Evidence That REM Sleep Is Controlled by the Activation of Brain Stem Pedunculopontine Tegmental Kainate Receptor

2002 ◽  
Vol 87 (4) ◽  
pp. 1790-1798 ◽  
Author(s):  
Subimal Datta
Keyword(s):  
Brain Stem ◽  
Rem Sleep ◽  
Kainate Receptors ◽  
Specific Receptor ◽  
Cell Compartment ◽  
Pharmacological Blockade ◽  
Specific Receptors ◽  
Cholinergic Cell ◽  
First Time ◽  
The Brain

Glutamate, the neurotransmitter, enhances rapid-eye-movement (REM) sleep when microinjected into the brain stem pedunculopontine tegmentum (PPT) of the cat and rat. Glutamate and its various receptors are normally present in the PPT cholinergic cell compartment. The aim of this study was to identify which specific receptor(s) in the cholinergic cell compartment of the PPT are involved in glutamate-induced-REM sleep. To identify these glutamate-induced REM-sleep-generating receptor(s) in the PPT cholinergic cell compartment, specific receptors were pharmacologically blocked differentially by localized pretreatment of specific glutamate receptor antagonists; glutamate was then microinjected into the PPT cholinergic cell compartment while quantifying the effects on REM sleep in freely moving chronically instrumented rats. The results demonstrate that when kainate receptors were blocked by pretreatment with a kainate-specific receptor antagonist, microinjection of glutamate was unable to induce REM sleep. Pharmacological blockade of specific N-methyl-d-aspartate and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors was unable to block glutamate-microinjection-induced-REM sleep. These findings suggest, for the first time, that the activation of kainate receptors within the cholinergic cell compartment of the PPT is an essential portion of the mechanism for the generation of glutamate-induced REM sleep in the rat.

Excitation of the Brain Stem Pedunculopontine Tegmentum Cholinergic Cells Induces Wakefulness and REM Sleep

1997 ◽  
Vol 77 (6) ◽  
pp. 2975-2988 ◽  
Author(s):  
Subimal Datta ◽  
Donald F. Siwek
Keyword(s):  
Brain Stem ◽  
Slow Wave ◽  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Cholinergic Neurons ◽  
Dependent Manner ◽  
Cell Compartment ◽  
Recording Time ◽  
Cholinergic Cell ◽  
The Brain

Datta, Subimal and Donald F. Siwek. Excitation of the brain stem pedunculopontine tegmentum cholinergic cells induces wakefulness and REM sleep. J. Neurophysiol. 77: 2975–2988, 1997. Considerable evidence suggests that brain stem pedunculopontine tegmentum (PPT) cholinergic cells are critically involved in the normal regulation of wakefulness and rapid eye movement (REM) sleep. However, much of this evidence comes from indirect studies. Thus, although involvement of PPT cholinergic neurons has been suggested by numerous investigations, the excitation of PPT cholinergic neurons causal to the behavioral state of wakefulness and REM sleep has never been directly demonstrated. In the present study we examined the effects of three different levels of activation of PPT cholinergic cells in wakefulness and sleep behavior. The effects of glutamate on the activity of PPT cholinergic cells were studied by microinjection of one of the three different doses of l-glutamate (0.3, 1.0, and 3.0 μg) or saline (vehicle control) into the PPT cholinergic cell compartment while quantifying the effects on wakefulness and sleep in free moving chronically instrumented cats. All microinjections were made during wakefulness and were followed by 4 h of recording. Polygraphic records were scored for wakefulness, slow-wave sleep states 1 and 2, slow-wave sleep with pontogeniculooccipital waves, and REM sleep. Dependent variables quantified after each microinjection included the percentage of recording time spent in each state, the latency to onset of REM sleep, the number of episodes per hour for REM sleep, and the duration of each REM sleep episode. A total of 48 microinjections was made into 12 PPT sites in six cats. Microinjection of 0.3- and 1.0-μg doses of l-glutamate into the cholinergic cell compartment of the PPT increased the total amount of REM sleep in a dose-dependent manner. Both doses of l-glutamate increased REM sleep at the expense of slow-wave sleep but not wakefulness. Microinjection of 3.0 μg l-glutamate kept animals awake for 2–3 h by eliminating slow-wave and REM sleep. The results show that the microinjection of the excitatory amino acid l-glutamate into the PPT cholinergic cell compartments can increase wakefulness and/or REM sleep depending on the l-glutamate dosage. These findings unambiguously confirm the hypothesis that the excitation of the PPT cholinergic cells is causal to the generation of wakefulness and REM sleep.

scholarly journals Spontaneous REM Sleep Is Modulated By the Activation of the Pedunculopontine Tegmental GABAB Receptors in the Freely Moving Rat

2004 ◽  
Vol 91 (4) ◽  
pp. 1822-1831 ◽  
Author(s):  
Jagadish Ulloor ◽  
Vijayakumar Mavanji ◽  
Subhash Saha ◽  
Donald F. Siwek ◽  
Subimal Datta
Keyword(s):  
Rem Sleep ◽  
Gabab Receptors ◽  
Optimum Dose ◽  
Dependent Manner ◽  
Specific Receptors ◽  
Cholinergic Cell ◽  
Freely Moving ◽  
Dose Dependent ◽  
The Brain

Considerable evidence suggests that the neurotransmitter γ-aminobutyric acid (GABA)-ergic system and pedunculopontine tegmentum (PPT) in the brain stem are critically involved in the regulation of rapid-eye-movement (REM) sleep. GABA and its various receptors are normally present in the PPT cholinergic cell compartment. The aim of this study was to identify the role of GABA and its receptors in the regulation of REM sleep. To achieve this aim, specific receptors were activated differentially by local microinjection of selective GABA receptor agonists into the PPT while quantifying its effects on REM sleep in freely moving chronically instrumented rats ( n = 21). The results demonstrated that when GABAB receptors were activated by local microinjection of a GABAB receptor selective agonist, baclofen, spontaneous REM sleep was suppressed in a dose-dependent manner. The optimum dose for REM sleep reduction was 1.5 nmol. In contrast, when GABAA and GABAC receptors were activated by microinjecting their receptor selective agonists, isoguvacine (ISGV) and cis-4-aminocrotonic acid (CACA), respectively, the total percentages of REM sleep did not change compared with the control values. In another eight freely moving rats, effects of baclofen application was tested on firing rates of REM-on cells ( n = 12). Of those 12 neurons, 11 stopped firing immediately after application of baclofen [latency: 50 ± 14 s (SD)] and remained almost silent for 130 ± 12 min. Findings of the present study provide direct evidence that the PPT GABAB receptors and REM-on cells are involved in the regulation of REM sleep.

scholarly journals Mouse IgG3 binding to macrophage-like cells is prevented by deglycosylation of the antibody or by Accutase treatment of the cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Alicja Karabasz ◽  
Monika Bzowska ◽  
Joanna Bereta ◽  
Maria Czarnek ◽  
Maja Sochalska ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Complex Network ◽  
Immune Cells ◽  
Specific Receptor ◽  
Fcγ Receptors ◽  
Specific Receptors ◽  
First Time

AbstractThe binding of mouse IgG3 to Fcγ receptors (FcγR) and the existence of a mouse IgG3-specific receptor have been discussed for 40 years. Recently, integrin beta-1 (ITGB1) was proposed to be a part of an IgG3 receptor involved in the phagocytosis of IgG3-coated pathogens. We investigated the interaction of mouse IgG3 with macrophage-like J774A.1 and P388D1 cells. The existence of an IgG3-specific receptor was verified using flow cytometry and a rosetting assay, in which erythrocytes clustered around the macrophage-like cells coated with an erythrocyte-specific IgG3. Our findings confirmed that receptors binding antigen-free IgG3 are present on J774A.1 and P388D1 cells. We demonstrated for the first time that the removal of N-glycans from IgG3 completely abolished its binding to the cells. Moreover, we discovered that the cells treated with Accutase did not bind IgG3, indicating that IgG3-specific receptors are substrates of this enzyme. The results of antibody-mediated blocking of putative IgG3 receptors suggested that apart from previously proposed ITGB1, FcγRII, FcγRIII, also additional, still unknown, receptor is involved in IgG3 binding. These findings indicate that there is a complex network of glycan-dependent interactions between mouse IgG3 and the surface of effector immune cells.

REM Sleep without Muscle Atonia (Stage 1-REM) and Its Relation to Delirious Behavior during Sleep in Patients with Degenerative Diseases Involving the Brain Stem

1990 ◽  
Vol 44 (4) ◽  
pp. 681-692 ◽  
Author(s):  
Tetsuo Shimizu ◽  
Yasushi Inami ◽  
Yoshio Sugita ◽  
Susami Iijima ◽  
Yoshio Teshima ◽  
...  
Keyword(s):  
Brain Stem ◽  
Rem Sleep ◽  
Degenerative Diseases ◽  
Muscle Atonia ◽  
Stage 1 ◽  
The Brain

The Latero-Medial Inferior Pontine Syndrome

1975 ◽  
Vol 84 (3) ◽  
pp. 379-383 ◽  
Author(s):  
Edward L. Applebaum ◽  
R. J. Lawrence Ferguson
Keyword(s):  
Brain Stem ◽  
Cranial Nerves ◽  
Complete Recovery ◽  
Vascular Lesion ◽  
Diagnostic Evaluation ◽  
Clinical Syndromes ◽  
Brain Scan ◽  
First Time ◽  
Total Deafness ◽  
The Brain

A case is presented with a pontine vascular lesion involving the V, VI, VII, and VIII cranial nerves. The diagnostic evaluation included audiometry and electronystagmography as well as arteriography, pneumoencephalography, and brain scan. Total deafness developed in the involved ear and was present for seven weeks before complete recovery occurred. Electronystagmographic findings consistent with a brain stem lesion also resolved following recovery of the patient. Audiometry and electronystagmography are described and documented for the first time in a report of a patient with a latero-medial inferior pontine syndrome. A discussion of some of the unique features of the brain stem vasculature and its relationship to clinical syndromes involving the brain stem is given.

Cluster Headache-Like Pain Caused by an Upper Cervical Meningioma

Cephalalgia ◽  
1984 ◽  
Vol 4 (3) ◽  
pp. 185-186 ◽  
Author(s):  
Arieh Kuritzky
Keyword(s):  
Cluster Headache ◽  
Lung Disease ◽  
Brain Stem ◽  
Chronic Lung Disease ◽  
Rem Sleep ◽  
Early Morning ◽  
Upper Cervical ◽  
Lower Brain Stem ◽  
The Brain

A 68-year-old man with chronic lung disease suffered from cluster headache (CH)-like pain associated with an upper cervical meningioma extending to compress the lower brain stem. The pain disappeared after tumour excision. We suggest that compression of the brain stem and hypoxemia associated with chronic lung disease might have caused the attacks. especially in the early morning when REM sleep hypoxia was prevalent. It is also suggested that in atypical resistant cases of CH-like pain where therapy fails. efforts should be made to rule

Chronic intermittent hypoxia alters neurotransmission from lateral paragigantocellular nucleus to parasympathetic cardiac neurons in the brain stem

2015 ◽  
Vol 113 (1) ◽  
pp. 380-389 ◽  
Author(s):  
Olga Dergacheva
Keyword(s):  
Brain Stem ◽  
Rem Sleep ◽  
Cardiovascular Events ◽  
Intermittent Hypoxia ◽  
Female Rats ◽  
Parasympathetic Activity ◽  
Male Rats ◽  
Chronic Intermittent Hypoxia ◽  
Gabaergic Neurotransmission ◽  
The Brain

Patients with sleep-related disorders, including obstructive sleep apnea (OSA), have an increased risk of cardiovascular diseases. OSA events are more severe in rapid eye movement (REM) sleep. REM sleep further increases the risk of adverse cardiovascular events by diminishing cardioprotective parasympathetic activity. The mechanisms underlying REM sleep-related reduction in parasympathetic activity likely include activation of inhibitory input to cardiac vagal neurons (CVNs) in the brain stem originating from the lateral paragigantocellular nucleus (LPGi), a nucleus that plays a role in REM sleep control. This study tests the hypothesis that chronic intermittent hypoxia and hypercapnia (CIHH), an animal model of OSA, inhibits CVNs because of exaggeration of the GABAergic pathway from the LPGi to CVNs. GABAergic neurotransmission to CVNs evoked by electrical stimulation of the LPGi was examined with whole cell patch-clamp recordings in an in vitro brain slice preparation in rats exposed to CIHH and control rats. GABAergic synaptic events were enhanced after 4-wk CIHH in both male and female rats, to a greater degree in males. Acute hypoxia and hypercapnia (H/H) reversibly diminished the LPGi-evoked GABAergic neurotransmission to CVNs. However, GABAergic synaptic events were enhanced after acute H/H in CIHH male animals. Orexin-A elicited a reversible inhibition of LPGi-evoked GABAergic currents in control animals but evoked no significant changes in CIHH male rats. In conclusion, exaggerated inhibitory neurotransmission from the LPGi to CVNs in CIHH animals would reduce cardioprotective parasympathetic activity and enhance the risk of adverse cardiovascular events.

scholarly journals Mapping pain activation and connectivity of the human habenula

2012 ◽  
Vol 107 (10) ◽  
pp. 2633-2648 ◽  
Author(s):  
L. Shelton ◽  
G. Pendse ◽  
N. Maleki ◽  
E. A. Moulton ◽  
A. Lebel ◽  
...  
Keyword(s):  
Brain Stem ◽  
Emotional Processing ◽  
Experimental Pain ◽  
Brain Regions ◽  
Periaqueductal Gray ◽  
Noxious Heat ◽  
Interpeduncular Nucleus ◽  
Efferent Connections ◽  
First Time ◽  
The Brain

The habenula, located in the posterior thalamus, is implicated in a wide array of functions. Animal anatomical studies have indicated that the structure receives inputs from a number of brain regions (e.g., frontal areas, hypothalamic, basal ganglia) and sends efferent connections predominantly to the brain stem (e.g., periaqueductal gray, raphe, interpeduncular nucleus). The role of the habenula in pain and its anatomical connectivity are well-documented in animals but not in humans. In this study, for the first time, we show how high-field magnetic resonance imaging can be used to detect habenula activation to noxious heat. Functional maps revealed significant, localized, and bilateral habenula responses. During pain processing, functional connectivity analysis demonstrated significant functional correlations between the habenula and the periaqueductal gray and putamen. Probabilistic tractography was used to assess connectivity of afferent (e.g., putamen) and efferent (e.g., periaqueductal gray) pathways previously reported in animals. We believe that this study is the first report of habenula activation by experimental pain in humans. Since the habenula connects forebrain structures with brain stem structures, we suggest that the findings have important implications for understanding sensory and emotional processing in the brain during both acute and chronic pain.

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