Protective effect of CCK-8 and ceruletide on glutamate-induced neuronal cell death in rat neuron cultures: Possible involvement of CCK-B receptors

Katsuura, Goro; Shinohara, Shunji; Shintaku, Haruyuki; Eigyo, Masami; Matsushita, Akira

doi:10.1016/0304-3940(91)90291-z

Cited by 28 publications

(11 citation statements)

References 14 publications

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“…From numerous studies on apoA-I mimetic peptides based on one or two amphiphilic ␣ -helical segments (22)(23)(24)(25)(26), a wide range of peptide sequences have been found that are more-or-less effective in various aspects of apoA-I mimicry. Many of these peptides have no sequence homology to apoA-I, as they capitalize on an amphiphilic ␣ -helical structural motif, and some are composed of all D -amino acids ( 21 ). Although in vivo effi cacy has been demonstrated for certain peptides in animal models of atherosclerosis, their mechanisms of action remain the subject of active research (27)(28)(29)(30)(31)(32)(33).…”

Section: In Vivo Effi Cacymentioning

confidence: 99%

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In vivo efficacy of HDL-like nanolipid particles containing multivalent peptide mimetics of apolipoprotein A-I

Zhao

Black

Bonnet

et al. 2014

Journal of Lipid Research

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Section: In Vivo Effi Cacymentioning

confidence: 99%

“…apoA-I mimetics previously reported (and administered parenterally) ( 21 ). Oral effi cacy was observed in spite of the peptide segments being comprised of L -amino acids, which would make them vulnerable to rapid proteolytic degradation.…”

mentioning

confidence: 93%

In vivo efficacy of HDL-like nanolipid particles containing multivalent peptide mimetics of apolipoprotein A-I

Zhao

Black

Bonnet

et al. 2014

Journal of Lipid Research

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“…Excitotoxity of glutamate was reduced in the presence of CCK. This action is thought to be mediated by CCKB receptors (Katsuura et al, 1991) and to occur via a reduction in glutamate-evoked intracellular Ca2+, but CCK itself seems to increase the intracellular Ca2+ concentration (Kaufmann et a/., 1994). In our study on neuronal activity, CCK-8S mainly enhanced the excitatory effect of glutamate.…”

Section: Discussionmentioning

confidence: 42%

“…Furthermore, since CCK receptors are reduced in the neostriatum of patients who suffer from degenerative diseases such as Huntington's disease (Hays et al, 1981a) and glutamate has been reported to be responsible for degeneration (Katsuura et al, 1991), we were interested in seeking possible interactions of CCK-8S with glutamate. Both transmitters may coexist in cortical fibres, and may be released from corticostriatal afferents (You et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Cholecystokinin Excites Neostriatal Neurons in Rats via CCKA or CCKB Receptors

Davidowa

Albrecht

Gabriel

et al. 1995

Eur J of Neuroscience

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The effect of iontophoretically applied cholecystokinin (CCK) on neurons of the neostriatum was studied in rats anaesthetized with urethane. The most frequently observed effect of the sulphated octapeptide (CCK-8S) on striatal neurons was excitation. Spontaneously active neurons responded more often to CCK-8S than quiescent cells. Silent, primarily non-responsive neurons could often be stimulated with CCK-8S using glutamate to induce an ongoing discharge. Thus, 45.8% of the 177 neurons studied changed their discharge rate by more than 30%. Certain CCK receptor antagonists could prevent the effect of CCK-8S, fully or at least partly, in the majority of CCK-responsive neurons. The data suggest that cholecystokinin modulates the firing of active neostriatal neurons via the CCKA or the CCKB receptor type. Furthermore, we compared neuronal responses to glutamate with those recorded during concomitant administration of CCK-8S in order to study the interaction of both transmitters, which may be colocalized in striatal afferents. CCK-8S mainly enhanced the excitatory effect of glutamate on striatal neurons, but in several neurons the response to glutamate was reduced. The CCKB receptor antagonist could prevent CCK-8S from increasing the glutamate-induced activation.

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“…Thus, it has been demonstrated that stimulation of CCK receptors with CCK-8 or ceruletide can protect cultured rat cortical neurones against the toxic effect of glutamate (Akaike, 1991;Katsuura et al, 1991). A CCKB selective antagonist, L365 260, counteracted this effect.…”

Section: Introductionmentioning

confidence: 96%

Cholecystokinin peptides and receptor binding in Alzheimer's disease

Löfberg

Harro

Gottfries³

et al. 1996

J. Neural Transmission

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Cholecystokinin (CCK) is a peptide that can be found in the cerebral cortex in high concentrations and is involved in learning and memory as well as neurodegenerative processes. Cortical brain samples from 9 patients with Alzheimer's disease and 9 matched control cases were studied with respect to the concentrations of various molecular forms of CCK and the CCK receptor binding characteristics. No differences were found between patients and controls in any of these measures. Significant correlations were found between the concentrations of CCK-8 sulphated and the three nonsulphated CCK peptides measured. In addition, the concentrations of CCK-4 and CCK-5 showed a highly significant and positive correlation.

show abstract

Protective effect of CCK-8 and ceruletide on glutamate-induced neuronal cell death in rat neuron cultures: Possible involvement of CCK-B receptors

Cited by 28 publications

References 14 publications

In vivo efficacy of HDL-like nanolipid particles containing multivalent peptide mimetics of apolipoprotein A-I

In vivo efficacy of HDL-like nanolipid particles containing multivalent peptide mimetics of apolipoprotein A-I

Cholecystokinin Excites Neostriatal Neurons in Rats via CCKA or CCKB Receptors

Cholecystokinin peptides and receptor binding in Alzheimer's disease

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