Age-Dependent Changes of the in Situ Protein Phosphorylation in Hippocampal Slices After Stimulation of Glutamate Receptors

1997 ◽  
pp. 1071-1075
Author(s):  
Frank Angenstein ◽  
Sabine Staak
Keyword(s):  
Protein Phosphorylation ◽  
Glutamate Receptors ◽  
Hippocampal Slices ◽  
Age Dependent ◽  
Stimulation Of

scholarly journals Activity-dependent regulation of synaptic strength by PSD-95 in CA1 neurons

2012 ◽  
Vol 107 (4) ◽  
pp. 1058-1066 ◽  
Author(s):  
Peng Zhang ◽  
John E. Lisman
Keyword(s):  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Synaptic Strength ◽  
Ca1 Neurons ◽  
Metabotropic Glutamate ◽  
Group I ◽  
Term Potentiation ◽  
Activity Dependent

CaMKII and PSD-95 are the two most abundant postsynaptic proteins in the postsynaptic density (PSD). Overexpression of either can dramatically increase synaptic strength and saturate long-term potentiation (LTP). To do so, CaMKII must be activated, but the same is not true for PSD-95; expressing wild-type PSD-95 is sufficient. This raises the question of whether PSD-95's effects are simply an equilibrium process [increasing the number of AMPA receptor (AMPAR) slots] or whether activity is somehow involved. To examine this question, we blocked activity in cultured hippocampal slices with TTX and found that the effects of PSD-95 overexpression were greatly reduced. We next studied the type of receptors involved. The effects of PSD-95 were prevented by antagonists of group I metabotropic glutamate receptors (mGluRs) but not by antagonists of ionotropic glutamate receptors. The inhibition of PSD-95-induced strengthening was not simply a result of inhibition of PSD-95 synthesis. To understand the mechanisms involved, we tested the role of CaMKII. Overexpression of a CaMKII inhibitor, CN19, greatly reduced the effect of PSD-95. We conclude that PSD-95 cannot itself increase synaptic strength simply by increasing the number of AMPAR slots; rather, PSD-95's effects on synaptic strength require an activity-dependent process involving mGluR and CaMKII.

scholarly journals STUDIES ON THE EFFECT OF CERTAIN TOXIC SUBSTANCES IN BACTERIAL CULTURES ON THE MOVEMENT OF THE INTESTINES

1926 ◽  
Vol 43 (6) ◽  
pp. 785-795 ◽  
Author(s):  
E. E. Ecker ◽  
A. Rademaekers
Keyword(s):  
Intravenous Injection ◽  
Toxic Substances ◽  
Propulsive Efficiency ◽  
Spasmodic Contraction ◽  
Strong Stimulation ◽  
Small Intestines ◽  
Slight Rise ◽  
Longitudinal Muscles ◽  
Stimulation Of

Following intravenous injection, filtrates of young cultures of B. paratyphosus B often produce marked diarrhea in rabbits. A study was made of the effect of these toxic filtrates on the motility of the small intestines of the rabbit. The observations were made on a segment of the small intestines in situ, and in the living animal. It was found that an immediate slight rise of tone of the longitudinal muscles occurred following intravenous injection of sterile broth. The same rise was noted after the injection of the toxic filtrate; but with these it was followed later (10 minutes elapsing at least) by a very strong but gradual rise of the diastolic and systolic tone, i.e., by spasmodic contraction of the intestinal muscle, which persisted at times for as long as 2 hours. In order to record simultaneously the effect on the longitudinal and circular muscles, and the propulsive efficiency of the segment the Sollmann and Rademaekers modification of Baur's technique was employed. This arrangement showed that the stimulation of the longitudinal muscles is accompanied by a similarly strong stimulation of the circular muscles, by peristalsis, and therefore by a greatly increased propulsion of intestinal contents which was sufficient to overcome the inhibition that usually occurs after preparation of the animal. With this arrangement an instance of peristaltic spasm was also noted. Broth alone failed to produce the phenomenon. Isotonic magnesium chloride or sulfate added to the bath relaxed the muscles again. Animals under deep urethane anesthesia did not show the diarrhea occurring in the intact controls, but sometimes exhibited it after the effect of the anesthetic had disappeared. So far no effects have been observed on the isolated strip (Magnus method), and further studies are being made to localize the effect, to neutralize it with a specific antiserum, and to observe the effect of filtrates of other members of the bacterial group including the dysentery bacilli.

Effects of stimulation of glutamate receptors in medial septum on some immune responses in rats

2013 ◽  
Vol 1538 ◽  
pp. 116-125 ◽  
Author(s):  
Goutam Dutta ◽  
Ananda Raj Goswami ◽  
Tusharkanti Ghosh
Keyword(s):  
Immune Responses ◽  
Glutamate Receptors ◽  
Medial Septum ◽  
Stimulation Of

On the Respective Roles of Nitric Oxide and Carbon Monoxide in Long-Term Potentiation in the Hippocampus

1999 ◽  
Vol 6 (1) ◽  
pp. 63-76 ◽  
Author(s):  
Min Zhuo ◽  
Jarmo T. Laitinen ◽  
Xiao-Ching Li ◽  
Robert D. Hawkins
Keyword(s):  
Nitric Oxide ◽  
Carbon Monoxide ◽  
Heme Oxygenase ◽  
Guanylyl Cyclase ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
No Synthase ◽  
Term Potentiation ◽  
Stimulation Of

Perfusion of hippocampal slices with an inhibitor nitric oxide (NO) synthase blocked induction of long-term potentiation (LTP) produced by a one-train tetanus and significantly reduced LTP by a two-train tetanus, but only slightly reduced LTP by a four-train tetanus. Inhibitors of heme oxygenase, the synthetic enzyme for carbon monoxide (CO), significantly reduced LTP by either a two-train or four-train tetanus. These results suggest that NO and CO are both involved in LTP but may play somewhat different roles. One possibility is that NO serves a phasic, signaling role, whereas CO provides tonic, background stimulation. Another possibility is that NO and CO are phasically activated under somewhat different circumstances, perhaps involving different receptors and second messengers. Because NO is known to be activated by stimulation of NMDA receptors during tetanus, we investigated the possibility that CO might be activated by stimulation of metabotropic glutamate receptors (mGluRs). Consistent with this idea, long-lasting potentiation by the mGluR agonist tACPD was blocked by inhibitors of heme oxygenase but not NO synthase. Potentiation by tACPD was also blocked by inhibitors of soluble guanylyl cyclase (a target of both NO and CO) or cGMP-dependent protein kinase, and guanylyl cyclase was activated by tACPD in hippocampal slices. However, biochemical assays indicate that whereas heme oxygenase is constitutively active in hippocampus, it does not appear to be stimulated by either tetanus or tACPD. These results are most consistent with the possibility that constitutive (tonic) rather than stimulated (phasic) heme oxygenase activity is necessary for potentiation by tetanus or tACPD, and suggest that mGluR activation stimulates guanylyl cyclase phasically through some other pathway.

scholarly journals Low-Intensity Ultrasound Decreases Ischemia-Induced Edema by Inhibiting N-Methyl-d-Aspartic Acid Receptors

2018 ◽  
Vol 45 (6) ◽  
pp. 675-681
Author(s):  
Binika Hada ◽  
Mrigendra Bir Karmacharya ◽  
So R. Park ◽  
Byung H. Choi
Keyword(s):  
Glutamate Receptors ◽  
Brain Edema ◽  
Aspartic Acid ◽  
Hippocampal Slices ◽  
Dependent Manner ◽  
Edema Formation ◽  
Mk 801 ◽  
Low Intensity ◽  
Low Intensity Ultrasound ◽  
Brain Edema Formation

AbstractBackground: We have previously shown that low-intensity ultrasound (LIUS), a noninvasive mechanical stimulus, inhibits brain edema formation induced by oxygen and glucose deprivation (OGD) or treatment with glutamate, a mediator of OGD-induced edema, in acute rat hippocampal slice model in vitro. Methods: In this study, we treated the rat hippocampal slices with N-methyl-d-aspartic acid (NMDA) or (S)-3,5-dihydroxyphenylglycine (DHPG) to determine whether these different glutamate receptor agonists induce edema. The hippocampal slices were then either sonicated with LIUS or treated with N-methyl-d-aspartic acid receptor (NMDAR) antagonists, namely, MK-801 and ketamine, and observed their effects on edema formation. Results: We observed that treatment with NMDA, an agonist of ionotropic glutamate receptors, induced brain edema at similar degrees compared with that induced by OGD. However, treatment with DHPG, an agonist of metabotropic glutamate receptors, did not significantly induce brain edema. Treatment with the NMDAR antagonists MK-801 or ketamine efficiently prevented brain edema formation by both OGD and NMDA in a concentration-dependent manner. N-Methyl-d-aspartic acid-induced brain edema was alleviated by LIUS in an intensity-dependent manner when ultrasound was administered at 30, 50, or 100 mW/cm2 for 20 minutes before the induction of the edema. Furthermore, LIUS reduced OGD- and NMDA-induced phosphorylation of NMDARs at Y1325. Conclusion: These results suggest that LIUS can inhibit OGD- or NMDA-induced NMDAR activation by preventing NMDAR phosphorylation, thereby reducing a subsequent brain edema formation. The mechanisms by which LIUS inhibits NMDAR phosphorylation need further investigation.

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