scholarly journals Chronic cocaine self-administration attenuates the anxiogenic-like and stress potentiating effects of the benzodiazepine inverse agonist, FG 7142

2011 ◽  
Vol 99 (3) ◽  
pp. 408-413 ◽  
Author(s):  
R. Parrish Waters ◽  
Ronald E. See
Keyword(s):  
Inverse Agonist ◽  
Fg 7142 ◽  
Self Administration ◽  
Chronic Cocaine ◽  
Benzodiazepine Inverse Agonist

scholarly journals BDNF-TrkB controls cocaine-induced dendritic spines in rodent nucleus accumbens dissociated from increases in addictive behaviors

2017 ◽  
Vol 114 (35) ◽  
pp. 9469-9474 ◽  
Author(s):  
Ethan M. Anderson ◽  
Anne Marie Wissman ◽  
Joyce Chemplanikal ◽  
Nicole Buzin ◽  
Daniel Guzman ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Dendritic Spine ◽  
Morphological Changes ◽  
Dominant Negative ◽  
Addictive Behaviors ◽  
Spine Density ◽  
Nucleus Accumbens Shell ◽  
Self Administration ◽  
Dendritic Spine Density ◽  
Chronic Cocaine

Chronic cocaine use is associated with prominent morphological changes in nucleus accumbens shell (NACsh) neurons, including increases in dendritic spine density along with enhanced motivation for cocaine, but a functional relationship between these morphological and behavioral phenomena has not been shown. Here we show that brain-derived neurotrophic factor (BDNF) signaling through tyrosine kinase B (TrkB) receptors in NACsh neurons is necessary for cocaine-induced dendritic spine formation by using either localized TrkB knockout or viral-mediated expression of a dominant negative, kinase-dead TrkB mutant. Interestingly, augmenting wild-type TrkB expression after chronic cocaine self-administration reverses the sustained increase in dendritic spine density, an effect mediated by TrkB signaling pathways that converge on extracellular regulated kinase. Loss of TrkB function after cocaine self-administration, however, leaves spine density intact but markedly enhances the motivation for cocaine, an effect mediated by specific loss of TrkB signaling through phospholipase Cgamma1 (PLCγ1). Conversely, overexpression of PLCγ1 both reduces the motivation for cocaine and reverses dendritic spine density, suggesting a potential target for the treatment of addiction in chronic users. Together, these findings indicate that BDNF-TrkB signaling both mediates and reverses cocaine-induced increases in dendritic spine density in NACsh neurons, and these morphological changes are entirely dissociable from changes in addictive behavior.

Barbiturates allosterically inhibit GABA antagonist and benzodiazepine inverse agonist binding

1984 ◽  
Vol 102 (2) ◽  
pp. 205-212 ◽  
Author(s):  
Erik H.F. Wong ◽  
Adele M. Snowman ◽  
L.M. Fredrik Leeb-Lundberg ◽  
Richard W. Olsen
Keyword(s):  
Inverse Agonist ◽  
Agonist Binding ◽  
Gaba Antagonist ◽  
Benzodiazepine Inverse Agonist

Behavioral neurobiology of inverse agonist FG 7142 induced anxiety syndrome in rats

1990 ◽  
Vol 14 (2) ◽  
pp. 249-260 ◽  
Author(s):  
Ravindranath Shanbhogue ◽  
Hiremagalur J. Hrishikeshavan ◽  
Kshama Devi ◽  
Sam Munonyedi
Keyword(s):  
Inverse Agonist ◽  
Fg 7142 ◽  
Behavioral Neurobiology

scholarly journals Effects of chronic cocaine self-administration and N-acetylcysteine on learning, cognitive flexibility, and reinstatement in nonhuman primates

2019 ◽  
Vol 236 (7) ◽  
pp. 2143-2153 ◽  
Author(s):  
Brian D. Kangas ◽  
Rachel J. Doyle ◽  
Stephen J. Kohut ◽  
Jack Bergman ◽  
Marc J. Kaufman
Keyword(s):  
Cognitive Flexibility ◽  
Nonhuman Primates ◽  
Self Administration ◽  
Chronic Cocaine
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