A5019352493- Sleep and Wakefulness Research
- Neuroscience of respiration and sleep
- Sleep and related disorders
- Circadian rhythm and melatonin
- Neuroscience and Neuropharmacology Research
- Neuroendocrine regulation and behavior
- Obstructive Sleep Apnea Research
- Parkinson's Disease Mechanisms and Treatments
- Regulation of Appetite and Obesity
- Photoreceptor and optogenetics research
- Respiratory Support and Mechanisms
- Restless Legs Syndrome Research
- Infant Health and Development
- Zebrafish Biomedical Research Applications
- Neonatal and fetal brain pathology
- Neonatal Respiratory Health Research
- Heart Rate Variability and Autonomic Control
- Obesity, Physical Activity, Diet
- Infant Development and Preterm Care
- Cannabis and Cannabinoid Research
- Biochemical Analysis and Sensing Techniques
- Neural dynamics and brain function
- Neurological disorders and treatments
- Olfactory and Sensory Function Studies
- Bipolar Disorder and Treatment
University of Toronto
2015-2025
Stem Cell Network
2019
Muscular Dystrophy Canada
2011
University of California, Los Angeles
2002-2003
Hypocretin (Hcrt or orexin) somas are located in the hypothalamus and project widely to forebrain brainstem regions, densely innervating monoaminergic cholinergic cells. Loss of Hcrt function results sleep disorder narcolepsy. However, normal pattern release across sleep–wake cycle is unknown. We monitored Hcrt-1 basal forebrain, perifornical hypothalamus, locus ceruleus (LC) using microdialysis freely moving cats a sensitive solid phase radioimmunoassay. found that peptide concentration...
Bipolar disorder is a debilitating psychopathology with unknown etiology. Accumulating evidence suggests the possible involvement of Na + ,K -ATPase dysfunction in pathophysiology bipolar disorder. Here we show that Myshkin mice carrying an inactivating mutation neuron-specific α3 subunit display behavioral profile remarkably similar to patients manic state. increased Ca 2+ signaling cultured cortical neurons and phospho-activation extracellular signal regulated kinase (ERK) Akt hippocampus....
During REM sleep the CNS is intensely active, but skeletal motor system paradoxically forced into a state of muscle paralysis. The mechanisms that trigger paralysis are matter intense debate. Two competing theories argue it caused by either active inhibition or reduced excitation somatic motoneuron activity. Here, we identify transmitter and receptor function to silence muscles during sleep. We used behavioral, electrophysiological, pharmacology neuroanatomical approaches determine how...
Rapid eye movement (REM) sleep behavior disorder (RBD) is a neurological disease characterized by loss of normal REM motor inhibition and subsequent dream enactment. RBD clinically relevant because it predicts neurodegenerative onset (e.g., Parkinson's disease) problematic disrupts results in patient injuries hospitalization. Even though the cause unknown, multiple lines evidence indicate that abnormal inhibitory transmission underlies disorder. Here, we show transgenic mice with deficient...
Narcolepsy is characterized by excessive sleepiness and cataplexy, sudden episodes of muscle weakness during waking that are thought to be an intrusion rapid eye movement sleep atonia into wakefulness. One the most striking aspects cataplexy it often triggered strong, generally positive emotions, but little known about neural pathways through which emotions trigger atonia. We hypothesized amygdala functionally important for because has a role in processing emotional stimuli contains neurons...
A hallmark of rapid eye movement (REM) sleep is a potent suppression postural muscle tone. Motor control in REM unique because it characterized by flurries intermittent twitches that punctuate atonia. Because somatic motoneurons are bombarded strychnine-sensitive IPSPs during sleep, assumed glycinergic inhibition underlies However, has never been determined whether indeed responsible for triggering the loss tone sleep. Therefore, we used reverse microdialysis, electrophysiology, and...
Skeletal muscle tone is modulated in a stereotypical pattern across the sleep-wake cycle. Abnormalities this modulation contribute to most of major sleep disorders; therefore, characterizing neurochemical substrate responsible for transmitting drive somatic motoneurons needs be determined. Glutamate an excitatory neurotransmitter that modulates motoneuron excitability; however, its role regulating excitability and during natural behaviors unknown. Therefore, we used reverse-microdialysis,...
Hypocretin-1 and -2 (Hcrt-1 -2, also called orexin-A -B) are newly identified neuropeptides synthesized by hypothalamic neurons. Defects in the Hcrt system underlie sleep disorder narcolepsy, which is characterized fragmentation involuntary loss of muscle tone cataplexy. neurons project to multiple brain regions including cranial spinal motor nuclei. In vitro studies suggest that application can modulate presynaptic glutamate release. Together these observations affect output glutamatergic...
Highlights•Muscle tone and arousal state are decoupled by manipulation of the SLD•SLD activation promotes cataplexy, whereas SLD silencing prevents cataplexy•SLD triggers cataplexy in wild-type mice•The couples motor activity during REM sleep wakefulnessSummaryAppropriate levels muscle needed to support waking behaviors such as sitting or standing. However, it is unclear how brain functions couple with behaviors. Cataplexy a unique experiment nature which paralysis involuntarily intrudes...
Abstract The respiratory control system can exhibit neuronal plasticity following exposures to repetitive challenges. For example, repeated obstructive apneas trigger a form of that results in the enhancement inspiratory hypoglossal (XII) motoneuron activity. This increase motor output is known as long‐term facilitation (hLTF). In adult male Sprague–Dawley rats, we demonstrate hLTF also be triggered absence by intermittent optogenetic stimulation locus coeruleus (LC) neurons, or through...
AnimalsExperiments used male, hypocretin KO mice on a C57BL/6 background (n = 17; age: 15.1 ± 1.0 weeks; mass: 29.2 0.8g) and male wild-type (WT) littermates 21; 15.9 0.8 28.1 0.9g).Mice were genotyped using PCR with genomic primers 5'-GACGACGGCCTCAGACTTCTT-GGG, 3'-TCACCCCCTTGGG ATAGCCCTTCC, 5'-CC-GCTATCAGGACATAGCGTTGGC (with forward DOPAMINERGIC REGULATION