The basolateral amygdala orexin 1 and 2 receptors’ involvement in modulating spatial reference memory

2019 ◽  
Vol 1704 ◽  
pp. 16-25 ◽  
Author(s):  
Motahareh Rouhi Ardeshiri ◽  
Narges Hosseinmardi ◽  
Esmaeil Akbari
Keyword(s):  
Basolateral Amygdala ◽  
Reference Memory ◽  
Spatial Reference ◽  
Spatial Reference Memory

Spatial reference memory in GluR-A-deficient mice using a novel hippocampal-dependent paddling pool escape task

Hippocampus ◽  
2004 ◽  
Vol 14 (2) ◽  
pp. 216-223 ◽  
Author(s):  
W.B. Schmitt ◽  
R.M.J. Deacon ◽  
D. Reisel ◽  
R. Sprengel ◽  
P.H. Seeburg ◽  
...  
Keyword(s):  
Reference Memory ◽  
Spatial Reference ◽  
Spatial Reference Memory ◽  
Deficient Mice

scholarly journals Neuroinflammation Induced by Surgery Does Not Impair the Reference Memory of Young Adult Mice

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Yanhua Zhao ◽  
Lili Huang ◽  
Huan Xu ◽  
Guangxi Wu ◽  
Mengyi Zhu ◽  
...  
Keyword(s):  
Risk Factor ◽  
Young Adult ◽  
Postoperative Cognitive Dysfunction ◽  
Underlying Mechanism ◽  
Reference Memory ◽  
Behavior Changes ◽  
Spatial Reference ◽  
Adult Mice ◽  
Spatial Reference Memory ◽  
Old Mice

Postoperative cognitive dysfunction (POCD) increases morbidity and mortality after surgery. But the underlying mechanism is not clear yet. While age is now accepted as the top one risk factor for POCD, results from studies investigating postoperative cognitive functions in adults have been controversial, and data about the very young adult individuals are lacking. The present study investigated the spatial reference memory, IL-1β, IL-6, and microglia activation changes in the hippocampus in 2-month-old mice after anesthesia and surgery. We found that hippocampal IL-1βand IL-6 increased at 6 hours after surgery. Microglia were profoundly activated in the hippocampus 6 to 24 hours after surgery. However, no significant behavior changes were found in these mice. These results indicate that although anesthesia and surgery led to neuroinflammation, the latter was insufficient to impair the spatial reference memory of young adult mice.

scholarly journals Ketamine affects the integration of developmentally generated granule neurons in the adult stage

2019 ◽  
Author(s):  
Zhanqiang Zhao ◽  
Bing Li ◽  
Yuqing Wu ◽  
Xujun Chen ◽  
Yan Guo ◽  
...  
Keyword(s):  
Functional Integration ◽  
Reference Memory ◽  
Control Group ◽  
Granule Neurons ◽  
Sprague Dawley ◽  
General Anesthetic ◽  
Spatial Reference ◽  
Spatial Reference Memory ◽  
Dividing Cells ◽  
Hippocampus Dependent Memory

Abstract Background Ketamine has been reported to cause neonatal neurotoxicity in a variety of developing animal models. Various studies have been conducted to study the mechanism of neurotoxicity for general anesthetic use during the neonatal period. Previous experiments have suggested that developmentally generated granule neurons in the hippocampus dentate gyrus (DG) supported hippocampus-dependent memory. Therefore, this study aimed to investigate whether ketamine affects the functional integration of developmentally generated granule neurons in the DG. For this purpose ， the postnatal day 7 (PND-7) Sprague-Dawley (SD) rats were divided into the control group and the ketamine group (rats who received 4 injections of 40 mg/kg ketamine at 1 h intervals). To label dividing cells, BrdU was administered for three consecutive days after the ketamine explore; NeuN+/BrdU+ cells were observed by using immunofluorescence. To evaluate the developmentally generated granule neurons that support hippocampus-dependent memory, spatial reference memory was tested by using Morris Water Maze at 3 months old, after which the immunofluorescence was used to detect c-Fos expression in the NeuN + /BrdU + cells. The expression of caspase-3 was measured by western blot to detect the apoptosis in the hippocampal DG. Results The present results showed that the neonatal ketamine exposure did not influence the survival rate of developmentally generated granule neurons at 2 and 3 months old, but ketamine interfered with the integration of these neurons into the hippocampal DG neural circuits and caused a deficit in hippocampal-dependent spatial reference memory tasks. Conclusions In summary, these findings may promote more studies to investigate the neurotoxicity of ketamine in the developing brain.

scholarly journals Ketamine affects the integration of developmentally generated granule neurons in the adult stage

2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Zhanqiang Zhao ◽  
Bing Li ◽  
Yuqing Wu ◽  
Xujun Chen ◽  
Yan Guo ◽  
...  
Keyword(s):  
Functional Integration ◽  
Reference Memory ◽  
Control Group ◽  
Granule Neurons ◽  
Sprague Dawley ◽  
General Anesthetic ◽  
Spatial Reference ◽  
Spatial Reference Memory ◽  
Dividing Cells ◽  
Hippocampus Dependent Memory

Abstract Background Ketamine has been reported to cause neonatal neurotoxicity in a variety of developing animal models. Various studies have been conducted to study the mechanism of neurotoxicity for general anesthetic use during the neonatal period. Previous experiments have suggested that developmentally generated granule neurons in the hippocampus dentate gyrus (DG) supported hippocampus-dependent memory. Therefore, this study aimed to investigate whether ketamine affects the functional integration of developmentally generated granule neurons in the DG. For this purpose,the postnatal day 7 (PND-7) Sprague-Dawley (SD) rats were divided into the control group and the ketamine group (rats who received 4 injections of 40 mg/kg ketamine at 1 h intervals). To label dividing cells, BrdU was administered for three consecutive days after the ketamine exposure; NeuN+/BrdU+cells were observed by using immunofluorescence. To evaluate the developmentally generated granule neurons that support hippocampus-dependent memory, spatial reference memory was tested by using Morris Water Maze at 3 months old, after which the immunofluorescence was used to detect c-Fos expression in the NeuN+/BrdU+ cells. The expression of caspase-3 was measured by western blot to detect the apoptosis in the hippocampal DG. Results The present results showed that the neonatal ketamine exposure did not influence the survival rate of developmentally generated granule neurons at 2 and 3 months old, but ketamine interfered with the integration of these neurons into the hippocampal DG neural circuits and caused a deficit in hippocampal-dependent spatial reference memory tasks. Conclusions In summary, these findings may promote more studies to investigate the neurotoxicity of ketamine in the developing brain.

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