Late developmental changes in the ability of adenosine A1 receptors to regulate synaptic transmission in the hippocampus

1998 ◽  
Vol 105 (1) ◽  
pp. 137-139 ◽  
Author(s):  
Theodore C Dumas ◽  
Thomas C Foster
Keyword(s):  
Synaptic Transmission ◽  
Developmental Changes ◽  
Adenosine A1 Receptors ◽  
Adenosine A1

Endogenous Activation of Adenosine A1 Receptors, but Not P2X Receptors, During High-Frequency Synaptic Transmission at the Calyx of Held

2006 ◽  
Vol 95 (6) ◽  
pp. 3336-3342 ◽  
Author(s):  
Adrian Y. C. Wong ◽  
Brian Billups ◽  
Jamie Johnston ◽  
Richard J. Evans ◽  
Ian D. Forsythe
Keyword(s):  
Synaptic Transmission ◽  
High Frequency ◽  
Atp Release ◽  
Physiological Role ◽  
P2x Receptors ◽  
Presynaptic Receptors ◽  
Calyx Of Held ◽  
Adenosine A1 Receptors ◽  
Medial Nucleus ◽  
Adenosine A1

Activation of presynaptic receptors plays an important role in modulation of transmission at many synapses, particularly during high-frequency trains of stimulation. Adenosine-triphosphate (ATP) is coreleased with several neurotransmitters and acts at presynaptic sites to reduce transmitter release; such presynaptic P2X receptors occur at inhibitory and excitatory terminals in the medial nucleus of the trapezoid body (MNTB). We have investigated the mechanism of purinergic modulation during high-frequency repetitive stimulation at the calyx of Held synapse. Suppression of calyceal excitatory postsynaptic currents (EPSCs) by ATP and ATPγS (100 μM) was mimicked by adenosine application and was blocked by DPCPX (10 μM), indicating mediation by adenosine A1 receptors. DPCPX enhanced EPSC amplitudes during high-frequency synaptic stimulation, suggesting that adenosine has a physiological role in modulating transmission at the calyx. The Luciferin-Luciferase method was used to probe for endogenous ATP release (at 37°C), but no release was detected. Blockers of ectonucleotidases also had no effect on endogenous synaptic depression, suggesting that it is adenosine acting on A1 receptors, rather than degradation of released ATP, which accounts for presynaptic purinergic suppression of synaptic transmission during physiological stimulus trains at this glutamatergic synapse.

scholarly journals Deletion of presynaptic adenosine A1 receptors impairs the recovery of synaptic transmission after hypoxia

Neuroscience ◽  
2005 ◽  
Vol 132 (3) ◽  
pp. 575-580 ◽  
Author(s):  
E. Arrigoni ◽  
A.J. Crocker ◽  
C.B. Saper ◽  
R.W. Greene ◽  
T.E. Scammell
Keyword(s):  
Synaptic Transmission ◽  
Adenosine A1 Receptors ◽  
Adenosine A1

Effect of dexamethasone on the expression of MMPs, adenosine A1 receptors and NFKB by human trabecular meshwork cells

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Normie Aida Mohd Nasir ◽  
Renu Agarwal ◽  
Anna Krasilnikova ◽  
Siti Hamimah Sheikh Abdul Kadir ◽  
Igor Iezhitsa
Keyword(s):  
Extracellular Matrix ◽  
Western Blot ◽  
Trabecular Meshwork ◽  
Culture Media ◽  
Smooth Muscle Actin ◽  
Adenosine A1 Receptors ◽  
Trabecular Meshwork Cells ◽  
Aqueous Humor Dynamics ◽  
Nfkb Activation ◽  
Adenosine A1

AbstractObjectivesSteroid-induced ocular hypertension and glaucoma are associated with extracellular matrix remodeling at the trabecular meshwork (TM) of the eye due to reduced secretion of matrix metalloproteinases (MMPs), a family of enzymes regulating extracellular matrix proteolysis. Several biological functions of steroids are known to involve regulation of adenosine A1 receptors (A1AR) and nuclear factor kappa B (NFKB). Since MMPs expression in TM has been shown to be regulated by A1AR as well as transcription factors, it is likely that dexamethasone-induced changes in aqueous humor dynamics involve reduced MMP and A1AR expression and reduced NFKB activation. Hence, the current study investigated the association of dexamethasone-induced reduction in MMP secretion with reduced NFKB activation and A1AR expression.MethodsHuman trabecular meshwork cells (HTMCs) were characterized by estimating myocilin and alpha smooth muscle actin expression and then were treated with dexamethasone 100 nM for 2, 5 and 7 days. The MMP secretion was estimated in culture media using Western blot. Immunocytochemistry (ICC) and ELISA were done to investigate the effect of dexamethasone on NFKB phosphorylation. A1AR expression in HTMCs was determined using Western blot and ELISA.ResultsDexamethasone caused a significant reduction in both MMP-2 and -9 expression compared to untreated group after five and seven days but not after two days of culture. Significantly reduced phosphorylated NFKB and A1AR protein levels were detected in dexamethasone treated compared to vehicle treated HTMCs after five days of culture.ConclusionsDexamethasone reduces MMP-2 and -9 secretion by HTMCs and this effect of dexamethasone is associated with reduced NFKB phosphorylation and A1AR expression.

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