scholarly journals Spatial Learning and Memory in Barnes Maze Test and Synaptic Potentiation in Schaffer Collateral-CA1 Synapses of Dorsal Hippocampus in Freely Moving Rats

2019 ◽  
pp. 461-468 ◽  
Author(s):  
Azam Sadeghian ◽  
Yaghoub Fathollahi ◽  
Mohammad Javan ◽  
Amir Shojaei ◽  
Nastaran Kosarmadar ◽  
...  
2016 ◽  
Vol 113 (51) ◽  
pp. 14835-14840 ◽  
Author(s):  
Kimberly A. Kempadoo ◽  
Eugene V. Mosharov ◽  
Se Joon Choi ◽  
David Sulzer ◽  
Eric R. Kandel

Dopamine neurotransmission in the dorsal hippocampus is critical for a range of functions from spatial learning and synaptic plasticity to the deficits underlying psychiatric disorders such as attention-deficit hyperactivity disorder. The ventral tegmental area (VTA) is the presumed source of dopamine in the dorsal hippocampus. However, there is a surprising scarcity of VTA dopamine axons in the dorsal hippocampus despite the dense network of dopamine receptors. We have explored this apparent paradox using optogenetic, biochemical, and behavioral approaches and found that dopaminergic axons and subsequent dopamine release in the dorsal hippocampus originate from neurons of the locus coeruleus (LC). Photostimulation of LC axons produced an increase in dopamine release in the dorsal hippocampus as revealed by high-performance liquid chromatography. Furthermore, optogenetically induced release of dopamine from the LC into the dorsal hippocampus enhanced selective attention and spatial object recognition via the dopamine D1/D5 receptor. These results suggest that spatial learning and memory are energized by the release of dopamine in the dorsal hippocampus from noradrenergic neurons of the LC. The present findings are critical for identifying the neural circuits that enable proper attention selection and successful learning and memory.


2000 ◽  
Vol 22 (4) ◽  
pp. 547-557 ◽  
Author(s):  
Sandra L. Inman-Wood ◽  
Michael T. Williams ◽  
LaRonda L. Morford ◽  
Charles V. Vorhees

2020 ◽  
Author(s):  
Kai-Yuan Jhan ◽  
Guan-Jhih Lai ◽  
Pi-Kai Chang ◽  
Ren-Yu Tang ◽  
Chien-Ju Cheng ◽  
...  

Abstract Background: Parasitic infections may cause significant effects on behavior, learning, and memory of the hosts. In the brain of mice heavily infected with Angiostrongylus cantonensis, severe damages have been observed in the hippocampus. This component has been considered to have associations with spatial learning and memory in human and vertebrates. This study was designed to determine the impairments in behavior, learning, and memory in BALB/c and C57BL/6 mice heavily infected with the parasite. Methods: Each mouse was inoculated with 50 third-stage larvae of A. cantonensis. After infection, daily changes in weight and dietary consumption, worm recoveries and survival rates were determined. The forced swimming test, open field test, and Morris water maze test were employed to evaluate depression- and anxiety-like behavior as well as impairments in spatial learning and memory, respectively. In addition, in the two strains of mice were also determined. Results: The worm recovery rate in the BALB/c mice was significantly lower than that of C57BL/6 mice since day 14 post-infection. The survival rate in infected BALB/c mice decreased to 0% by day 25 whereas those with swim-training survived three more days. On day 42, the C57BL/6 mice had a survival rate of 85.7% in the swimming group and 70% in the non-swimming group. Significant differences were found in weight between infected and non-infected BALB/c and C57BL/6 mice since day 13 and day 12, respectively with corresponding changes in the dietary consumption. Depression-like behavior was found in the infected BALB/c mice but not in C57BL/6 mice. However, anxiety-like behavior was found to occur only in C57BL/6 mice. Impaired spatial learning and memory were also found in the two strains of mice occurred since day 14 post-infection. Conclusions: Results of this study indicate that A. cantonensis causes depression, anxiety, and impairments in spatial learning and memory in heavily infected mice. Moreover, significantly higher severity was observed in the Th-2 dominant BALB/c mice. Keywords: Angiostrongyliasis cantonensis, mice, behavior, learning, memory, forced swimming test, open field test, Morris water maze test


2020 ◽  
Vol 32 (5) ◽  
pp. 257-264
Author(s):  
S.S. Zulu ◽  
O. Abboussi ◽  
N. Simola ◽  
M.V. Mabandla ◽  
W.M.U. Daniels

AbstractObjectives:Growing evidence suggested that antiretroviral (ARV) drugs may promote amyloid beta (Aβ) accumulation in HIV-1-infected brain and the persistence of HIV-associated neurocognitive disorders (HANDs). It has also been shown that lipid peroxidation upregulates β-site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1) expression and subsequently promotes Aβ peptide production. In the present study, we examined whether chronic exposure to the anti-HIV drugs tenofovir disoproxil fumarate (TDF) and nevirapine induces lipid peroxidation thereby promoting BACE1 and Aβ generation and consequently impair cognitive function in mice.Methods:TDF or nevirapine was orally administered to female BALB/c mice once a day for 8 weeks. On the 7th week of treatment, spatial learning and memory were assessed using the Morris water maze test. The levels of lipid peroxidation, BACE1, amyloid β 1-42 (Aβ1-42) and Aβ deposits were measured in the hippocampal tissue upon completion of treatment.Results:Chronic administration of nevirapine induced spatial learning and memory impairment in the Morris water maze test, whereas TDF did not have an effect. TDF and nevirapine administration increased hippocampal lipid peroxidation and Aβ1-42 concentration. Nevirapine further upregulated BACE1 expression and Aβ deposits.Conclusion:Our results suggest that chronic exposure to TDF and nevirapine contributes to hippocampal lipid peroxidation and Aβ accumulation, respectively, as well as spatial learning and memory deficits in mice even in the absence of HIV infection. These findings further support a possible link between ARV drug toxicity, Aβ accumulation and the persistence of HANDs.


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