The dorsal subiculum is not necessary for step-through inhibitory avoidance acquisition and consolidation in rats.

2021 ◽  
Author(s):  
Márcio Braga de Melo ◽  
Maria Gabriela Menezes Oliveira ◽  
Vanessa Manchim Favaro
2020 ◽  
Vol 34 (4) ◽  
pp. 383-390
Author(s):  
Thatiane De Oliveira Sergio ◽  
Alana Tercino Frias ◽  
Heloisa Helena Vilela-Costa ◽  
Danielle CG De Oliveira ◽  
Antônio W Zuardi ◽  
...  

Introduction and objectives: Oxytocin (OT) has been widely linked to positive social interactions, and there is great interest in OT as a therapy for a variety of neuropsychiatric conditions. Recent evidence also suggests that OT can play an important role in the mediation of anxiety-associated defensive responses, including a role for serotonin (5-HT) neurotransmission in this action. However, it is presently unknown whether OT additionally regulates the expression of panic-related behaviors, such as escape, by acting in the dorsal periaqueductal gray (dPAG), a key panic-regulating area. This study aimed to investigate the consequence of OT injection in the dPAG on escape expression and whether facilitation of 5-HT neurotransmission in this midbrain area is implicated in this action. Methods: Male Wistar rats were injected with OT in the dPAG and tested for escape expression in the elevated T-maze (ETM) and dPAG electrical stimulation tests. Using the latter test, OT’s effect was also investigated after previous intra-dPAG injection of the OT receptor antagonist atosiban, the preferential antagonists of 5-HT1A and 5-HT2A receptors, WAY-100635 and ketanserin, respectively, or systemic pretreatment with the 5-HT synthesis inhibitor p-CPA. Results: OT impaired escape expression in the two tests used, suggesting a panicolytic-like effect. In the ETM, the peptide also facilitated inhibitory avoidance acquisition, indicating an anxiogenic effect. Previous administration of atosiban, WAY-100635, ketanserin, or p-CPA counteracted OT’s anti-escape effect. Conclusions: OT and 5-HT in the dPAG interact in the regulation of panic- and anxiety-related defensive responses. These findings open new perspectives for the development of novel therapeutic strategies for the treatment of anxiety disorders.


2018 ◽  
Vol 147 ◽  
pp. 28-32 ◽  
Author(s):  
J. Raya ◽  
C.E.N. Girardi ◽  
L.A. Esumi ◽  
L.B.T. Ferreira ◽  
D.C. Hipólide

2010 ◽  
Vol 211 (2) ◽  
pp. 191-197 ◽  
Author(s):  
Cristiane do Socorro Ferraz Maia ◽  
Vania Maria Moraes Ferreira ◽  
Júlia Silva Valério Diniz ◽  
Fabiana Pirani Carneiro ◽  
João Batista de Sousa ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Andressa Radiske ◽  
Maria Carolina Gonzalez ◽  
Diana A. Nôga ◽  
Janine I. Rossato ◽  
Lia R. M. Bevilaqua ◽  
...  

AbstractExtinction memory destabilized by recall is restabilized through mTOR-dependent reconsolidation in the hippocampus, but the upstream pathways controlling these processes remain unknown. Hippocampal NMDARs drive local protein synthesis via mTOR signaling and may control active memory maintenance. We found that in adult male Wistar rats, intra dorsal-CA1 administration of the non-subunit selective NMDAR antagonist AP5 or of the GluN2A subunit-containing NMDAR antagonist TCN201 after step down inhibitory avoidance (SDIA) extinction memory recall impaired extinction memory retention and caused SDIA memory recovery. On the contrary, pre-recall administration of AP5 or of the GluN2B subunit-containing NMDAR antagonist RO25-6981 had no effect on extinction memory recall or retention per se but hindered the recovery of the avoidance response induced by post-recall intra-CA1 infusion of the mTOR inhibitor rapamycin. Our results indicate that GluN2B-containing NMDARs are necessary for extinction memory destabilization whereas GluN2A-containing NMDARs are involved in its restabilization, and suggest that pharmacological modulation of the relative activation state of these receptor subtypes around the moment of extinction memory recall may regulate the dominance of extinction memory over the original memory trace.


1989 ◽  
Vol 493 (2) ◽  
pp. 258-268 ◽  
Author(s):  
Catherine A. Cornwell-Jones ◽  
Michael W. Decker ◽  
Julia W. Chang ◽  
Barry Cole ◽  
Kimberly M. Goltz ◽  
...  

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