scholarly journals Molecular and Functional Characterization ofBacopa monniera: A Retrospective Review

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Koilmani Emmanuvel Rajan ◽  
Jayakumar Preethi ◽  
Hemant K. Singh
Keyword(s):  
Neural Plasticity ◽  
Functional Characterization ◽  
Memory Formation ◽  
Pharmacological Effect ◽  
Aminobutyric Acid ◽  
Antioxidant Mechanism ◽  
Different Dimensions ◽  
Memory Enhancer ◽  
With Memory ◽  
Fine Tune

Over the last 50 years, laboratories around the world analyzed the pharmacological effect ofBacopa monnieraextract in different dimensions, especially as a nerve tonic and memory enhancer. Studies in animal model evidenced thatBacopatreatment can attenuate dementia and enhances memory. Further, they demonstrate thatBacopaprimarily either acts via antioxidant mechanism (i.e., neuroprotection) or alters different neurotransmitters (serotonin (5-hydroxytryptamine, 5-HT), dopamine (DA), acetylcholine (ACh),γ-aminobutyric acid (GABA)) to execute the pharmacological effect. Among them, 5-HT has been shown to fine tune the neural plasticity, which is a substrate for memory formation. This review focuses on the studies which trace the effect ofBacopatreatment on serotonergic system and 5-HT mediated key molecular changes that are associated with memory formation.

scholarly journals Coordinated Plasticity between Barrel Cortical Glutamatergic and GABAergic Neurons during Associative Memory

2016 ◽  
Vol 2016 ◽  
pp. 1-20 ◽  
Author(s):  
Fenxia Yan ◽  
Zilong Gao ◽  
Pin Chen ◽  
Li Huang ◽  
Dangui Wang ◽  
...  
Keyword(s):  
Associative Memory ◽  
Neural Plasticity ◽  
High Throughput Sequencing ◽  
Memory Formation ◽  
Gabaergic Neurons ◽  
Glutamatergic Neurons ◽  
Sensory Cortices ◽  
With Memory ◽  
Odor Signal ◽  
Epigenetic Processes

Neural plasticity is associated with memory formation. The coordinated refinement and interaction between cortical glutamatergic and GABAergic neurons remain elusive in associative memory, which we examine in a mouse model of associative learning. In the mice that show odorant-induced whisker motion after pairing whisker and odor stimulations, the barrel cortical glutamatergic and GABAergic neurons are recruited to encode the newly learnt odor signal alongside the innate whisker signal. These glutamatergic neurons are functionally upregulated, and GABAergic neurons are refined in a homeostatic manner. The mutual innervations between these glutamatergic and GABAergic neurons are upregulated. The analyses by high throughput sequencing show that certain microRNAs related to regulating synapses and neurons are involved in this cross-modal reflex. Thus, the coactivation of the sensory cortices through epigenetic processes recruits their glutamatergic and GABAergic neurons to be the associative memory cells as well as drive their coordinated refinements toward the optimal state for the storage of the associated signals.

Role of MicroRNA Genes miR-1000 and miR-375 in Forming Olfactory Conditional Memory in Drosophila melanogaster

MicroRNA ◽  
2020 ◽  
Vol 09 ◽  
Author(s):  
Sadniman Rahman ◽  
Chaity Modak ◽  
Mousumi Akter ◽  
Mohammad Shamimul Alam
Keyword(s):  
Learning And Memory ◽  
Short Term Memory ◽  
Memory Loss ◽  
Memory Formation ◽  
Neural Integration ◽  
Significant Difference ◽  
Locomotion Speed ◽  
Microrna Genes ◽  
With Memory

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.

scholarly journals Regional synapse gain and loss accompany memory formation in larval zebrafish

2022 ◽  
Vol 119 (3) ◽  
pp. e2107661119
Author(s):  
William P. Dempsey ◽  
Zhuowei Du ◽  
Anna Nadtochiy ◽  
Colton D. Smith ◽  
Karl Czajkowski ◽  
...  
Keyword(s):  
Classical Conditioning ◽  
Structural Changes ◽  
Memory Formation ◽  
Excitatory Synapses ◽  
Microscopy Imaging ◽  
Functional Changes ◽  
Larval Zebrafish ◽  
Before And After ◽  
Synaptic Changes ◽  
With Memory

Defining the structural and functional changes in the nervous system underlying learning and memory represents a major challenge for modern neuroscience. Although changes in neuronal activity following memory formation have been studied [B. F. Grewe et al., Nature 543, 670–675 (2017); M. T. Rogan, U. V. Stäubli, J. E. LeDoux, Nature 390, 604–607 (1997)], the underlying structural changes at the synapse level remain poorly understood. Here, we capture synaptic changes in the midlarval zebrafish brain that occur during associative memory formation by imaging excitatory synapses labeled with recombinant probes using selective plane illumination microscopy. Imaging the same subjects before and after classical conditioning at single-synapse resolution provides an unbiased mapping of synaptic changes accompanying memory formation. In control animals and animals that failed to learn the task, there were no significant changes in the spatial patterns of synapses in the pallium, which contains the equivalent of the mammalian amygdala and is essential for associative learning in teleost fish [M. Portavella, J. P. Vargas, B. Torres, C. Salas, Brain Res. Bull. 57, 397–399 (2002)]. In zebrafish that formed memories, we saw a dramatic increase in the number of synapses in the ventrolateral pallium, which contains neurons active during memory formation and retrieval. Concurrently, synapse loss predominated in the dorsomedial pallium. Surprisingly, we did not observe significant changes in the intensity of synaptic labeling, a proxy for synaptic strength, with memory formation in any region of the pallium. Our results suggest that memory formation due to classical conditioning is associated with reciprocal changes in synapse numbers in the pallium.

scholarly journals The entorhinal cortex modulates trace fear memory formation and neuroplasticity in the mouse lateral amygdala via cholecystokinin

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Hemin Feng ◽  
Junfeng Su ◽  
Wei Fang ◽  
Xi Chen ◽  
Jufang He
Keyword(s):  
Entorhinal Cortex ◽  
Neural Plasticity ◽  
Long Term Potentiation ◽  
Fear Memory ◽  
Memory Formation ◽  
Loss Of Function ◽  
Trace Fear Conditioning ◽  
Term Potentiation ◽  
Auditory Response ◽  
Trace Fear

Although fear memory formation is essential for survival and fear-related mental disorders, the neural circuitry and mechanism are incompletely understood. Here, we utilized trace fear conditioning to study the formation of trace fear memory in mice. We identified the entorhinal cortex (EC) as a critical component of sensory signaling to the amygdala. We adopted both loss-of-function and gain-of-function experiments to demonstrate that release of the cholecystokinin (CCK) from the EC is required for trace fear memory formation. We discovered that CCK-positive neurons project from the EC to the lateral nuclei of the amygdala (LA), and inhibition of CCK-dependent signaling in the EC prevented long-term potentiation of the auditory response in the LA and formation of trace fear memory. In summary, high-frequency activation of EC neurons triggers the release of CCK in their projection terminals in the LA, potentiating auditory response in LA neurons. The neural plasticity in the LA leads to trace fear memory formation.

scholarly journals Bilateral Inhibition of γ-Aminobutyric Acid Type A Receptor Function within the Basolateral Amygdala Blocked Propofol-induced Amnesia and Activity-regulated Cytoskeletal Protein Expression Inhibition in the Hippocampus

2008 ◽  
Vol 109 (5) ◽  
pp. 775-781 ◽  
Author(s):  
Yu Ren ◽  
Fu-Jun Zhang ◽  
Qing-Sheng Xue ◽  
Xin Zhao ◽  
Bu-Wei Yu
Keyword(s):  
Protein Expression ◽  
Basolateral Amygdala ◽  
Mrna Level ◽  
Type A ◽  
Memory Formation ◽  
Aminobutyric Acid ◽  
Receptor Function ◽  
Amnesic Effect ◽  
Bicuculline Methiodide ◽  
Acid Type

Background It has been reported that bilateral lesions of the basolateral amygdala complex (BLA) blocked propofol-induced amnesia of inhibitory avoidance (IA) training. Based on these results, the authors hypothesized that the amnesia effect of propofol was partly due to its impairment of memory formation in the hippocampus through activating the BLA gamma-aminobutyric acid type A receptor function. The authors determined the changes in activity-regulated cytoskeleton-associated protein (Arc) expression to be an indicator of IA memory formation. Methods Male Sprague-Dawley rats received bilateral injection of bicuculline methiodide (10, 50, or 100 pmol/0.5 microl) or saline (0.5 microl) into the BLA. Fifteen minutes later, the rats were intraperitoneally injected with either propofol (25 mg/kg) or saline. After 5 min, the one-trial IA training was conducted. Rats intraperitoneally infused with saline served as controls and only received saline injections into the BLA. Twenty-four hours later, the IA retention latency was tested. Separate groups of rats treated the same way were killed either 30 min after IA training for hippocampal Arc mRNA measurement or after 45 min for protein level quantification. Results The largest dose of bicuculline methiodide (100 pmol) not only blocked the propofol-induced amnesia but also reversed the inhibition effect of propofol on Arc protein expression in the hippocampus (P < 0.05). However, the mRNA level of Arc showed no significant changes after propofol and bicuculline methiodide administration. Conclusions The amnesic effect of propofol seems to involve the modulation of Arc protein expression in the hippocampus, occurring through a network interaction with the BLA.

7-Chloro-4-(Phenylselanyl) Quinoline with Memory Enhancer Action in Aging Rats: Modulation of Neuroplasticity, Acetylcholinesterase Activity, and Cholesterol Levels

2019 ◽  
Vol 56 (9) ◽  
pp. 6398-6408 ◽  
Author(s):  
Anelise Barth ◽  
Ane G. Vogt ◽  
Angélica S. dos Reis ◽  
Mikaela P. Pinz ◽  
Roberta Krüger ◽  
...  
Keyword(s):  
Acetylcholinesterase Activity ◽  
Aging Rats ◽  
Cholesterol Levels ◽  
Memory Enhancer ◽  
With Memory

scholarly journals An Emerging Role of m6A in Memory: A Case for Translational Priming

2020 ◽  
Vol 21 (20) ◽  
pp. 7447
Author(s):  
Amanda M. Leonetti ◽  
Ming Yin Chu ◽  
Fiona O. Ramnaraign ◽  
Samuel Holm ◽  
Brandon J. Walters
Keyword(s):  
Learning And Memory ◽  
Memory Consolidation ◽  
Protein Translation ◽  
Memory Formation ◽  
Current Data ◽  
Neuron Development ◽  
Neuronal Functions ◽  
The Brain ◽  
Fine Tune

Investigation into the role of methylation of the adenosine base (m6A) of RNA has only recently begun, but it quickly became apparent that m6A is able to control and fine-tune many aspects of mRNA, from splicing to translation. The ability of m6A to regulate translation distally, away from traditional sites near the nucleus, quickly caught the eye of neuroscientists because of implications for selective protein translation at synapses. Work in the brain has demonstrated how m6A is functionally required for many neuronal functions, but two in particular are covered at length here: The role of m6A in 1) neuron development; and 2) memory formation. The purpose of this review is not to cover all data about m6A in the brain. Instead, this review will focus on connecting mechanisms of m6A function in neuron development, with m6A’s known function in memory formation. We will introduce the concept of “translational priming” and discuss how current data fit into this model, then speculate how m6A-mediated translational priming during memory consolidation can regulate learning and memory locally at the synapse.

scholarly journals Sensory Cortical Plasticity Participates in the Epigenetic Regulation of Robust Memory Formation

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Mimi L. Phan ◽  
Kasia M. Bieszczad
Keyword(s):  
Epigenetic Regulation ◽  
Neural Plasticity ◽  
Cortical Plasticity ◽  
Memory Formation ◽  
Sensory Cortex ◽  
Long Term Memory ◽  
Epigenetic Mechanisms ◽  
Significant Information ◽  
Expression Of Genes ◽  
Open Question

Neuroplasticity remodels sensory cortex across the lifespan. A function of adult sensory cortical plasticity may be capturing available information during perception for memory formation. The degree of experience-dependent remodeling in sensory cortex appears to determine memory strength and specificity for important sensory signals. A key open question is how plasticity is engaged to induce different degrees of sensory cortical remodeling. Neural plasticity for long-term memory requires the expression of genes underlying stable changes in neuronal function, structure, connectivity, and, ultimately, behavior. Lasting changes in transcriptional activity may depend on epigenetic mechanisms; some of the best studied in behavioral neuroscience are DNA methylation and histone acetylation and deacetylation, which, respectively, promote and repress gene expression. One purpose of this review is to propose epigenetic regulation of sensory cortical remodeling as a mechanism enabling the transformation of significant information from experiences into content-rich memories of those experiences. Recent evidence suggests how epigenetic mechanisms regulate highly specific reorganization of sensory cortical representations that establish a widespread network for memory. Thus, epigenetic mechanisms could initiate events to establish exceptionally persistent and robust memories at a systems-wide level by engaging sensory cortical plasticity for gatingwhatandhow muchinformation becomes encoded.

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