The dorsal hippocampus is essential for context discrimination but not for contextual conditioning.

1998 ◽  
Vol 112 (4) ◽  
pp. 863-874 ◽  
Author(s):  
Paul W. Frankland ◽  
Vincenzo Cestari ◽  
Robert K. Filipkowski ◽  
Robert J. McDonald ◽  
Alcino J. Silva
1994 ◽  
Vol 1 (1) ◽  
pp. 34-44
Author(s):  
R G Phillips ◽  
J E LeDoux

The effects of hippocampal lesions on the conditioning of fear responses (freezing responses) to contextual stimuli (static, continuously present stimuli) were examined in three conditioning paradigms: forward pairing of a phasic tone conditioned stimulus (CS) with a footshock unconditioned stimulus (US), unpaired presentations of the CS and US, or presentations of the US alone. All three procedures resulted in the acquisition of conditioned freezing to contextual stimuli. Lesions of the dorsal hippocampus prevented the acquisition of contextual conditioning in the Paired procedure, as reported previously, but not in the Unpaired or US Alone procedures. In the Paired procedure, static contextual cues occur in the background, with the phasic tone CS being the primary stimulus that enters into the association with the US. However, in the other two procedures, where there is no phasic CS, the primary associations with the US involve static contextual stimuli, which are therefore in the foreground. We refer to these types of contextual conditioning as background and foreground contextual conditioning, respectively, and argue that the hippocampus is only involved in background contextual conditioning. These results have implications for understanding both fear conditioning and hippocampal function.


Author(s):  
Cristina Rosell-Valle ◽  
Magdalena Martínez-Losa ◽  
Elisa Matas-Rico ◽  
Estela Castilla-Ortega ◽  
Emma Zambrana-Infantes ◽  
...  

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 610
Author(s):  
Jessica C. Gaspar ◽  
Catherine Healy ◽  
Mehnaz I. Ferdousi ◽  
Michelle Roche ◽  
David P. Finn

Peroxisome proliferator-activated receptors (PPARs) are ligand-dependent transcription factors that exist in three isoforms: PPARα, PPARβ/δ and PPARγ. Studies suggest that the PPAR signalling system may modulate pain, anxiety and cognition. The aim of the present study was to investigate whether endogenous signalling via PPARs differentially modulates innate anxiety responses and mnemonic function in the presence and absence of inflammatory pain. We examined the effects of intraperitoneal administration of GW6471 (PPARα antagonist), GSK0660 (PPARβ/δ antagonist), GW9662 (PPARγ antagonist), and N-palmitoylethanolamide (PEA) on rat behaviour in the elevated plus maze (EPM), open field (OF), light-dark box (LDB), and novel object recognition (NOR) tests in the presence or absence of chronic inflammatory pain. Complete Freund’s Adjuvant (CFA)-injected rats exhibited impaired recognition and spatial mnemonic performance in the NOR test and pharmacological blockade of PPARα further impaired spatial memory in CFA-treated rats. N-oleoylethanolamide (OEA) levels were higher in the dorsal hippocampus in CFA-injected animals compared to their counterparts. The results suggest a modulatory effect of CFA-induced chronic inflammatory pain on cognitive processing, but not on innate anxiety-related responses. Increased OEA-PPARα signalling may act as a compensatory mechanism to preserve spatial memory function following CFA injection.


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