Characterization of subtypes of excitatory amino acid receptors involved in the stimulation of inositol phosphate synthesis in rat brain synaptoneurosomes

Récasens, Max; Sassetti, Isabelle; Nourigat, Agnès; Sladeczek, Fritz; Bockaert, Joël

doi:10.1016/0014-2999(87)90413-4

Cited by 131 publications

(19 citation statements)

References 25 publications

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“…In connection with this, our in vitro data from hypothalamic neurons in primary culture, have shown that GLU exerts a stimulatory action on SRIF release essentially through NMDA-type receptor sites (4). The present data show that these findings obtained in foetal cells can also be obtained in adult animals despite the decline in GLU transduction mechanisms observed in other cerebral tissues during postnatal development (15,16). Direct evidence of SRIF release from the ME in conscious animals when a pharmacological agent is peripherally administered, represents an original approach to push-pull perfusion (8).…”

Section: Discussionsupporting

confidence: 78%

Glutamate Peripherally Administered Exerts Somatostatin‐Releasing Action in the Conscious Rat

Benyassi

Tapia‐Arancibia

Arancibia

1991

J Neuroendocrinology

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This study was designed to determine whether glutamate is able to stimulate somatostatin release from in vivo conscious animals when somatostatin release is monitored in unanaesthetized rats stereotaxically implanted with a push-pull cannula in the median eminence. One week after implantation, the median eminence was perfused with artificial cerebrospinal fluid alone or with the addition of either CGS 19755, an N-methyl-D-aspartate (NMDA) receptor antagonist M). The latter (which is able to cross the brain-blood barrier at large doses) was also peripherally administered (1 g/kg ip). Median eminence perfusate samples were collected every 15 min and somatostatin was measured by a sensitive radioimmunoassay. In rats receiving ip glutamate injection, somatostatin release from the median eminence was significantly increased (73.3+ 10.4 versus 24.8k6.2; P

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Section: Discussionsupporting

confidence: 78%

Glutamate Peripherally Administered Exerts Somatostatin‐Releasing Action in the Conscious Rat

Benyassi

Tapia‐Arancibia

Arancibia

1991

J Neuroendocrinology

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“…Although consistent with the 'covariance' hypothesis and with similar experiments performed in neocortical area (Baranyi & Szente, 1987;Bindman, Murphy & Pockett, 1988;Fregnac et al 1988), the underlying mechanisms may well be different, again because-of the absence of NMDA receptors on PCs. Interestingly, stimulation of ionotropic and of metabotropic QA receptors (Sladeezek, Pin, Recasens, Bockaert & Weiss, 1985;Recasens, Sassetti, Nourigat, Sladeczek & Bockaert, 1987;Sugiyama, Ito & Hirono, 1987), coupled with sodium channel activation, triggers arachidonic acid release in cultured striatal neurones (Dumuis, Pin, Sebben & Bockaert, 1990). In the hippocampus, this molecule acts as a retrograde messenger released by the postsynaptic cell to increase Glu release by presynaptic terminals, and thus contributes to maintenance of LTP Williams, Errington, Lynch & Bliss, 1989).…”

Section: Pairing Of Pf-mediated Epsps With Ca2l Spikesmentioning

confidence: 99%

Pairing of pre‐ and postsynaptic activities in cerebellar Purkinje cells induces long‐term changes in synaptic efficacy in vitro.

Crépel

Jaillard

1991

The Journal of Physiology

240

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SUMMARY1. An in vitro slice preparation of rat cerebellar cortex was used to analyse longlasting modifications of synaptic transmission at parallel fibre (PF)-Purkinje cell (PC) synapses. These use-dependent changes were induced by pairing PF-mediated EPSPs evoked at low frequency (1 Hz) with different levels of membrane polarization (or bioelectrical activities) of PCs for 15 min.2. Experiments were performed on forty-eight PCs recorded intracellularly in a conventional perfused chamber, and in fifty other cells maintained in a static chamber either in the presence (n = 21) or in the absence (n = 29) of 400 nM-phorbol 12,13-dibutyrate (PDBu).3. In these three experimental conditions, PF-mediated EPSPs were always measured on PCs maintained at a holding potential of -75 mV, and further hyperpolarized by constant hyperpolarizing pulses. This allowed us both to test the input resistance of PCs and to avoid their firing during PF-mediated EPSPs.4. In all cells retained for the present study, latencies of PF-mediated EPSPs evoked at 0-2 Hz were stable during the pre-pairing period, and the same was true for their amplitude and time course.5. In the perfused chamber, pairing of PF-mediated EPSPs with the same hyperpolarization of PCs as that used for measurements of synaptic responses had no effect on these EPSPs in 30% of PCs. It induced long-term depression (LTD) and long-term potentiation (LTP) in 23 and 47 % of the tested cells respectively (n = 17).6. In the perfused chamber, pairing of PF-mediated EPSPs with moderate depolarization of PCs (n = 19) giving rise to a sustained firing of sodium spikes significantly favoured the appearance of LTP as compared to the previous pairing protocol. However, there were still 27 and 15 % of cells which showed no modification and LTD respectively.7. In contrast, pairing of PF-mediated EPSPs with calcium (Ca2") spikes evoked by strong depolarization of PCs (n = 12) led to LTD of synaptic transmission in nearly half of the tested cells, whereas LTP was now observed in less than 20 % of them. MS 8485F. CREPEL AND D. JAILLARD 8. In the static chamber and in the absence of PDBu, LTD of PF-mediated EPSPs was observed in most cells, whatever the pairing protocol with sodium or Ca2+ spikes.9. This shift towards LTD was significantly reversed by PDBu in the pairing protocol using firing of sodium spikes, but not in the case of pairings with Ca2+ spikes.10. Whatever the protocol used, long-term synaptic changes were not accompanied by any significant variation of cell input resistance or latency of EPSPs. In all cases, LTP and LTD were accompanied by increase and decrease of the initial slope of PF-mediated EPSPs.11. These results, together with those from previous studies, suggest that induction of LTP at PF-PC synapses is at least partly presynaptic and can be increased by direct activation of protein kinase C. They also suggest that PCs can reinforce this LTP or alternatively can convert it into LTD depending on their firing on sodium or Ca2+ spikes.

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“…Plasma membranes were obtained from bovine brain as described by Olsen et al [2l] and Recasens et al [22]. Coated vesicles were obtained by Shephacryl S 1000 gel filtration as described by Bar-Zvi and Branton [23] and modified by Gonzjlez-Calero et al [18].…”

Section: Prepararion Of Metnbranes and Coaled Vesiclesmentioning

confidence: 99%

Presence of phospholipase C in coated vesicles from bovine brain Dual regulatory effects of GTP‐analogs

Martı́n¹,

Ros²,

González-Calero³

et al. 1991

FEBS Letters

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Bovine brain coated vesicles display free calcium‐dependent phospholipase C activity. Gpp(NH)p and GTPγS inhibited phospholipase C at nanomolar concentrations. Increasing concentrations of Gpp(NH)p and GTPγS reversed the inhibitory effects and stimulated phospholipase C activity. Preincubation of coated vesicles with pertussis toxin blocked the poorly‐hydrolyzable GTP‐analogs' inhibitory effects on phospholipase C. These data indicate that guanine nucleotides exert a dual regulatory control of phospholipase C in coated vesicles and that the inhibitory pathway is mediated by a pertussis toxin‐sensitive G‐protein.

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Characterization of subtypes of excitatory amino acid receptors involved in the stimulation of inositol phosphate synthesis in rat brain synaptoneurosomes

Cited by 131 publications

References 25 publications

Glutamate Peripherally Administered Exerts Somatostatin‐Releasing Action in the Conscious Rat

Glutamate Peripherally Administered Exerts Somatostatin‐Releasing Action in the Conscious Rat

Pairing of pre‐ and postsynaptic activities in cerebellar Purkinje cells induces long‐term changes in synaptic efficacy in vitro.

Presence of phospholipase C in coated vesicles from bovine brain Dual regulatory effects of GTP‐analogs

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