. elegans. A large microfluidic device facilitates population-wide assessment of long-term sleep behavior over 12 h, including effects of fluid flow, oxygen, feeding, odors, and genetic perturbations. Smaller devices allow simultaneous recording of sleep behavior and neuronal activity, and a closed-loop sleep detection system delivers chemical stimuli to individual animals to assess sleepdependent changes to neural responses. Sleep increased the arousal threshold to aversive chemical stimulation, yet sensory neuron (ASH) and first-layer interneuron (AIB) responses were unchanged. This localizes adult sleep-dependent neuromodulation within interneurons presynaptic to the AVA premotor interneurons, rather than afferent sensory circuits. Supplementary Information Automated analysis of sleep in adult C. elegans with closed-loop assessment of state-dependent neural activity Lawler, et al.

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