SLEEP 2011 Abstract Supplement

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A. Basic Science IV. Neurobiology μM) and APV (40 μM) to block fast synaptic transmission. Whole-cell patch clamp was used to record subthreshold oscillations in SubC neurons in current clamp mode before and after application of the sodium channel blocker tetrodotoxin (TTX, 1-10 μM). Results: Subthreshold oscillations in the gamma frequency range were observed using ramp and various membrane holding potential protocols in all SubC cells (n=12) in the presence of fast synaptic blockers. These oscillations were blocked by application of TTX (n=8, p
A. Basic Science IV. Neurobiology the interactive effects of stimulation of the CNA and the PPT on the intracellularly recorded activity of NPO neurons were examined. Methods: Experiments were performed on urethane-anesthetized, adult male Sprague-Dawley rats. NPO neurons were recorded with glass micropipettes filled with 3 M KCl in conjunction with ipsilateral electrical stimulation of the CNA (100 to 400 μA) and the PPT (10 to 50 μA). Results: Stimulation of either the CNA or the PPT evoked short-latency EPSPs in neurons within the NPO. Concurrent stimulation of the CNA and the PPT potentiated the effects of stimulation of either site by itself. The amplitude of PPT-evoked EPSPs in NPO neurons increased by 20 to 58% when stimulation of the PPT was preceded by stimulation of the CNA at an interval of 3 to 15 ms, and vice-versa. Maximal facilitation occurred when the CNA and PPT were stimulated with an interval of 8 to 10 ms. Simultaneous subthreshold stimuli of the CNA and the PPT resulted in the discharge of NPO neurons. Conclusion: The present data provide evidence that there are converging excitatory synaptic inputs from the amygdala and the PPT that facilitate the discharge of neurons in the NPO. Therefore, we suggest that the amygdala is capable of inducing active sleep by promoting the discharge of active sleep-on neurons in the NPO and by its interactions with projections from the PPT. Support (If Any): USPHS Grant NS060917 0092 ELECTROPHYSIOLOGICAL IDENTIFICATION OF SLEEP ACTIVE NEURONS IN RAT BASAL FOREBRAIN Van Dort CJ 1,2 , Flores FJ 1,2 , Wilson MA 2,3 , Brown EN 1,2,4 1 Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA, 2 Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA, 3 Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA, USA, 4 Harvard-MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology, Cambridge, MA, USA Introduction: Inhibitory neurons in the preoptic area are important for induction of non-rapid eye movement (NREM) sleep in many species. Cholinergic neurons in the brainstem and basal forebrain mediate rapid eye movement (REM) sleep induction. Sleep-active neurons have also been found by electrophysiological recordings in the medial basal forebrain of cat - specifically the horizontal limb of the diagonal band of Broca (hDB). Electrical stimulation of this area in the cat induces sleep, suggesting that these neurons are involved in sleep induction. However, no one has identified sleep active cells in the corresponding area of the hDB in rodents. Therefore, this study investigated the sleep state dependent firing patterns of neurons in the hDB of rat. Methods: Adult male Sprague-Dawley rats were implanted with microdrives containing movable tetrodes aimed for the hDB and electroencephalogram (EEG) and electromyogram (EMG) recording electrodes. The tetrodes were adjusted to yield single unit isolation across the hDB. Spikes, EEG, and EMG were recorded across multiple spontaneous sleep wake cycles. Single neurons were clustered offline using M-Clust in Matlab and sleep was scored visually using Spike2. Results: Four main categories of neurons were identified that demonstrated state dependent firing. There were 5 Wake-on neurons, 5 Wake/ REM-on neurons, 14 NREM/REM-on neurons, and 14 REM-on neurons. Significant differences in firing rate between states were determined using 95% confidence intervals computed with a non-parametric bootstrap. Conclusion: While much of the cholinergic basal forebrain is involved in arousal and REM sleep generation, approximately 37% of recorded cells in the hDB showed an increased firing rate during both NREM and REM sleep compared to wakefulness. These data suggest that in addition to cholinergic arousal promoting neurons in the rat basal forebrain, a non-cholinergically mediated sleep induction mechanism may also exist. Support (If Any): National Institutes of Health grants OD003646-01 and HL07901 0093 STATE-SPECIFIC ACTIVITY OF CORTICAL SLEEP-ACTIVE NEURONS DOES NOT REQUIRE PRESENCE OF NEURONAL NITRIC OXIDE SYNTHASE Dittrich L, Morairty S, Warrier D, Silveira K, Kilduff TS Biosciences Division, SRI International, Menlo Park, CA, USA Introduction: Recently, our lab identified a population of sleep-active cortical neurons. These neurons express Fos during sleep but not during wake and can be readily identified histochemically because they express the enzyme neuronal nitric oxide synthase (nNOS). However, it is unclear what functions cortical nNOS neurons have in sleep and whether the nitric oxide produced feeds back (directly or indirectly) on the activation of this neuronal population. In the present study, we asked whether the enzymatic activity of nNOS is critical for the regulation of the state-specific activity of cortical sleep-active neurons. Methods: Of the 15 male nNOS knockout (KO) mice (B6;129S4-Nos- 1tm1Plh) and 20 nNOS control mice (B6129SF2/J) implanted for EEG and EMG recordings using either telemetry or conventional techniques described in the accompanying abstract by Morairty et al., 13 nNOS KO and 15 controls were sleep deprived (SD) for 6 h by gentle handling. 5 nNOS KO and 6 controls were perfused immediately following SD, 8 nNOS KO and 9 controls mice were allowed 2.5 h recovery sleep (RS) before perfusion (ZT 8.5 for all animals). In the absence of nNOS, the sleep-active cortical neurons were identified by immunoreactivity for NK1, the cortical expression of which occurs almost exclusively in nNOS-immunoreactive neurons in wild type mice. Neuronal activity was assessed by double-labeling with Fos. Results: The proportion of Fos-positive cells among the cortical NK1- immunoreactive neuronal population was greater during RS than during SD in both controls and nNOS KO mice. The proportion of Fos-positive cells did not differ between the genotypes. Conclusion: These results indicate that nNOS is not necessary for the activation of cortical interneurons during sleep. Support (If Any): Supported by the NIH grant R01 HL59658. 0094 SLEEP ACTIVE NEURONS IN THE CAUDAL BRAIN STEM Thankachan S, Lu J Neurology, Beth Israel Deaconess Medical Center & Harvard Medical School, Boston, MA, USA Introduction: Early brainstem transection studies indicated the existence of a sleep promoting system in the medullary brainstem although its precise location has been never identified. Electrical stimulation of the solitary tract nucleus (NTS) and dorsal reticular formation produced cortical EEG synchronization suggestive of inducing NREM sleep. Although the nucleus of solitary tract (NTS) in the caudal medulla has been proposed to be a potential candidate for the medullary sleep system, the evidence for this claim has been not substantiated. A recent observations from our lab showed that cell specific lesions using orexin-saporin of NTS had no affect on the sleep-wake percentages, but, lesion of the structure rostral to NTS; dorsal and lateral to facial nerve (referred to as parafacial zone; PZ) showed about 50% increase in wakefulness. Interestingly, the PZ also corresponds to the region where stroke caused severe insomnia in a human case. In order to get a direct evidence for the presence of the sleep active neurons in this area, we did extracellular single-unit recordings of the neurons in PZ in the freely behaving animals. Methods: Male Sprague-Dawley rats were implanted with electrodes to record sleep-wake behavior and a microwire assembly to record single neurons from the parafacial zone (PZ). After post-surgical recovery and A35 SLEEP, Volume 34, Abstract Supplement, 2011
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