scholarly journals The Dorsal Agranular Insular Cortex Regulates the Cued Reinstatement of Cocaine-Seeking, but not Food-Seeking, Behavior in Rats

2015 ◽  
Vol 40 (10) ◽  
pp. 2425-2433 ◽  
Author(s):  
Caitlin V Cosme ◽  
Andrea L Gutman ◽  
Ryan T LaLumiere

2017 ◽  
Vol 234 (16) ◽  
pp. 2431-2441 ◽  
Author(s):  
Amy A. Arguello ◽  
Rong Wang ◽  
Carey M. Lyons ◽  
Jessica A. Higginbotham ◽  
Matthew A. Hodges ◽  
...  


2017 ◽  
Author(s):  
Hillary Schiff ◽  
Anna Lien Bouhuis ◽  
Kai Yu ◽  
Mario A. Penzo ◽  
Haohong Li ◽  
...  

AbstractPredicting which substances are suitable for consumption during foraging is critical for animals to survive. While food-seeking behavior is extensively studied, the neural circuit mechanisms underlying avoidance of potentially poisonous substances remain poorly understood. Here we examined the role of the insular cortex (IC) to central amygdala (CeA) circuit in the establishment of such avoidance behavior. Using anatomic tracing approaches combined with optogenetics-assisted circuit mapping, we found that the gustatory region of the IC sends direct excitatory projections to the lateral division of the CeA (CeL), making monosynaptic excitatory connections with distinct populations of CeL neurons. Specific inhibition of neurotransmitter release from the CeL-projecting IC neurons prevented mice from acquiring the “no-go” response, while leaving the “go” response largely unaffected in a tastant (sucrose/quinine)-reinforced “go/no-go” task. Furthermore, selective activation of the IC-CeL pathway with optogenetics drove unconditioned lick suppression in thirsty animals, induced aversive responses, and was sufficient to instruct conditioned action suppression in response to a cue predicting the optogenetic activation. These results indicate that activity in the IC-CeL circuit is necessary for establishing anticipatory avoidance responses to an aversive tastant, and is also sufficient to drive learning of such anticipatory avoidance. This function of the IC-CeL circuit is likely important for guiding avoidance of substances with unpleasant tastes during foraging in order to minimize the chance of being poisoned.Significance StatementThe ability to predict which substances are suitable for consumption is critical for survival. Here we found that activity in the insular cortex (IC) to central amygdala (CeA) circuit is necessary for establishing avoidance responses to an unpleasant tastant, and is also sufficient to drive learning of such avoidance responses. These results suggest that the IC-CeA circuit is critical for behavioral inhibition in anticipation of potentially poisonous substances during foraging.



2021 ◽  
Vol 09 ◽  
Author(s):  
Kenneth Blum ◽  
Mark S Gold ◽  
Jean L. Cadet ◽  
David Baron ◽  
Abdalla Bowirrat ◽  
...  

Background: Repeated cocaine administration changes histone acetylation and methylation on Lys residues and Deoxyribonucleic acid (DNA) within the nucleus accumbens (NAc). Recently Nestler’s group explored histone Arg (R) methylation in reward processing models. Damez-Werno et al. (2016) reported that during investigator and selfadministration experiments, the histone mark protein-R-methyltransferase-6 (PRMT6) and asymmetric dimethylation of R2 on histone H3 (H3R2me2a) decreased in the rodent and cocaine-dependent human NAc. Overexpression of PRMT6 in D2-MSNs in all NAc neurons increased cocaine seeking, whereas PRMT6 overexpression in D1-MSNs protects against cocaine-seeking. Hypothesis: Hypothesizing that dopaminylation (H3R2me2a binding) occurs in psychostimulant use disorder (PSU), and the binding inhibitor Srcin1, like the major DRD2 A2 allelic polymorphism, protects against psychostimulant seeking behavior by normalizing nucleus accumbens (NAc) dopamine expression. Discussion: Numerous publications confirmed the association between the DRD2 Taq A1 allele (30-40 lower D2 receptor numbers) and severe cocaine dependence. Lepack et al. (2020) found that acute cocaine increases dopamine in NAc synapses, results in histone H3 glutamine 5 dopaminylation (H3Q5dop), and consequent inhibition of D2 expression. The inhibition increases with chronic cocaine use and accompanies cocaine withdrawal. They also found that the Src kinase sig-naling inhibitor 1 (Srcin1 or p140CAP) during cocaine withdrawal reduced H3R2me2a binding. Consequently, this inhibited dopaminylation induced a “homeostatic brake.” Conclusion: The decrease in Src signaling in NAc D2-MSNs, like the DRD2 Taq A2 allele, a well-known genetic mechanism protective against SUD normalized nucleus accumbens (NAc) dopamine expression and decreased cocaine reward and motivation to self-administer cocaine. The Srcin1 may be an important therapeutic target.



2009 ◽  
Vol 14 (4) ◽  
pp. 419-430 ◽  
Author(s):  
Nathan S. Pentkowski ◽  
Jazmin I. Acosta ◽  
Jenny R. Browning ◽  
Elizabeth C. Hamilton ◽  
Janet L. Neisewander


2017 ◽  
pp. 407-415
Author(s):  
B.J. Tunstall ◽  
D.N. Kearns


2003 ◽  
Vol 29 (4) ◽  
pp. 660-668 ◽  
Author(s):  
Jeffrey J Burmeister ◽  
Erin M Lungren ◽  
Kenneth F Kirschner ◽  
Janet L Neisewander


2014 ◽  
Vol 39 (13) ◽  
pp. 2974-2988 ◽  
Author(s):  
Javier Gutiérrez-Cuesta ◽  
Aurelijus Burokas ◽  
Samantha Mancino ◽  
Sami Kummer ◽  
Elena Martín-García ◽  
...  


Sign in / Sign up

Export Citation Format

Share Document