scholarly journals Mapping and Identification of GABAergic Neurons in Transgenic Mice Projecting to Cardiac Vagal Neurons in the Nucleus Ambiguus Using Photo-Uncaging

2009 ◽  
Vol 101 (4) ◽  
pp. 1755-1760 ◽  
Author(s):  
J. G. Frank ◽  
H. S. Jameson ◽  
C. Gorini ◽  
D. Mendelowitz
Keyword(s):  
Neural Control ◽  
Gabaergic Neurons ◽  
Nucleus Ambiguus ◽  
Gabaergic Neurotransmission ◽  
Transgenic Mouse Line ◽  
Bötzinger Complex ◽  
Green Florescent Protein ◽  
Caged Glutamate ◽  
The Brain ◽  
Synaptic Responses

The neural control of heart rate is determined primarily by the activity of preganglionic parasympathetic cardiac vagal neurons (CVNs) originating in the nucleus ambiguus (NA) in the brain stem. GABAergic inputs to CVNs play an essential role in determining the activity of these neurons including a robust inhibition during each inspiratory burst. The origin of GABAergic innervation has yet to be determined however. A transgenic mouse line expressing green florescent protein (GFP) in GABAergic cells was used in conjunction with caged glutamate to identify both clusters and individual GABAergic neurons that evoke inhibitory GABAergic synaptic responses in CVNs. Transverse slices were taken with CVNs patch-clamped in the whole cell configuration. Sections containing both the pre-Botzinger complex as well as the calamus scriptorius were divided into ∼90 quadrants, each 200 × 200 μm and were sequentially photostimulated. Inhibitory post synaptic currents (IPSCs) were recorded in CVNs after a 5-ms photostimulation of 50 μM caged glutamate. The four areas that contained GABAergic cells projecting to CVNs were 200 μm medial, 400 μm medial, 200 μm ventral, and 1,200 μm dorsal and 1,000 μm medial to patched CVNs. Once foci of GABAergic cells projecting to CVNs were determined, photostimulation of individual GABAergic neurons was conducted. The results from this study suggest that GABAergic cells located in four specific areas project to CVNs, and that these cells can be individually identified and stimulated using photouncaging to recruit GABAergic neurotransmission to CVNs.

scholarly journals A Transgenic Mouse Line Expressing the Red Fluorescent Protein tdTomato in GABAergic Neurons

PLoS ONE ◽  
2015 ◽  
Vol 10 (6) ◽  
pp. e0129934 ◽  
Author(s):  
Stefanie Besser ◽  
Marit Sicker ◽  
Grit Marx ◽  
Ulrike Winkler ◽  
Volker Eulenburg ◽  
...  
Keyword(s):  
Transgenic Mouse ◽  
Fluorescent Protein ◽  
Gabaergic Neurons ◽  
Mouse Line ◽  
Red Fluorescent Protein ◽  
Transgenic Mouse Line

scholarly journals Significance of the Thalamic Reticular Nucleus GABAergic Neurons in Normal and Pathological Activity of the Brain

2012 ◽  
Vol 02 (04) ◽  
pp. 436-444 ◽  
Author(s):  
Zakaria I. Nanobashvili ◽  
Arkadi G. Surmava ◽  
Irine G. Bilanishvili ◽  
Maia G. Barbaqadze ◽  
Magda D. Mariamidze ◽  
...  
Keyword(s):  
Gabaergic Neurons ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
The Brain

Bidirectional Electrical Coupling Between Inspiratory Motoneurons in the Newborn Mouse Nucleus Ambiguus

1997 ◽  
Vol 78 (6) ◽  
pp. 3508-3510 ◽  
Author(s):  
Jens C. Rekling ◽  
Jack L. Feldman
Keyword(s):  
Brain Stem ◽  
Impulse Activity ◽  
Electrical Coupling ◽  
Postnatal Period ◽  
The Other ◽  
Nucleus Ambiguus ◽  
Newborn Mouse ◽  
Coupling Ratio ◽  
Newborn Mice ◽  
The Brain

Rekling, Jens C. and Jack L. Feldman. Bidirectional electrical coupling between inspiratory motoneurons in the newborn mouse nucleus ambiguus. J. Neurophysiol. 78: 3508–3510, 1997. Some spinal and brain stem motoneurons are electrically coupled in the early postnatal period. To test whether respiratory motoneurons in the brain stem are electrically coupled, we performed single and dual whole cell patch recordings from presumptive motoneurons in the nucleus ambiguus in a rhythmically active brain stem slice from newborn mice. Two of eight (25%) biocytin-injected neurons showed dye-coupling and 4 of 11 (36%) of intracellularly recorded pairs of neurons showed evidence of bidirectional electrical coupling. Impulse activity in one cell elicited small spikelets in the other and hyperpolarization of one cell led to hyperpolarization of the other with a coupling ratio (Δ V 2:Δ V 1) of 0.03–0.14. We conclude that inspiratory ambiguus motoneurons in the newborn mouse brain stem are bidirectionally electrically coupled, which may serve to transmit or coordinate signals, chemical or electrical.

scholarly journals Electroacupuncture Involved in Motor Cortex and Hypoglossal Neural Control to Improve Voluntary Swallowing of Poststroke Dysphagia Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-18
Author(s):  
Shuai Cui ◽  
Shuqi Yao ◽  
Chunxiao Wu ◽  
Lulu Yao ◽  
Peidong Huang ◽  
...  
Keyword(s):  
Motor Cortex ◽  
Neural Control ◽  
Primary Motor Cortex ◽  
Hypoglossal Nerve ◽  
Field Potential ◽  
Pyramidal Cells ◽  
Laser Speckle ◽  
Nucleus Ambiguus ◽  
Ventrolateral Medulla ◽  
Contrast Imaging

The descending motor nerve conduction of voluntary swallowing is mainly launched by primary motor cortex (M1). M1 can activate and regulate peripheral nerves (hypoglossal) to control the swallowing. Acupuncture at “Lianquan” acupoint (CV23) has a positive effect against poststroke dysphagia (PSD). In previous work, we have demonstrated that electroacupuncture (EA) could regulate swallowing-related motor neurons and promote swallowing activity in the essential part of central pattern generator (CPG), containing nucleus ambiguus (NA), nucleus of the solitary tract (NTS), and ventrolateral medulla (VLM) under the physiological condition. In the present work, we have investigated the effects of EA on the PSD mice in vivo and sought evidence for PSD improvement by electrophysiology recording and laser speckle contrast imaging (LSCI). Four main conclusions can be drawn from our study: (i) EA may enhance the local field potential in noninfarction area of M1, activate the swallowing-related neurons (pyramidal cells), and increase the motor conduction of noninfarction area in voluntary swallowing; (ii) EA may improve the blood flow in both M1 on the healthy side and deglutition muscles and relieve PSD symptoms; (iii) EA could increase the motor conduction velocity (MCV) in hypoglossal nerve, enhance the EMG of mylohyoid muscle, alleviate the paralysis of swallowing muscles, release the substance P, and restore the ability to drink water; and (iv) EA can boost the functional compensation of M1 in the noninfarction side, strengthen the excitatory of hypoglossal nerve, and be involved in the voluntary swallowing neural control to improve PSD. This research provides a timely and necessary experimental evidence of the motor neural regulation in dysphagia after stroke by acupuncture in clinic.

scholarly journals Endogenous opioids in the nucleus accumbens promote approach to high-fat food in the absence of caloric need

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Kevin Caref ◽  
Saleem M Nicola
Keyword(s):  
Nucleus Accumbens ◽  
Receptor Antagonist ◽  
Neural Control ◽  
Neural Mechanism ◽  
Endogenous Opioids ◽  
Neuronal Firing ◽  
Palatable Food ◽  
Sugar Consumption ◽  
High Fat ◽  
The Brain

When relatively sated, people (and rodents) are still easily tempted to consume calorie-dense foods, particularly those containing fat and sugar. Consumption of such foods while calorically replete likely contributes to obesity. The nucleus accumbens (NAc) opioid system has long been viewed as a critical substrate for this behavior, mainly via contributions to the neural control of consumption and palatability. Here, we test the hypothesis that endogenous NAc opioids also promote appetitive approach to calorie-dense food in states of relatively high satiety. We simultaneously recorded NAc neuronal firing and infused a µ-opioid receptor antagonist into the NAc while rats performed a cued approach task in which appetitive and consummatory phases were well separated. The results reveal elements of a neural mechanism by which NAc opioids promote approach to high-fat food despite the lack of caloric need, demonstrating a potential means by which the brain is biased towards overconsumption of palatable food.

Recent progress on the role of GABAergic neurotransmission in the pathogenesis of Alzheimer’s disease

2016 ◽  
Vol 27 (4) ◽  
pp. 449-455 ◽  
Author(s):  
Ghulam Abbas ◽  
Wajahat Mahmood ◽  
Nurul Kabir
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Gaba Receptor ◽  
Amyloid Β ◽  
Receptor Subtypes ◽  
Causative Role ◽  
Gabaergic Neurotransmission ◽  
Promising Target ◽  
The Brain

AbstractDespite their possible causative role, targeting amyloidosis, tau phosphorylation, acetylcholine esterase, glutamate, oxidative stress and mitochondrial metabolism have not yet led to the development of drugs to cure Alzheimer’s disease (AD). Recent preclinical and clinical reports exhibit a surge in interest in the role of GABAergic neurotransmission in the pathogenesis of AD. The interaction among GABAergic signaling, amyloid-β and acetylcholine is shown to affect the homeostasis between excitation (glutamate) and inhibition (GABA) in the brain. As a consequence, over-excitation leads to neurodegeneration (excitotoxicity) and impairment in the higher level functions. Previously, the glutamate arm of this balance received the most attention. Recent literature suggests that over-excitation is primarily mediated by dysfunctional GABA signaling and can possibly be restored by rectifying anomalous metabolism observed in the GABAergic neurons during AD. Additionally, neurogenesis and synaptogenesis have also been linked with GABAergic signaling. This association may provide a basis for the needed repair mechanism. Furthermore, several preclinical interventional studies revealed that targeting various GABA receptor subtypes holds potential in overcoming the memory deficits associated with AD. In conclusion, the recent scientific literature suggests that GABAergic signaling presents itself as a promising target for anti-AD drug development.

Recovery of breathing pattern after 15 min of cerebral ischemia in rabbits

1990 ◽  
Vol 69 (5) ◽  
pp. 1676-1681 ◽  
Author(s):  
R. Pluta ◽  
J. R. Romaniuk
Keyword(s):  
Cerebral Ischemia ◽  
Neural Control ◽  
Breathing Pattern ◽  
Respiratory Pattern ◽  
Lung Inflation ◽  
Brachiocephalic Trunk ◽  
Precise Analysis ◽  
Neural Control Of Breathing ◽  
Recurrent Laryngeal Nerves ◽  
The Brain

The study was undertaken to ascertain the neural control of breathing and vagal reflexes during and after cerebral ischemia. The experiments were performed on anesthetized, paralyzed, and artificially ventilated rabbits. Cerebral ischemia was induced by reversible intrathoracic occlusion of the brachiocephalic trunk and the left subclavian and both internal thoracic arteries for 15 min. The effect of cerebral ischemia on breathing pattern was assessed by monitoring the integrated activities of phrenic and recurrent laryngeal nerves. Ischemia produced enhancement of breathing followed by apnea and gasping. During enhanced breathing as well as during gasping, the inspiratory-inhibiting effect of lung inflation (Breuer-Hering reflex) was abolished. When brain circulation was restored, respiratory activity started with gasps, which later were intermingled with eupneic type of inspirations. During the onset of a eupneic breath, lung inflation produced inspiratory facilitation but never an inhibition. However, after 30 min of recovery from cerebral ischemia, the Breuer-Hering reflex was restored. Results show that precise analysis of vagal reflexes and respiratory pattern during ischemia and resuscitation may be used as an indicator of resumption of autonomic activity in the brain stem.

Decreased energy metabolism in brain stem during central respiratory depression in response to hypoxia

1996 ◽  
Vol 81 (4) ◽  
pp. 1772-1777 ◽  
Author(s):  
J. C. Lamanna ◽  
M. A. Haxhiu ◽  
K. L. Kutina-Nelson ◽  
S. Pundik ◽  
B. Erokwu ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Brain Stem ◽  
Respiratory Depression ◽  
Intracellular Ph ◽  
Metabolic Changes ◽  
Nucleus Ambiguus ◽  
Electromyographic Activity ◽  
Respiratory Drive ◽  
Energy Deficiency ◽  
The Brain

LaManna, J. C., M. A. Haxhiu, K. L. Kutina-Nelson, S. Pundik, B. Erokwu, E. R. Yeh, W. D. Lust, and N. S. Cherniack.Decreased energy metabolism in brain stem during central respiratory depression in response to hypoxia. J. Appl. Physiol. 81(4): 1772–1777, 1996.—Metabolic changes in the brain stem were measured at the time when oxygen deprivation-induced respiratory depression occurred. Eucapnic ventilation with 8% oxygen in vagotomized urethan-anesthetized rats resulted in cessation of respiratory drive, monitored by recording diaphragm electromyographic activity, on average within 11 min (range 5–27 min), presumably via central depressant mechanisms. At that time, the brain stems were frozen in situ for metabolic analyses. By using 20-μm lyophilized sections from frozen-fixed brain stem, microregional analyses of ATP, phosphocreatine, lactate, and intracellular pH were made from 1) the ventral portion of the nucleus gigantocellularis and the parapyramidal nucleus; 2) the compact and ventral portions of the nucleus ambiguus; 3) midline neurons; 4) nucleus tractus solitarii; and 5) the spinal trigeminal nucleus. At the time of respiratory depression, lactate was elevated threefold in all regions. Both ATP and phosphocreatine were decreased to 50 and 25% of control, respectively. Intracellular pH was more acidic by 0.2–0.4 unit in these regions but was relatively preserved in the chemosensitive regions near the ventral and dorsal medullary surfaces. These results show that hypoxia-induced respiratory depression was accompanied by metabolic changes within brain stem regions involved in respiratory and cardiovascular control. Thus it appears that there was significant energy deficiency in the brain stem after hypoxia-induced respiratory depression had occurred.

scholarly journals Neural Control of Immunity in Hypertension: Council on Hypertension Mid Career Award for Research Excellence, 2019

Hypertension ◽  
2020 ◽  
Vol 76 (3) ◽  
pp. 622-628
Author(s):  
Daniela Carnevale
Keyword(s):  
Immune Response ◽  
Nervous System ◽  
Neural Control ◽  
Neural Signals ◽  
The Past ◽  
Target Organs ◽  
Long Time ◽  
The Common ◽  
The Brain

The nervous system and the immune system share the common ability to exert gatekeeper roles at the interfaces between internal and external environment. Although interaction between these 2 evolutionarily highly conserved systems has been recognized for long time, the investigation into the pathophysiological mechanisms underlying their crosstalk has been tackled only in recent decades. Recent work of the past years elucidated how the autonomic nervous system controls the splenic immunity recruited by hypertensive challenges. This review will focus on the neural mechanisms regulating the immune response and the role of this neuroimmune crosstalk in hypertension. In this context, the review highlights the components of the brain-spleen axis with a focus on the neuroimmune interface established in the spleen, where neural signals shape the immune response recruited to target organs of high blood pressure.

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