scholarly journals Spatial learning and memory deficit of low level polybrominated diphenyl ethers-47 in male adult rat is modulated by intracellular glutamate receptors

2012 ◽  
Vol 37 (2) ◽  
pp. 223-233 ◽  
Author(s):  
Tang Yan ◽  
Li Xiang ◽  
Jiang Xuejun ◽  
Chen Chengzhi ◽  
Qi Youbin ◽  
...  
Keyword(s):  
Glutamate Receptors ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Polybrominated Diphenyl Ethers ◽  
Memory Deficit ◽  
Spatial Learning And Memory ◽  
Male Adult ◽  
Adult Rat ◽  
Diphenyl Ethers ◽  
Learning And Memory Deficit

scholarly journals Prenatal Stress Induced Spatial Memory Deficit in a Sex-Specific Manner in Mice: Possible Involvement of Hippocampal Insulin Resistance

2021 ◽  
Author(s):  
Massomeh Mohammadi ◽  
◽  
Ali Haeri-Rohani ◽  
Parichehr Yaghmaei ◽  
Hedayat Sahraei ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Prenatal Stress ◽  
Insulin Receptors ◽  
Memory Deficit ◽  
Spatial Learning And Memory ◽  
Control Male ◽  
Control Female ◽  
Learning And Memory Deficit

Introduction: In the present study, the effects of prenatal stress on spatial learning and memory deficit and its relationship with hippocampal insulin resistance was examined in male and female offspring. Method: Female NMRI mice were mate with males overnight and the zero day of pregnancy was detected (Gestational day zero-GD0). The pregnant mice were then randomly divided into stress and control groups. The stress group received stress from the GD0 to GD10. On post natal day 30 (PND30) the offspring were divided into for subgroups namely: male-control, female-control, male-stress, and female-stress. Barnes maze (BM) method was used for spatial learning evaluation. Plasma cortisol and insulin levels were measured at the beginning of the experiments. At the end of the experiments, the animals’ brains were removed and their hippocampus was extracted. The hippocampus was homogenized and its insulin and insulin receptor contents were evaluated. Results: The stressed animals needed more time for reaching to target hole. In addition, they spend more distance for finding the target hole, which was more pronounced in the male offspring. Both plasma and hippocampal insulin content were reduced in stressed groups. Moreover, the hippocampal insulin receptors protein was reduced in the stressed animals. There was a positive relationship between plasma and hippocampal content and memory deficit in the stressed groups. Conclusion: These results indicated that prenatal stress can induce spatial learning and memory deficit in offspring which is associated with plasma and hippocampal insulin and receptor content reduction (hippocampal insulin resistance) in these animals.

scholarly journals Intranasal Insulin Prevents Anesthesia-Induced Spatial Learning and Memory Deficit in Mice

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Yongli Zhang ◽  
Chun-ling Dai ◽  
Yanxing Chen ◽  
Khalid Iqbal ◽  
Fei Liu ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Spatial Learning ◽  
Memory Deficit ◽  
Spatial Learning And Memory ◽  
Intranasal Insulin ◽  
Learning And Memory Deficit

Effect of neonatal handling on adult rat spatial learning and memory following acute stress

Stress ◽  
2008 ◽  
Vol 11 (2) ◽  
pp. 148-159 ◽  
Author(s):  
A. Stamatakis ◽  
A. Stamatakis ◽  
S. Pondiki ◽  
A. Stamatakis ◽  
S. Pondiki ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Spatial Learning ◽  
Acute Stress ◽  
Spatial Learning And Memory ◽  
Neonatal Handling ◽  
Adult Rat

scholarly journals Calcium sensor regulation of the CaV2.1 Ca2+ channel contributes to long-term potentiation and spatial learning

2016 ◽  
Vol 113 (46) ◽  
pp. 13209-13214 ◽  
Author(s):  
Evanthia Nanou ◽  
Todd Scheuer ◽  
William A. Catterall
Keyword(s):  
Synaptic Plasticity ◽  
Glutamate Receptors ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Long Term Potentiation ◽  
Spatial Learning And Memory ◽  
Calcium Sensor ◽  
Short Term ◽  
Sensor Proteins

Many forms of short-term synaptic plasticity rely on regulation of presynaptic voltage-gated Ca2+ type 2.1 (CaV2.1) channels. However, the contribution of regulation of CaV2.1 channels to other forms of neuroplasticity and to learning and memory are not known. Here we have studied mice with a mutation (IM-AA) that disrupts regulation of CaV2.1 channels by calmodulin and related calcium sensor proteins. Surprisingly, we find that long-term potentiation (LTP) of synaptic transmission at the Schaffer collateral-CA1 synapse in the hippocampus is substantially weakened, even though this form of synaptic plasticity is thought to be primarily generated postsynaptically. LTP in response to θ-burst stimulation and to 100-Hz tetanic stimulation is much reduced. However, a normal level of LTP can be generated by repetitive 100-Hz stimulation or by depolarization of the postsynaptic cell to prevent block of NMDA-specific glutamate receptors by Mg2+. The ratio of postsynaptic responses of NMDA-specific glutamate receptors to those of AMPA-specific glutamate receptors is decreased, but the postsynaptic current from activation of NMDA-specific glutamate receptors is progressively increased during trains of stimuli and exceeds WT by the end of 1-s trains. Strikingly, these impairments in long-term synaptic plasticity and the previously documented impairments in short-term synaptic plasticity in IM-AA mice are associated with pronounced deficits in spatial learning and memory in context-dependent fear conditioning and in the Barnes circular maze. Thus, regulation of CaV2.1 channels by calcium sensor proteins is required for normal short-term synaptic plasticity, LTP, and spatial learning and memory in mice.

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