scholarly journals Long-term nicotine treatment down-regulates α6β2* nicotinic receptor expression and function in nucleus accumbens

2013 ◽  
Vol 127 (6) ◽  
pp. 762-771 ◽  
Author(s):  
Xiomara A. Perez ◽  
J.Michael McIntosh ◽  
Maryka Quik
Keyword(s):  
Nucleus Accumbens ◽  
Nicotinic Receptor ◽  
Receptor Expression ◽  
Nicotine Treatment ◽  
And Function

scholarly journals Sex Specific Alterations in α4*Nicotinic Receptor Expression in the Nucleus Accumbens

2018 ◽  
Vol 8 (4) ◽  
pp. 70 ◽  
Author(s):  
Joan Holgate ◽  
Josephine Tarren ◽  
Selena Bartlett
Keyword(s):  
Nucleus Accumbens ◽  
Nicotinic Receptor ◽  
Receptor Expression

Long-Term Nicotine Treatment Decreases Striatal α6* Nicotinic Acetylcholine Receptor Sites and Function in Mice

2005 ◽  
Vol 67 (5) ◽  
pp. 1639-1647 ◽  
Author(s):  
Albert Lai ◽  
Neeraja Parameswaran ◽  
Mirium Khwaja ◽  
Paul Whiteaker ◽  
Jon M. Lindstrom ◽  
...  
Keyword(s):  
Acetylcholine Receptor ◽  
Nicotinic Acetylcholine Receptor ◽  
Nicotinic Acetylcholine ◽  
Nicotine Treatment ◽  
Receptor Sites ◽  
And Function

Abstract 281: Long-term Exposure of PM2.5 Causes Hypertension by Impaired Renal D1 Receptor Mediated Sodium Excretion via Up-regulation of GRK4 Expression in SD rats

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Xi Lu ◽  
Ken Chen ◽  
Jing Zeng ◽  
Hongmei Ren ◽  
Chunyu Zeng
Keyword(s):  
Sodium Excretion ◽  
D1 Receptor ◽  
Receptor Expression ◽  
Sd Rats ◽  
Induced Hypertension ◽  
Pm2.5 Exposure ◽  
And Function

Introduction: Epidemiological evidence supports an important association between PM2.5 exposure and hypertension. There are reports that PM2.5 induced hypertension with impaired sodium excretion, however, the mechanisms are not clear. Hypothesis: We hypothesize that PM2.5, via increased ROS levels, increased GRK4 expression, consequently impaired renal D1 receptor function, and lead to hypertension. Methods: We used Sprague-Dawley (SD) rats with in-vivo PM2.5 exposure, and immortalized renal proximal tubule (RPT) cells from Wistar-Kyoto (WKY) rats in-vitro, which behave similarly to freshly obtained RPT cells. Results: Our present study found that long-term exposure of PM2.5 caused hypertension and impaired renal sodium excretion, which might be ascribed to lower D1 receptor expression and higher D1 receptor phosphorylation, accompanied with higher GRK4 expression. The in-vivo results were confirmed in in-vitro study, i.e. PM2.5 increased basal Na+-K+ ATPase activity, decreased D1 receptor mediated inhibitory effect on Na+-K+ ATPase activity, decreased D1 receptor expression and increased D1 receptor phosphorylation in RPT cells. The downregulation of D1 receptor expression and function might be due to higher GRK4 expression, because down-regulation of GRK4 by siRNA reversed the D1 receptor expression and function. Due to the role of ROS on D1 receptor dysfunction, we checked ROS levels, and found plasma ROS levels were higher in PM2.5 treated SD rats. Inhibition of ROS by tempol reduced blood pressure and increased sodium excretion in PM2.5 treated SD rats, accompanied by increased the lower D1 receptor expression, and decreased the hyperphosphorylated D1 receptor and GRK4 expression. Conclusions: Long-term exposure of PM2.5 increases blood pressure by decreased D1 receptor expression and function; ROS, via regulation of GRK4 expression, is taken part in the pathogenesis of PM2.5-induced hypertension.

scholarly journals Long-Term Nicotine Treatment Differentially Regulates Striatal α6α4β2* and α6(Nonα4)β2* nAChR Expression and Function

2008 ◽  
Vol 74 (3) ◽  
pp. 844-853 ◽  
Author(s):  
Xiomara A. Perez ◽  
Tanuja Bordia ◽  
J. Michael McIntosh ◽  
Sharon R. Grady ◽  
Maryka Quik
Keyword(s):  
Nicotine Treatment ◽  
And Function

scholarly journals Estrogen Receptor Expression and Function in Long-Term Estrogen-Deprived Human Breast Cancer Cells1

Endocrinology ◽  
1998 ◽  
Vol 139 (10) ◽  
pp. 4164-4174 ◽  
Author(s):  
Meei-Huey Jeng ◽  
Margaret A. Shupnik ◽  
Timothy P. Bender ◽  
Eric H. Westin ◽  
Debdutta Bandyopadhyay ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Human Breast Cancer ◽  
Receptor Expression ◽  
Estrogen Receptor Expression ◽  
Human Breast ◽  
And Function

scholarly journals Increases in alpha4* but not alpha3*/alpha6* nicotinic receptor sites and function in the primate striatum following chronic oral nicotine treatment

2006 ◽  
Vol 96 (4) ◽  
pp. 1028-1041 ◽  
Author(s):  
Sarah E. McCallum ◽  
Neeraja Parameswaran ◽  
Tanuja Bordia ◽  
Hong Fan ◽  
Rachel F. Tyndale ◽  
...  
Keyword(s):  
Nicotinic Receptor ◽  
Nicotine Treatment ◽  
Receptor Sites ◽  
And Function ◽  
Oral Nicotine

scholarly journals Kalirin and Trio proteins serve critical roles in excitatory synaptic transmission and LTP

2016 ◽  
Vol 113 (8) ◽  
pp. 2264-2269 ◽  
Author(s):  
Bruce E. Herring ◽  
Roger A. Nicoll
Keyword(s):  
Ampa Receptor ◽  
Rho Gtpases ◽  
Imaging Techniques ◽  
Long Term Potentiation ◽  
Structure And Function ◽  
Receptor Expression ◽  
Term Potentiation ◽  
And Function ◽  
Necessary And Sufficient

The molecular mechanism underlying long-term potentiation (LTP) is critical for understanding learning and memory. CaMKII, a key kinase involved in LTP, is both necessary and sufficient for LTP induction. However, how CaMKII gives rise to LTP is currently unknown. Recent studies suggest that Rho GTPases are necessary for LTP. Rho GTPases are activated by Rho guanine exchange factors (RhoGEFs), but the RhoGEF(s) required for LTP also remain unknown. Here, using a combination of molecular, electrophysiological, and imaging techniques, we show that the RhoGEF Kalirin and its paralog Trio play critical and redundant roles in excitatory synapse structure and function. Furthermore, we show that CaMKII phosphorylation of Kalirin is sufficient to enhance synaptic AMPA receptor expression, and that preventing CaMKII signaling through Kalirin and Trio prevents LTP induction. Thus, our data identify Kalirin and Trio as the elusive targets of CaMKII phosphorylation responsible for AMPA receptor up-regulation during LTP.

Long-term effects of prenatal stress and diazepam on D2 receptor expression in the nucleus accumbens of adult rats

2015 ◽  
Vol 594 ◽  
pp. 133-136 ◽  
Author(s):  
S. Lakehayli ◽  
N. Said ◽  
M. El Khachibi ◽  
M. El Ouahli ◽  
S. Nadifi ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Prenatal Stress ◽  
D2 Receptor ◽  
Receptor Expression ◽  
Long Term Effects ◽  
Adult Rats
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