167 research outputs found
Restoring arm function with a soft robotic wearable for individuals with amyotrophic lateral sclerosis
No full textC1 Neurons in the RVLM: Are they catecholaminergic in name only? (Commentary on Abbott et al.)
No full textAdvances in Parasympathetic Control of Heart Rate and Cardiac Function
No full textIt is well known that the neuronal projections from the brain to the heart strongly influence cardiac function, and an abnormal activity has been implicated in diseases such as cardiac arrhythmia and sudden infant death syndrome. This short review describes recent advances focused on the neurobiology of cardiac vagal neurons, utilizing cellular techniques.</jats:p
Intranasal Oxytocin Administration in Patients Suffering from Obstructive Sleep Apnea
No full textObstructive sleep apnea is a condition that affects millions of people yet very few treatment options exist. People with OSA cease breathing multiple times during the night. If left untreated, besides poor sleep quality and excessive daytime fatigue, OSA can lead to more serious conditions such as hypertension, arrhythmias and other cardiovascular consequences. The current recommended treatment is continuous positive airway pressure with which many patients are poorly compliant. Previous work in the Mendelowitz lab has demonstrated a cardioprotective role of oxytocin in a rodent model of OSA. We therefore hypothesized intranasal administration of oxytocin to patients suffering from OSA can have similar benefits on autonomic function. Patients suffering from OSA underwent sleep studies on two consecutive nights. Night one served as a control while intranasal oxytocin was administered on the second night at the start of the sleep study. The recorded sleep studies were then analyzed examining differences in heart rate, oxygen saturation and air flow during apneic events between the two nights
Role of Purinergic and Nicotinic Receptors in the Hypoxia/Hypercapnia Evoked Excitation of Parasympathetic Cardiac Vagal Neurons in the Brainstem
No full textAbstractHypoxia and hypercapnia are among the strongest challenges to the cardiorespiratory system, and these responses are altered by prenatal nicotine exposure. However the mechanism(s) responsible for these cardiorespiratory responses, and their alteration by prenatal nicotine exposure are unknown. We used an in vitro medullary slice that allows simultaneous examination of rhythmic respiratory-related activity and synaptic neurotransmission to cardiac vagal neurons (CVNs) that control heart rate. Respiratory-related increases in excitatory neurotransmission only occurred upon recovery from hypoxia/hypercapnia in unexposed animals. These responses were mediated in part by purinergic receptors. Prenatal nicotine exposure transformed central cardiorespiratory responses; CVNs received a respiratory-related neurotransmission not during recovery but during hypoxia/hypercapnia which was wholly dependent upon nicotinic receptor activation. In the presence of nicotinic antagonists, the responses in prenatal nicotine animals reverted to the pattern of responses in unexposed animals. These data identify a new functional role for purinergic receptors in the cardiorespiratory responses to hypoxia/hypercapnia and their role in occluding nicotinic receptor activation with prenatal nicotine exposure. [Tzu Chi Med J 2008;20(1):1–10
Superior laryngeal neurons directly excite cardiac vagal neurons within the nucleus ambiguus
No full textThe aim of this study was to test whether superior laryngeal neurons have axon collaterals that synapse upon cardiac vagal neurons. Superior laryngeal neurons were tested as likely mediators of cardio-respiratory interaction because these neurons are active in post-inspiration, co- localized with cardiac vagal neurons, and have many axon collaterals within the nucleus ambiguus. Nontoxic fluorescent tracers were utilized to identify, in vitro, both superior laryngeal neurons that innervated the crico-thyroid muscle, and cardiac vagal neurons that projected to cardiac ganglia. Co- localization of these two populations of neurons demonstrated that cardiac vagal and superior laryngeal neurons are both co-localized in the nucleus ambiguus. Simultaneous dual patch clamp recordings were used to either inject depolarizing current and evoke an action potential (current clamp configuration) or control the voltage and depolarize an identified single superior laryngeal neuron (voltage clamp configuration) while simultaneously recording from a cardiac vagal neuron. Depolarization of some, but not all, individual superior laryngeal neurons elicited post-synaptic excitatory currents in cardiac vagal neurons, indicating that at least some superior laryngeal neurons monosynaptically synapse upon cardiac vagal neurons within the nucleus ambiguus. (C) 2000 Elsevier Science Inc
How Does Angiotensin Activate Hypothalamic Neurons Essential for Controlling Sympathetic Activity and Blood Pressure?
No full textNicotine excites cardiac vagal neurons via three sites of action
No full text1. Nicotine is involved in many cardio-respiratory diseases, including hypertension and sudden infant death syndrome (SIDS), which is the most common cause of death in infants between 1 month and 1 year of age. While the aetiology of SIDS remains largely unknown, recent clinical studies suggest maternal cigarette smoking is a major risk factor in SIDS and an abnormality of cardio-respiratory control, particularly a centrally mediated slowing of the heart that precedes or accompanies apnoea, is involved. 2. Because the sites, mechanisms of action and diverse receptor types of nicotine within the central nervous system are controversial and poorly understood, in the present study we examined the effects of nicotine on specific brainstem neurons that control heart rate. Cardiac vagal neurons were identified in an in vitro slice preparation using a retrograde fluorescent tracer and were studied using both whole-cell and perforated patch-clamp electrophysiological techniques. 3. We have found there are different pre- and post-synaptic nicotinic receptors that have dramatic effects on glutamatergic neurotransmission as well as directly activating vagal cardioinhibitory neurons
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