scholarly journals Distinct CCK-positive SFO neurons are involved in persistent or transient suppression of water intake

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Takashi Matsuda ◽  
Takeshi Y. Hiyama ◽  
Kenta Kobayashi ◽  
Kazuto Kobayashi ◽  
Masaharu Noda
Keyword(s):  
Water Intake ◽  
Neural Mechanisms ◽  
Gabaergic Interneurons ◽  
Water Drinking ◽  
Pathological Conditions ◽  
Increase Water Intake ◽  
The Central Nervous System ◽  
Response To Water ◽  
The Brain ◽  
Excessive Water

Abstract The control of water-intake behavior is critical for life because an excessive water intake induces pathological conditions, such as hyponatremia or water intoxication. However, the brain mechanisms controlling water intake currently remain unclear. We previously reported that thirst-driving neurons (water neurons) in the subfornical organ (SFO) are cholecystokinin (CCK)-dependently suppressed by GABAergic interneurons under Na-depleted conditions. We herein show that CCK-producing excitatory neurons in the SFO stimulate the activity of GABAergic interneurons via CCK-B receptors. Fluorescence-microscopic Ca2+ imaging demonstrates two distinct subpopulations in CCK-positive neurons in the SFO, which are persistently activated under hyponatremic conditions or transiently activated in response to water drinking, respectively. Optical and chemogenetic silencings of the respective types of CCK-positive neurons both significantly increase water intake under water-repleted conditions. The present study thus reveals CCK-mediated neural mechanisms in the central nervous system for the control of water-intake behaviors.

Impairment in fluid ingestion in rats with lesions of the zona incerta

1977 ◽  
Vol 233 (1) ◽  
pp. R53-R58 ◽  
Author(s):  
M. D. Evered ◽  
G. J. Mogenson
Keyword(s):  
Water Intake ◽  
Water Deprivation ◽  
Zona Incerta ◽  
Subsequent Reduction ◽  
Fluid Ingestion ◽  
Daily Water Intake ◽  
Daily Water ◽  
Ad Libitum ◽  
The Brain ◽  
Excessive Water

Rats with lesions of the zona incerta (ZI) dorsal to the lateral hypothalamus drink as much water as controls following intracellular or extracellular dehydration but restrict their daily water intake to minimal requirements for fluid balance, suggesting a specific impairment in secondary drinking. Following water deprivation, however, rats with ZI lesions responded to changes in palatability of the water as if they were experiencing slightly greater difficulty or aversiveness in drinking than controls. The cause appears to be an impairment in the ability to lick fluids from a spout. When water was available ad libitum or when water or liquid diet were provided after water or food deprivation, rats with ZI damage were unable to obtain as much fluid per lick as controls. It is concluded that lesions in this region of the brain impair the motor act of drinking and that the subsequent reduction in the efficiency of drinking is the cause of the attenuation of excessive water intake.

scholarly journals The Role of GPNMB in Inflammation

2021 ◽  
Vol 12 ◽  
Author(s):  
Marina Saade ◽  
Giovanna Araujo de Souza ◽  
Cristoforo Scavone ◽  
Paula Fernanda Kinoshita
Keyword(s):  
Neurodegenerative Diseases ◽  
Innate Immune ◽  
Inflammatory Conditions ◽  
Pathological Conditions ◽  
Published Evidence ◽  
The Central Nervous System ◽  
Inflammation Resolution ◽  
The Brain ◽  
Lps Treatment

Inflammation is a response to a lesion in the tissue or infection. This process occurs in a specific manner in the central nervous system and is called neuroinflammation, which is involved in neurodegenerative diseases. GPNMB, an endogenous glycoprotein, has been recently related to inflammation and neuroinflammation. GPNMB is highly expressed in macrophages and microglia, which are cells involved with innate immune response in the periphery and the brain, respectively. Some studies have shown increased levels of GPNMB in pro-inflammatory conditions, such as LPS treatment, and in pathological conditions, such as neurodegenerative diseases and cancer. However, the role of GPNMB in inflammation is still not clear. Even though most studies suggest that GPNMB might have an anti-inflammatory role by promoting inflammation resolution, there is evidence that GPNMB could be pro-inflammatory. In this review, we gather and discuss the published evidence regarding this interaction.

Loss of cholecystokinin and glucagon-like peptide-1-induced satiation in mice lacking serotonin 2C receptors

2009 ◽  
Vol 296 (1) ◽  
pp. R51-R56 ◽  
Author(s):  
Lori Asarian
Keyword(s):  
Neural Mechanisms ◽  
Wild Type ◽  
Gut Peptides ◽  
Serotonin Signaling ◽  
The Central Nervous System ◽  
Fos Expression ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
The Brain

To investigate the role of serotonin 2C receptors (2CR), which are expressed only in the central nervous system, in the satiating actions of the gut peptides CCK and glucagon-like peptide 1 (GLP-1), we examined 1) the effect of null mutations of serotonin 2CR (2CR KO) on the eating-inhibitory potencies of dark-onset intraperitoneal injections of 0.9, 1.7, or 3.5 nmol/kg (1, 2, or 4 μg/kg) CCK and 100, 200, and 400 nmol/kg (33, 66, or 132 μg/kg) GLP-1, and 2) the effects of intraperitoneal injections of 1.7 nmol//kg CCK and 100 nmol/kg GLP-1 on neuronal activation in the brain, as measured by c-Fos expression. All CCK and GLP-1 doses decreased 30-min food intake in wild-type (WT) mice, but none of them did in 2CR KO mice. CCK increased the number of cells expressing c-Fos in the nucleus tractus solitarii (NTS) of WT, but not 2CR KO mice. CCK induced similar degrees of c-Fos expression in the paraventricular (PVN) and arcuate (Arc) nuclei of the hypothalamus of both genotypes. GLP-1, on the other hand, increased c-Fos expression similarly in the NTS of both genotypes and increased c-Fos expression more in the PVN and Arc of 2CR KO mice, but not WT mice. These results indicate that serotonin signaling via serotonin 2CR is necessary for the full satiating effects of CCK and GLP-1. In addition, they suggest that the satiating effects of the two peptides are mediated by different neural mechanisms.

Delirium – a common complication of severe pathological conditions

2014 ◽  
Vol 155 (48) ◽  
pp. 1895-1901
Author(s):  
István Szendi
Keyword(s):  
Critical State ◽  
The Elderly ◽  
Evidence Based ◽  
Pathological Conditions ◽  
High Prevalence ◽  
Targeted Screening ◽  
The Central Nervous System ◽  
Professional Guidelines ◽  
The Brain ◽  
Pathophysiologic Mechanisms

Delirium is a complex syndrome caused most often by secondary neuronal dysfuncions due to systemic disorders. Because of the central nervous system manifestations of the general disease processes that are getting through the blood-brain barrier, the vigilance of attention flucutates and, therefore, the integration of incoming stimuli fails – resulting in inadequate behavioral answers. Delirium is one of the most common and serious complications of diseases, particularly in the elderly and patients in critical state. It cannot be traced back to a single etiologic process; one should consider all those pathophysiologic mechanisms that are interacting with one another simultaneously impairing the integrated functioning of the brain. Despite the high prevalence rate of delirium and the marked adverse effects on the outcome of the underlying disorders, management and therapy are basically lacking professional guidelines. The syndrome is a threatening state, requiring increased clinical attention and often intensive care. Beside evidence based therapeutic methods, conscious, targeted screening of the known risk factors and measures against them when they present themselves may exert remarkable influence on the prevention of delirium, which is also an exceptionally important aspect of the care of patients in critical state. Orv. Hetil., 2014, 155(48), 1895–1901.

Effects of water deprivation on immunoreactive angiotensin II levels in plasma, cerebroventricular perfusate and hypothalamus of the rat

1981 ◽  
Vol 97 (1) ◽  
pp. 137-144 ◽  
Author(s):  
K. Yamaguchi
Keyword(s):  
Central Nervous System ◽  
Angiotensin Ii ◽  
Water Intake ◽  
Water Deprivation ◽  
Potassium Concentration ◽  
Plasma Osmolality ◽  
Sodium Concentration ◽  
Anaesthetized Rats ◽  
The Central Nervous System ◽  
The Brain

Abstract. To examine whether endogenous angiotensin — which has been suggested to produce increased vasopressin (ADH) release and water intake under dehydration, by stimulating the central nervous system — is derived from the brain or from the circulating blood or from both, the effects of water deprivation for 46 h on immunoreactive angiotensin II (AII) concentrations of plasma, cerebroventricular perfusate and the hypothalamus were studied in conscious and urethane-anaesthetized rats. Immunoreactive AII in plasma and the hypothalamus was extracted with acetone and petroleum ether preceding the determination by radioimmunoassay. The water deprivation significantly increased plasma immunoreactive AII concentration (P < 0.002) together with plasma osmolality and sodium concentration, and reduced the potassium concentration. However, neither the immunoreactive AII concentration of the ventricular perfusate nor that of the hypothalamus was affected. Both the perfusate and the hypothalamus were very poor in immunoreactive AII (< 35.0 pg/ml and < 46.7 pg/g wet tissue, respectively). These results may suggest that increased ADH release and water intake under dehydration are brought about by the angiotensin formed in the circulating blood rather than in the brain.

scholarly journals Emerging Roles of Extracellular Vesicles in the Central Nervous System: Physiology, Pathology, and Therapeutic Perspectives

2021 ◽  
Vol 15 ◽  
Author(s):  
Yadaly Gassama ◽  
Alexandre Favereaux
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Extracellular Vesicles ◽  
Cell Types ◽  
Cellular Processes ◽  
Pathological Conditions ◽  
The Central Nervous System ◽  
System Physiology ◽  
The Brain

Extracellular vesicles or EVs are secreted by most, if not all, eukaryote cell types and recaptured by neighboring or distant cells. Their cargo, composed of a vast diversity of proteins, lipids, and nucleic acids, supports the EVs’ inter-cellular communication. The role of EVs in many cellular processes is now well documented both in physiological and pathological conditions. In this review, we focus on the role of EVs in the central nervous system (CNS) in physiological as well as pathological conditions such as neurodegenerative diseases or brain cancers. We also discuss the future of EVs in clinical research, in particular, their value as biomarkers as well as innovative therapeutic agents. While an increasing number of studies reveal EV research as a promising field, progress in the standardization of protocols and innovation in analysis as well as in research tools is needed to make a breakthrough in our understanding of their impact in the pathophysiology of the brain.

scholarly journals Glymphatic System as a Gateway to Connect Neurodegeneration From Periphery to CNS

2021 ◽  
Vol 15 ◽  
Author(s):  
Gianfranco Natale ◽  
Fiona Limanaqi ◽  
Carla L. Busceti ◽  
Federica Mastroiacovo ◽  
Ferdinando Nicoletti ◽  
...  
Keyword(s):  
Interstitial Fluid ◽  
Lymphatic Vessels ◽  
Normal Pressure ◽  
Lymphatic Drainage ◽  
Brain Parenchyma ◽  
Waste Products ◽  
Pathological Conditions ◽  
The Central Nervous System ◽  
Glymphatic Pathway ◽  
The Brain

The classic concept of the absence of lymphatic vessels in the central nervous system (CNS), suggesting the immune privilege of the brain in spite of its high metabolic rate, was predominant until recent times. On the other hand, this idea left questioned how cerebral interstitial fluid is cleared of waste products. It was generally thought that clearance depends on cerebrospinal fluid (CSF). Not long ago, an anatomically and functionally discrete paravascular space was revised to provide a pathway for the clearance of molecules drained within the interstitial space. According to this model, CSF enters the brain parenchyma along arterial paravascular spaces. Once mixed with interstitial fluid and solutes in a process mediated by aquaporin-4, CSF exits through the extracellular space along venous paravascular spaces, thus being removed from the brain. This process includes the participation of perivascular glial cells due to a sieving effect of their end-feet. Such draining space resembles the peripheral lymphatic system, therefore, the term “glymphatic” (glial-lymphatic) pathway has been coined. Specific studies focused on the potential role of the glymphatic pathway in healthy and pathological conditions, including neurodegenerative diseases. This mainly concerns Alzheimer’s disease (AD), as well as hemorrhagic and ischemic neurovascular disorders; other acute degenerative processes, such as normal pressure hydrocephalus or traumatic brain injury are involved as well. Novel morphological and functional investigations also suggested alternative models to drain molecules through perivascular pathways, which enriched our insight of homeostatic processes within neural microenvironment. Under the light of these considerations, the present article aims to discuss recent findings and concepts on nervous lymphatic drainage and blood–brain barrier (BBB) in an attempt to understand how peripheral pathological conditions may be detrimental to the CNS, paving the way to neurodegeneration.

scholarly journals The Brain Entangled: The Contribution of Neutrophil Extracellular Traps to the Diseases of the Central Nervous System

Cells ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 1477 ◽  
Author(s):  
Aneta Manda-Handzlik ◽  
Urszula Demkow
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Proteolytic Enzymes ◽  
Neutrophil Extracellular Traps ◽  
Brain Parenchyma ◽  
Free Oxygen Radicals ◽  
Extracellular Traps ◽  
Pathological Conditions ◽  
The Central Nervous System ◽  
The Brain

Under normal conditions, neutrophils are restricted from trafficking into the brain parenchyma and cerebrospinal fluid by the presence of the brain–blood barrier (BBB). Yet, infiltration of the central nervous system (CNS) by neutrophils is a well-known phenomenon in the course of different pathological conditions, e.g., infection, trauma or neurodegeneration. Different studies have shown that neutrophil products, i.e., free oxygen radicals and proteolytic enzymes, play an important role in the pathogenesis of BBB damage. It was recently observed that accumulating granulocytes may release neutrophil extracellular traps (NETs), which damage the BBB and directly injure surrounding neurons. In this review, we discuss the emerging role of NETs in various pathological conditions affecting the CNS.

Roles of glutamine in neurotransmission

2010 ◽  
Vol 6 (4) ◽  
pp. 263-276 ◽  
Author(s):  
Jan Albrecht ◽  
Marta Sidoryk-Węgrzynowicz ◽  
Magdalena Zielińska ◽  
Michael Aschner
Keyword(s):  
Amino Acids ◽  
Significant Proportion ◽  
Brain Slices ◽  
Amino Butyric Acid ◽  
Pathological Conditions ◽  
The Central Nervous System ◽  
Activity Dependent ◽  
The Brain

Glutamine (Gln) is found abundantly in the central nervous system (CNS) where it participates in a variety of metabolic pathways. Its major role in the brain is that of a precursor of the neurotransmitter amino acids: the excitatory amino acids, glutamate (Glu) and aspartate (Asp), and the inhibitory amino acid, γ-amino butyric acid (GABA). The precursor–product relationship between Gln and Glu/GABA in the brain relates to the intercellular compartmentalization of the Gln/Glu(GABA) cycle (GGC). Gln is synthesized from Glu and ammonia in astrocytes, in a reaction catalyzed by Gln synthetase (GS), which, in the CNS, is almost exclusively located in astrocytes (Martinez-Hernandez et al., 1977). Newly synthesized Gln is transferred to neurons and hydrolyzed by phosphate-activated glutaminase (PAG) to give rise to Glu, a portion of which may be decarboxylated to GABA or transaminated to Asp. There is a rich body of evidence which indicates that a significant proportion of the Glu, Asp and GABA derived from Gln feed the synaptic, neurotransmitter pools of the amino acids. Depolarization-induced-, calcium- and PAG activity-dependent releases of Gln-derived Glu, GABA and Asp have been observed in CNS preparations in vitro and in the brain in situ. Immunocytochemical studies in brain slices have documented Gln transfer from astrocytes to neurons as well as the location of Gln-derived Glu, GABA and Asp in the synaptic terminals. Patch-clamp studies in brain slices and astrocyte/neuron co-cultures have provided functional evidence that uninterrupted Gln synthesis in astrocytes and its transport to neurons, as mediated by specific carriers, promotes glutamatergic and GABA-ergic transmission. Gln entry into the neuronal compartment is facilitated by its abundance in the extracellular spaces relative to other amino acids. Gln also appears to affect neurotransmission directly by interacting with the NMDA class of Glu receptors. Transmission may also be modulated by alterations in cell membrane polarity related to the electrogenic nature of Gln transport or to uncoupled ion conductances in the neuronal or glial cell membranes elicited by Gln transporters. In addition, Gln appears to modulate the synthesis of the gaseous messenger, nitric oxide (NO), by controlling the supply to the cells of its precursor, arginine. Disturbances of Gln metabolism and/or transport contribute to changes in Glu-ergic or GABA-ergic transmission associated with different pathological conditions of the brain, which are best recognized in epilepsy, hepatic encephalopathy and manganese encephalopathy.

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