Background:
Learning and memory is basic aspects in neurogenetics as most of the neurological disorders start with dementia or memory loss. Several genes associated with memory formation have been discovered. MicroRNA genes miR-1000 and miR-375 were reported to be associated with neural integration and glucose homeostasis in some insects and vertebrates. However, neuronal function of these genes is yet to be established in D. melanogaster.
Objective:
Possible role of miR-1000 and miR-375 in learning and memory formation in this fly has been explored in the present study.
Methods:
Both appetitive and aversive olfactory conditional learning were tested in the miR-1000 and miR-375 knockout (KO) strains and compared with wild one. Five days old third instar larvae were trained by allowing them to be associated with an odor with reward (fructose) or punishment (salt). Then, the larvae were tested to calculate their preferences to the odor trained with. Learning index (LI) values and larval locomotion speed were calculated for all strains.
Results:
No significant difference was observed for larval locomotion speed in mutant strains. Knockout strain of miR-1000 showed significant deficiency in both appetitive and aversive memory formation whereas miR-375 KO strain showed a significantly lower response only in appetitive one.
Conclusion:
The results of the present study indicate important role played by these two genes in forming short-term memory in D. melanogaster.
Aluminum exposure has been reported to be related to learning and memory impairment. This study examines the role of aluminum in alterating amino acids of the cerebral cortex of rats. The Step-down type tests were performed to investigate the alteration of learning and memory of rats induced by aluminum. The amino acids in the cerebral cortex were detected by high performance liquid chromatography (HLPC). Results show that the amounts of aluminum in the cerebral cortex increased by 5.0mgAl3+/(Kg·BW) group and 10.0mg Al3+/(Kg·BW) group. In the Step-down type test, the EN1 increased significantly in the Al3+ 10.0mg/(Kg·BW) group. The latency shortened obviously and the EN2 increased significantly in the 10.0mg Al3+/(Kg·BW) group. The content of Glu (Glutamic acid) increased but the content of GABA (gamma-aminobutyric acid) decreased significantly in the 10.0mg Al3+/(Kg·BW) group. This present study shows evidence that the disorder of amino acid neurotransmitters system plays an important role in the impairment of learning and memory of rats induced by aluminum.
Learning and memory requires coordinated activity between different regions of the brain. Here we studied the interaction between medial prefrontal cortex (mPFC) and hippocampal dorsal CA1 during associative odorant discrimination learning in the mouse. We found that as the animal learns to discriminate odorants in a go-no go task the coupling of high frequency neural oscillations to the phase of theta oscillations (phase-amplitude coupling or PAC) changes in a manner that results in divergence between rewarded and unrewarded odorant-elicited changes in the theta-phase referenced power (tPRP) for beta and gamma oscillations. In addition, in the proficient animal there was a decrease in the coordinated oscillatory activity between CA1 and mPFC in the presence of the unrewarded odorant. Furthermore, the changes in PAC resulted in a marked increase in the accuracy for decoding odorant identity from tPRP when the animal became proficient. Finally, we studied the role of Ca2+/calmodulin-dependent protein kinase II α (CaMKIIα), a protein involved in learning and memory, in oscillatory neural processing in this task. We find that the accuracy for decoding the odorant identity from tPRP decreases in CaMKIIα knockout mice and that this accuracy correlates with behavioral performance. These results implicate a role for PAC and CaMKIIα in olfactory go-no go associative learning in the hippocampal-prefrontal circuit.
Role of Endoplasmic Reticulum Stress in Learning and Memory Impairment and Alzheimer's Disease-Like Neuropathology in the PS19 and APPSwe Mouse Models of Tauopathy and Amyloidosis
