Neuroprotective effect of Centella asiatica leaf extract on hippocampal CA3 neurons: A quantitative study in mice

2016 ◽  
Vol 65 ◽  
pp. S40
Author(s):  
Hemamalini ◽  
M.S. Rao
Keyword(s):  
Quantitative Study ◽  
Leaf Extract ◽  
Neuroprotective Effect ◽  
Centella Asiatica ◽  
Hippocampal Ca3 ◽  
Ca3 Neurons

scholarly journals Centella asiatica (L.) Leaf Extract Treatment During the Growth Spurt Period Enhances Hippocampal CA3 Neuronal Dendritic Arborization in Rats

2006 ◽  
Vol 3 (3) ◽  
pp. 349-357 ◽  
Author(s):  
K. G. Mohandas Rao ◽  
S. Muddanna Rao ◽  
S. Gurumadhva Rao
Keyword(s):  
Body Weight ◽  
Leaf Extract ◽  
Centella Asiatica ◽  
Growth Spurt ◽  
Fresh Leaf ◽  
Dendritic Length ◽  
Branching Points ◽  
Dendritic Branching ◽  
Hippocampal Ca3 ◽  
Ca3 Neurons

Centella asiatica(CeA) is a creeping plant growing in damp places in India and other Asian countries. The leaves of CeA are used for memory enhancement in the Ayurvedic system of medicine, an alternative system of medicine in India. In this study, we have investigated the effect during the rat growth spurt period of CeA fresh leaf extract treatment on the dendritic morphology of hippocampal CA3 neurons, one of the regions of the brain concerned with learning and memory. Neonatal rat pups (7 days old) were fed with 2, 4 or 6 ml kg−1 body weight of fresh leaf extract of CeA for 2, 4 or 6 weeks. After the treatment period the rats were killed, their brains were removed and the hippocampal neurons were impregnated with silver nitrate (Golgi staining). Hippocampal CA3 neurons were traced using a camera lucida, and dendritic branching points (a measure of dendritic arborization) and intersections (a measure of dendritic length) were quantified. These data were compared with data for age-matched control rats. The results showed a significant increase in the dendritic length (intersections) and dendritic branching points along the length of both apical and basal dendrites in rats treated with 4 and 6 ml kg−1 body weight per day of CeA for longer periods of time (i.e. 4 and 6 weeks). We conclude that the constituents/active principles present in CeA fresh leaf extract have a neuronal dendritic growth stimulating property; hence, the extract can be used for enhancing neuronal dendrites in stress and neurodegenerative and memory disorders.

scholarly journals Neuroprotective Efficacy of Clitoria Ternacea Root Extract on Hippocampal CA3 Neurons – A Quantitative Study in Mice

2018 ◽  
Vol 35 (02) ◽  
pp. 090-095 ◽  
Author(s):  
Shetty Hemamalini ◽  
Muddanna Rao
Keyword(s):  
Neuroprotective Effect ◽  
Group Iv ◽  
Wire Mesh ◽  
Control Group ◽  
Group Iii ◽  
Group I ◽  
Branching Points ◽  
Dendritic Branching ◽  
Hippocampal Ca3 ◽  
Ca3 Neurons

Abstract Clitoria ternatea is a vigorous, herbaceous perennial legume that belongs to the Fabaceae family. All parts of the plant are used in the preparations of Ayurvedic drugs. It is an astringent, an aphrodisiac, a rejuvenator, and a brain tonic. It also has anti-inflammatory, analgesic, and antipyretic properties. Baidyanath Shankapushpi, which contains extracts of herbs such as C. ternatea, Bacopa monnieri, Withania somnifera and Asparagus racemosus, is clinically administered for memory improvement, blood purification and to improve digestion. However, its neuroprotective effect has not been reported so far. In the present study, the neuroprotective effect of C. ternatea root (CTR) extract on hippocampal CA3 neurons was investigated. Three-month-old albino mice were divided into four groups. Group I was the normal control, group II was the saline control, group III was the stress group, and group IV was the stress + CTR-treated group. Group-III mice were stressed in a wire mesh restrainer for 6 hours/day for 6 weeks. Grou-IV mice were also stressed like group III, but received CTR extract orally throughout the stress period. After 6 weeks, their brain was removed, and their hippocampi were dissected and processed for Golgi staining. The hippocampal neurons were traced using a camera lucida focused at 400x magnification. The Sholl concentric circle method was used to quantify the dendrites. The results showed a decrease in the number of dendritic branching points and of dendritic intersections in the stressed group. On the other hand, there was an increase in the number of dendritic branching points and of dendritic intersections of hippocampal CA3 neurons in group IV, which was subjected to restraint stress and was treated with the CTR extract. The results showed that the oral administration of CTR significantly increased the dendritic branching points and the dendritic intersections of hippocampal CA3 neurons.

scholarly journals Neurotrophic factor-α1, a novel tropin is critical for the prevention of stress-induced hippocampal CA3 cell death and cognitive dysfunction in mice: comparison to BDNF

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Lan Xiao ◽  
Vinay Kumar Sharma ◽  
Leila Toulabi ◽  
Xuyu Yang ◽  
Cheol Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Learning And Memory ◽  
Cognitive Dysfunction ◽  
Neurotrophic Factor ◽  
Maternal Separation ◽  
Pyramidal Neurons ◽  
Neuroprotective Activity ◽  
Weaning Stress ◽  
Hippocampal Ca3 ◽  
Ca3 Neurons

AbstractStress leads to brain pathology including hippocampal degeneration, cognitive dysfunction, and potential mood disorders. Hippocampal CA3, a most stress-vulnerable region, consists of pyramidal neurons that regulate cognitive functions e.g. learning and memory. These CA3 neurons express high levels of the neuroprotective protein, neurotrophic factor-α1 (NF-α1), also known as carboxypeptidase E (CPE), and receive contacts from granule cell projections that release BDNF which has neuroprotective activity. Whether NF-α1-CPE and/or BDNF are critical in protecting these CA3 neurons against severe stress-induced cell death is unknown. Here we show that social combined with the physical stress of maternal separation, ear tagging, and tail snipping at weaning in 3-week-old mice lacking NF-α1-CPE, led to complete hippocampal CA3 degeneration, despite having BDNF and active phosphorylated TrkB receptor levels similar to WT animals. Mice administered TrkB inhibitor, ANA12 which blocked TrkB phosphorylation showed no degeneration of the CA3 neurons after the weaning stress paradigm. Furthermore, transgenic knock-in mice expressing CPE-E342Q, an enzymatically inactive form, replacing NF-α1-CPE, showed no CA3 degeneration and exhibited normal learning and memory after the weaning stress, unlike NF-α1-CPE-KO mice. Mechanistically, we showed that radio-labeled NF-α1-CPE bound HT22 hippocampal cells in a saturable manner and with high affinity (Kd = 4.37 nM). Subsequently, treatment of the HT22cpe−/− cells with NF-α1-CPE or CPE-E342Q equivalently activated ERK signaling and increased BCL2 expression to protect these neurons against H2O2-or glutamate-induced cytotoxicity. Our findings show that NF-α1-CPE is more critical compared to BDNF in protecting CA3 pyramidal neurons against stress-induced cell death and cognitive dysfunction, independent of its enzymatic activity.

Hyperexcitability of hippocampal CA3 neurons in spontaneously epileptic rats (SER) by intracellular recording

1991 ◽  
Vol 14 ◽  
pp. S47
Author(s):  
Masashi Sasa ◽  
Kumatoshi Ishihara ◽  
Tadao Serikawa ◽  
Shuji Takaori
Keyword(s):  
Intracellular Recording ◽  
Hippocampal Ca3 ◽  
Ca3 Neurons

Altered Regulation of Potassium and Calcium Channels by GABAB and Adenosine Receptors in Hippocampal Neurons From Mice Lacking Gαo

2000 ◽  
Vol 83 (2) ◽  
pp. 1010-1018 ◽  
Author(s):  
Gabriela J. Greif ◽  
Deborah L. Sodickson ◽  
Bruce P. Bean ◽  
Eva J. Neer ◽  
Ulrike Mende
Keyword(s):  
Time Constant ◽  
Hippocampal Neurons ◽  
Ionic Currents ◽  
Absolute Requirement ◽  
Voltage Dependent ◽  
Hippocampal Ca3 ◽  
Ca3 Neurons ◽  
Inwardly Rectifying ◽  
G Protein Coupled

To examine the role of Go in modulation of ion channels by neurotransmitter receptors, we characterized modulation of ionic currents in hippocampal CA3 neurons from mice lacking both isoforms of Gαo. In CA3 neurons from Gαo −/− mice, 2-chloro-adenosine and the GABAB-receptor agonist baclofen activated inwardly rectifying K+ currents and inhibited voltage-dependent Ca2+ currents just as effectively as in Gαo +/+ littermates. However, the kinetics of transmitter action were dramatically altered in Gαo −/− mice in that recovery on washout of agonist was much slower. For example, recovery from 2-chloro-adenosine inhibition of calcium current was more than fourfold slower in neurons from Gαo −/− mice [time constant of 12.0 ± 0.8 (SE) s] than in neurons from Gαo +/+ mice (time constant of 2.6 ± 0.2 s). Recovery from baclofen effects was affected similarly. In neurons from control mice, effects of both baclofen and 2-chloro-adenosine on Ca2+ currents and K+currents were abolished by brief exposure to external N-ethyl-maleimide (NEM). In neurons lacking Gαo, some inhibition of Ca2+ currents by baclofen remained after NEM treatment, whereas baclofen activation of K+ currents and both effects of 2-chloro-adenosine were abolished. These results show that modulation of Ca2+ and K+ currents by G protein-coupled receptors in hippocampal neurons does not have an absolute requirement for Gαo. However, modulation is changed in the absence of Gαo in having much slower recovery kinetics. A likely possibility is that the very abundant Gαo is normally used but, when absent, can readily be replaced by G proteins with different properties.

scholarly journals Synapse type-specific proteomic dissection identifies IgSF8 as a hippocampal CA3 microcircuit organizer

2019 ◽  
Author(s):  
Nuno Apóstolo ◽  
Samuel N. Smukowski ◽  
Jeroen Vanderlinden ◽  
Giuseppe Condomitti ◽  
Vasily Rybakin ◽  
...  
Keyword(s):  
Cell Surface ◽  
Pyramidal Neurons ◽  
Mossy Fiber ◽  
Surface Protein ◽  
Guidance Cue ◽  
Hippocampal Ca3 ◽  
Cell Surface Interactions ◽  
Ca3 Pyramidal Neurons ◽  
Ca3 Neurons ◽  
Multiple Ligand

SummarySynaptic diversity is a key feature of neural circuits. The structural and functional diversity of closely spaced inputs converging on the same neuron suggests that cell-surface interactions are essential in organizing input properties. Here, we analyzed the cell-surface protein (CSP) composition of hippocampal mossy fiber (MF) inputs on CA3 pyramidal neurons to identify regulators of MF-CA3 synapse properties. We uncover a rich cell-surface repertoire that includes adhesion proteins, guidance cue receptors, extracellular matrix (ECM) proteins, and uncharacterized CSPs. Interactome screening reveals multiple ligand-receptor modules and identifies ECM protein Tenascin-R (TenR) as a ligand of the uncharacterized neuronal receptor IgSF8. Presynaptic Igsf8 deletion impairs MF-CA3 synaptic architecture and robustly decreases the density of bouton filopodia that provide feedforward inhibition of CA3 neurons. Consequently, loss of IgSF8 increases CA3 neuron excitability. Our findings identify IgSF8 as a regulator of CA3 microcircuit development and suggest that combinations of CSP modules define input identity.

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