scholarly journals Central neuronal functions of histamine H4 receptors

Oncotarget ◽  
2017 ◽  
Vol 8 (8) ◽  
pp. 12556-12557 ◽  
Author(s):  
Maria Domenica Sanna ◽  
Nicoletta Galeotti
Keyword(s):  
Neuronal Functions ◽  
Histamine H4 Receptors

Differential effects of human and pork insulin-induced hypoglycemia on neuronal functions in humans

Diabetes ◽  
1990 ◽  
Vol 39 (9) ◽  
pp. 1091-1098 ◽  
Author(s):  
W. Kern ◽  
K. Lieb ◽  
W. Kerner ◽  
J. Born ◽  
H. L. Fehm
Keyword(s):  
Differential Effects ◽  
Neuronal Functions

scholarly journals An Endogenous RNA Transcript Antisense to CNGα1 Cation Channel mRNA

2002 ◽  
Vol 13 (10) ◽  
pp. 3696-3705 ◽  
Author(s):  
Chin-Hung Cheng ◽  
David Tai-Wai Yew ◽  
Hiu-Yee Kwan ◽  
Qing Zhou ◽  
Yu Huang ◽  
...  
Keyword(s):  
Expression System ◽  
Expression Patterns ◽  
Long Term Potentiation ◽  
Information Storage ◽  
Term Potentiation ◽  
Hippocampal Ca1 ◽  
Oocyte Expression System ◽  
Neuronal Functions ◽  
Rna Transcript

CNG channels are cyclic nucleotide-gated Ca2+-permeable channels that are suggested to be involved in the activity-dependent alterations of synaptic strength that are thought to underlie information storage in the CNS. In this study, we isolated an endogenous RNA transcript antisense to CNGα1 mRNA. This transcript was capable of down-regulating the expression of sense CNGα1 in theXenopus oocyte expression system. RT-PCR, Northern blot, and in situ hybridization analyses showed that the transcript was coexpressed with CNGα1 mRNA in many regions of human brain, notably in those regions that were involved in long-term potentiation and long-term depression, such as hippocampal CA1 and CA3, dentate gyrus, and cerebellar Purkinje layer. Comparison of expression patterns between adult and fetal cerebral cortex revealed that there were concurrent developmental changes in the expression levels of anti-CNG1 and CNGα1. Treatment of human glioma cell T98 with thyroid hormone T3 caused a significant increase in anti-CNG1 expression and a parallel decrease in sense CNGα1 expression. These data suggest that the suppression of CNGα1 expression by anti-CNG1 may play an important role in neuronal functions, especially in synaptic plasticity and cortical development. Endogenous antisense RNA-mediated regulation may represent a new mechanism through which the activity of ion channels can be regulated in the human CNS.

Localization of histamine H4 receptors in the central nervous system of human and rat

2009 ◽  
Vol 1250 ◽  
pp. 41-48 ◽  
Author(s):  
Marina I. Strakhova ◽  
Arthur L. Nikkel ◽  
Arlene M. Manelli ◽  
Gin C. Hsieh ◽  
Timothy A. Esbenshade ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
The Central Nervous System ◽  
Histamine H4 Receptors

Histamine H4 receptors in normal conjunctiva and in vernal keratoconjunctivitis

Allergy ◽  
2011 ◽  
Vol 66 (10) ◽  
pp. 1360-1366 ◽  
Author(s):  
A. Leonardi ◽  
A. Di Stefano ◽  
C. Vicari ◽  
L. Motterle ◽  
P. Brun
Keyword(s):  
Vernal Keratoconjunctivitis ◽  
Histamine H4 Receptors

Pathomechanisms in hepatic encephalopathy

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Dieter Häussinger ◽  
Markus Butz ◽  
Alfons Schnitzler ◽  
Boris Görg
Keyword(s):  
Hepatic Encephalopathy ◽  
Nitrosative Stress ◽  
Cortical Excitability ◽  
Brain Activity ◽  
System Level ◽  
Low Grade ◽  
Motor Impairments ◽  
Chronic Liver Failure ◽  
Oscillatory Brain Activity ◽  
Neuronal Functions

Abstract Hepatic encephalopathy (HE) is a frequent neuropsychiatric complication in patients with acute or chronic liver failure. Symptoms of HE in particular include disturbances of sensory and motor functions and cognition. HE is triggered by heterogeneous factors such as ammonia being a main toxin, benzodiazepines, proinflammatory cytokines and hyponatremia. HE in patients with liver cirrhosis is triggered by a low-grade cerebral edema and cerebral oxidative/nitrosative stress which bring about a number of functionally relevant alterations including posttranslational protein modifications, oxidation of RNA, gene expression changes and senescence. These alterations are suggested to impair astrocyte/neuronal functions and communication. On the system level, a global slowing of oscillatory brain activity and networks can be observed paralleling behavioral perceptual and motor impairments. Moreover, these changes are related to increased cerebral ammonia, alterations in neurometabolite and neurotransmitter concentrations and cortical excitability in HE patients.

Activation of Protein Kinase C Increases Neuronal Excitability by Regulating Persistent Na+ Current in Mouse Neocortical Slices

1998 ◽  
Vol 80 (3) ◽  
pp. 1547-1551 ◽  
Author(s):  
Nadav Astman ◽  
Michael J. Gutnick ◽  
Ilya A. Fleidervish
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Action Potential ◽  
Neuronal Excitability ◽  
Specific Protein ◽  
Protein Kinase C Inhibitors ◽  
Cationic Current ◽  
Kinase C ◽  
Layer V ◽  
Neuronal Functions

Astman, Nadav, Michael J. Gutnick, and Ilya A. Fleidervish. Activation of protein kinase C increases neuronal excitability by regulating persistent Na+ current in mouse neocortical slices. J. Neurophysiol. 80: 1547–1551, 1998. Effects of the protein kinase C activating phorbol ester, phorbol 12-myristate 13-acetate (PMA), were studied in whole cell recordings from layer V neurons in slices of mouse somatosensory neocortex. PMA was applied intracellularly (100 nM to 1 μM) to restrict its action to the cell under study. In current-clamp recordings, it enhanced neuronal excitability by inducing a 10- to 20-mV decrease in voltage threshold for action-potential generation. Because spike threshold in neocortical neurons critically depends on the properties of persistent Na+ current ( I NaP), effects of PMA on this current were studied in voltage clamp. After blocking K+ and Ca2+ currents, I NaP was revealed by applying slow depolarizing voltage ramps from −70 to 0 mV. Intracellular PMA induced a decrease in I NaP at very depolarized membrane potentials. It also shifted activation of I NaP in the hyperpolarizing direction, however, such that there was a significant increase in persistent inward current at potentials more negative than −45 mV. When tetrodotoxin (TTX) was added to the bath, blocking I NaP and leaving only an outward nonspecific cationic current ( I cat), PMA had no apparent effect on responses to voltage ramps. Thus PMA did not affect I cat, and it did not induce any additional current. Intracellular application of the inactive PMA analogue, 4α-PMA, did not affect I NaP. The specific protein kinase C inhibitors, chelerythrine (20 μM) and calphostin C (10 μM), blocked the effect of PMA on I NaP. The data suggest that PMA enhances neuronal excitability via a protein kinase C–mediated increase in I NaP at functionally critical subthreshold voltages. This novel effect would modulate all neuronal functions that are influenced by I NaP, including synaptic integration and active backpropagation of action potential from the soma into the dendrites.

scholarly journals Neuronal Functions of ESCRTs

2012 ◽  
Vol 21 (1) ◽  
pp. 9-15 ◽  
Author(s):  
Jin-A Lee ◽  
Fen-Biao Gao
Keyword(s):  
Neuronal Functions
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