Inhibition by Forskolin of Excitatory Amino Acid‐Induced Accumulation of Cyclic AMP in Guinea Pig Hippocampal Slices

Baba, Akemichi; Nishiuchi, Yukiko; Uemura, Akinori; Tatsuno, Tohru; Iwata, Hisato

doi:10.1111/j.1471-4159.1988.tb04861.x

Cited by 9 publications

(7 citation statements)

References 36 publications

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“…In the present studies tetanic stimulation of the Schaffer collateral inputs into area CAl induced LTP in greater than 90% of tetanized slices. The same tetanic stimulation paradigm was found to elicit increases in cAMP in area CAl, assayed 1 min after tetanus (146% ± 10%o of control, n = 20) ( If the tetanus-induced rise in cAMP is mediated by NMDA receptor activation, then application of NMDA receptor agonists should also produce elevations in cAMP (19). We found that bath application of NMDA to hippocampal slices produced concentration-dependent elevation of cAMP in area CAl (Fig.…”

Section: Resultssupporting

confidence: 52%

N-methyl-D-aspartate receptor activation increases cAMP levels and voltage-gated Ca2+ channel activity in area CA1 of hippocampus.

Chetkovich

Gray

Johnston³

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

246

111

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Tetanic stimulation of the Schaffer collateral inputs into area CA1 of the hippocampus causes N-methyl-Daspartate (NMDA) receptor activation, an effect that contributes to the induction of long-term potentiation (LTP) in this region. The present studies demonstrate that LTP-inducing tetanic stimulation in rat hippocampal area CA1 elicited increased levels of cAMP. The elevation of cAMP was blocked by the NMDA receptor antagonist DL-2-amino-5-phosphonovaleric acid (APV). Bath application of NMDA also resulted in an increase in cAMP in CA1, an effect that was blocked by both APV and removal of extracellular Ca2+. These frndings suggest that activation of NMDA receptors elicits a Ca2+-dependent increase in cAMP, and taken together with the data from tetanic stimulation, suggest that NMDA-receptor-mediated increases in cAMP could play a role in the induction of LTP in area CAL. One role for cAMP may be to increase Ca2+ influx through voltage-gated Ca21 channels, as it was observed that application of either Long-term potentiation of synaptic transmission (LTP) is a robust form of synaptic plasticity that is a strong candidate mechanism for learning and memory in the mammalian brain (for reviews, see refs. 1 and 2). The induction of the most commonly studied form of LTP in area CA1 of the hippocampus requires activation of N-methyl-D-aspartate (NMDA) receptors (3, 4). NMDA receptor activation allows the influx of Ca2+ into neurons, an effect that has been causally linked to the induction of LTP (5-8). The biochemical sequelae of the NMDA-receptor-mediated Ca2+ influx, however, are not well characterized. Available evidence suggests that the activation of Ca2+-dependent protein kinases contributes to the induction of LTP (9-12). Ca2+ is a pleuripotent second messenger, and many biochemical effects of Ca2' are well documented in the central nervous system, including activation, through calmodulin, ofadenylyl cyclase (13,14). In the experiments reported here, we tested the hypothesis that NMDA receptor activation increases cAMP in area CA1 of the hippocampus and that a physiological consequence of increased cAMP is an increase in the activity of voltage-gated Ca2+ channels. (1) in the CA1 region were monitored for 20 min to assure a stable baseline. Tetanic stimulation consisted of three one-s trains of stimuli (100 Hz) every 5 s at the minimum stimulus current needed to elicit a maximal population excitatory postsynaptic potential (EPSP). This stimulus was sufficient to induce LTP in >90%o of slices (20 of 22). LTP was defined as a 20% or greater increase in initial EPSP slope, or in initial experiments it was defined as a 30% or greater increase in population spike amplitude. When present, DL-2-amino-5-phosphonovaleric acid (APV) was 50 ,AM in the bath, a concentration that was found to block LTP induced by this stimulus paradigm (n = 6). MATERIALS AND METHODSMeasurement of cAMP. Slices were allowed to adjust to the recording chamber for 1.5-2 hr to allow cAMP levels to stabilize (15). Slices were removed fr...

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Section: Resultssupporting

confidence: 52%

N-methyl-D-aspartate receptor activation increases cAMP levels and voltage-gated Ca2+ channel activity in area CA1 of hippocampus.

Chetkovich

Gray

Johnston³

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

246

111

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“…However, the binding of kainate to the glutamate receptor subtype which appears to be responsible for the observed potentiation is not modulated by chloride (Simon et al, 1976;Foster and Fagg, 1984;Cowburn et al, 1989). Interestingly, the glutamate-stimulated cAMP accumulation reported in rat hippocampal slices was also Cl--dependent (Baba et al, 1988). Thus chloride may be involved at another level of signal transduction.…”

Section: Discussionmentioning

confidence: 85%

Modulation of VIP‐Stimulated cAMP Formation by Excitatory Amino Acids in Mouse Cerebral Cortex

Schaad

Schorderet

Magistretti³

1990

Eur J of Neuroscience

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We have investigated the modulatory action of excitatory amino acids (EAA) on vasoactive intestinal polypeptide (VIP)-stimulated cAMP formation in mouse cerebral cortical slices. Glutamate and aspartate potentiate in a concentration-dependent manner the effect of VIP. In order to characterize the type of receptor involved, we have used three prototypical EAA receptor agonists, that is, kainate, N-methyl-d-aspartate (NMDA) and quisqualate. Kainate mimicked the effect of glutamate, NMDA was inactive and quisqualate displayed an inhibitory action. Furthermore, ibotenate also potentiated the effect of VIP on cAMP formation, while l-homocysteate exhibited an inhibitory action. Ibotenate was 4-fold more potent and 2.5 times more effective than glutamate. However, the effects of kainate and ibotenate were not additive, suggesting the activation of a common receptor. Thus, based on this metabotropic action, EAA can be categorized into the following classes: (i) those that potentiate the effect of VIP, such as glutamate, aspartate, kainate and ibotenate; (ii) those that inhibit the effect of VIP, such as l-homocysteate and quisqualate; and (iii) those that are ineffective, such as NMDA and d-homocysteate. The effects of glutamate or ibotenate on VIP-stimulated cAMP formation were completely inhibited by l-phosphoserine and only partially by kynurenate. In a low chloride medium, or in the presence of 8-(N,N-diethylamino) octyl-3,4,5-trimethoxybenzoate-hydrochloride (TMB-8), an inhibitor of calcium release from internal stores, EAA did not potentiate the effect of VIP, thus stressing the importance of these ions for the transduction of the glutamatergic signal. Our results indicate the existence of marked interactions between EAA and VIP on cAMP formation; the pharmacology of these interactions is, however, clearly distinct from the classical pharmacology of EAA which is mainly based on electrophysiological and binding studies.

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“…In guinea-pig brain, responses to adenosine or its analogue 2-chloroadenosine are greatly enhanced by both 5-HT and by histamine HI-receptor activation (Schultz & Daly, 1973;Donaldson et al, 1990) but in the human cortical slices the 2-chloroadenosine dose-response curve was not significantly affected by the inclusion of either 5-HT or histamine (Figure 6). Excitatory amino acids also potentiate the cyclic AMP response to 2-chloroadenosine in guinea-pig (Baba et al, 1988;Donaldson et al, 1990) but in the human slices, quisqualic acid and glutamate were without effect (data not shown).…”

Section: I-t-l-mentioning

confidence: 98%

Direct and indirect stimulations of cyclic AMP formation in human brain

Kendall

Millns

Firth

1992

British J Pharmacology

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1 Adenosine 3':5'-cyclic monophosphate (cyclic AMP) formation, by use of an [3H]-adenine prelabelling assay, was measured in fragments of human cerebral cortex, taken in the course of various neurosurgical procedures. 2 Large accumulations of [3H]-cyclic AMP due to isoprenaline, noradrenaline and adenosine and small effects due to forskolin were observed. Histamine, 5-hydroxytryptamine (5-HT) and the excitatory amino acids glutamate and quisqualate were ineffective.3 The response to noradrenaline consisted of two components; a direct P-adrenoceptor response and an enhancement mediated by an a-adrenoceptor which appears to be similar to that in rat cerebral cortex.4 The response to isoprenaline was also potentiated by histamine H, receptor stimulation but the direct effect of 2-chloroadenosine was not altered by histamine, 5-HT or quisqualate. 5 It is concluded that some, but not all, of the indirect modulations of cyclic AMP formation previously observed in experimental animal brain exist in human cerebral cortex.

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Inhibition by Forskolin of Excitatory Amino Acid‐Induced Accumulation of Cyclic AMP in Guinea Pig Hippocampal Slices

Cited by 9 publications

References 36 publications

N-methyl-D-aspartate receptor activation increases cAMP levels and voltage-gated Ca2+ channel activity in area CA1 of hippocampus.

N-methyl-D-aspartate receptor activation increases cAMP levels and voltage-gated Ca2+ channel activity in area CA1 of hippocampus.

Modulation of VIP‐Stimulated cAMP Formation by Excitatory Amino Acids in Mouse Cerebral Cortex

Direct and indirect stimulations of cyclic AMP formation in human brain

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