Induction of glutamate binding sites in hippocampal membranes by transient exposure to high concentrations of glutamate or glutamate analogs

Kessler, Markus; Baudry, Michel; Jt, Cummins; Way, Stanley; Lynch, Gary

doi:10.1523/jneurosci.06-02-00355.1986

Cited by 14 publications

(4 citation statements)

References 18 publications

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“…The idea that LTP is due to a presynaptic mechanism is also suggested by other studies in a variety of tissues (Baxter, Bittner & Brown, 1985; Koyano, Kuba & Minota, 1985;Walters & Byrne, 1985;Bliss, Douglas, Errington & Lynch, 1986;Desmond & Levy, 1986;Feasey, Lynch & Bliss, 1986;Goelet, Castellucci, Schacher & Kandel, 1986;Applegate, Kerr & Landfield, 1987). However, others have suggested that an increase in the postsynaptic sensitivity to transmitter explains or contributes to LTP (Lynch & Baudry, 1984;Koyano et al 1985;Kessler, Baudry, Cummins, Way & Lynch, 1986; but see Lynch, Errington & Bliss, 1985;Goh, Ho-Asjoe & Sastry, 1986).…”

Section: Discussionmentioning

confidence: 76%

Long‐term potentiation at nicotinic synapses in the rat superior cervical ganglion.

Briggs

McAfee

1988

The Journal of Physiology

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SUMMARY1. Nicotinic fast excitatory postsynaptic potentials (fast EPSPs) were recorded intracellularly from postganglionic neurones in the isolated rat superior cervical ganglion.2. An hours-long potentiation of the fast EPSP could be induced by brief tetanic stimulation of the preganglionic nerve (5 Hz for 5 s to 20 Hz for 20 s). While longterm potentiation (LTP) can be detected in every ganglion by extracellular techniques, LTP was induced in only two-thirds of the nicotinic synaptic responses.3. Muscarinic blockade with atropine did not prevent LTP of the fast EPSP. 4. LTP of the fast EPSP did not correlate with changes in input resistance nor cell potential, as recorded in the soma.5. The formation of nicotinic LTP appeared to depend upon stimulation of the nerve terminals. Non-synaptic tetanic depolarization of the postganglionic neurone, effected by injecting depolarizing current pulses through the intracellular microelectrode, was not sufficient. LTP could be induced by synaptic tetani in two-thirds of the same neurones.6. The response to exogenous 1,1-dimethyl-4-phenylpiperazinium (DMPP), a selective nicotinic agonist, was not increased during nicotinic synaptic LTP. This was true whether DMPP was applied by pressure-ejection from an extracellular micropipette during intracellular recording, or by brief superfusion during sucrosegap recording of postganglionic responses.7. Responses to exogenous acetylcholine and carbachol were increased during nicotinic LTP when these non-selective cholinergic agonists were applied by pressure-ejection during intracellular recording. However, the potentiation of the fast EPSP was always at least twofold greater than the potentiation of the response to these exogenous agonists.8. Potentiation of the responses to acetylcholine and carbachol may have been due to long-term enhancement of muscarinic responses. Thus, no postsynaptic basis for nicotinic LTP was uncovered in these studies.

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Section: Discussionmentioning

confidence: 76%

Long‐term potentiation at nicotinic synapses in the rat superior cervical ganglion.

Briggs

McAfee

1988

The Journal of Physiology

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“…However, others suggest that postsynaptic processes explain or contribute to the expression of l.t.p. (Lynch & Baudry, 1984;Koyano et al, 1985;Kessler et al, 1986;Desmond & Levy, 1987). There may be more than one type of l.t.p., even in one tissue.…”

Section: Discussionmentioning

confidence: 99%

Long‐term regulation of synaptic acetylcholine release and nicotinic transmission: the role of cyclic AMP

Briggs

McAfee

McCaman

1988

British J Pharmacology

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1 Using the rat superior cervical ganglion in vitro, the relative efficacy of nicotinic synaptic transmission was estimated by recording the postganglionic compound action potential and the amount of endogenous acetylcholine (ACh) released. These two parameters were correlated in individual ganglia by sampling the bathing medium for the assay of ACh while simultaneously recording the postganglionic response.2 The P-adrenoceptor agonist isoprenaline potentiated both the evoked release of ACh and the postganglionic response by about 20% during preganglionic stimulation at 0.2 Hz. 3 The adenosine receptor agonist 2-chloroadenosine inhibited ACh release and the postganglionic response by about 35%. 4 Tetanic preganglionic stimulation for a few seconds induced a long-term potentiation of nicotinic responses and of ACh release. Both of these potentiations were dependent upon extracellular Ca2l during the tetani. 5 Forskolin and analogues of cyclic AMP also caused a long-lasting potentiation of both the evoked release ofACh and the postganglionic response, indicating that cyclic AMP may regulate transmission by a presynaptic mechanism. The specificity of the cyclic AMP analogues was tested using various butyryl-and bromo-purine nucleotides. 6 The effects of forskolin and 8-bromo-cyclic AMP did not appear to be dependent upon extracellular Ca2+. 7 The potentiation caused by forskolin was consistently augmented by three phosphodiesterase inhibitors -AH 21-132, papaverine and SQ 20-006. However, the effect of forskolin was not consistently enhanced by theophylline, nor was it reduced by the adenylate cyclase inhibitor SQ 22-536. 8 The neurogenic long-term potentiation was augmented by two of the phosphodiesterase inhibitors that also augmented the forskolin-induced potentiation -papaverine and SQ 20-006. 9 It was concluded that cyclic AMP can enhance nicotinic transmission, and can do so by increasing the evoked release of ACh. However, it was not possible to prove that cyclic AMP mediates the longterm potentiation induced by tetanic preganglionic stimulation.

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“…It has been found that pretreatment of rat hippocampal membranes with 10 mM L-glutamate induced new L-glutamate binding sites (Kessler et al, 1984). However, pretreatment of either canine brain CTX-SPM or CTX-PSD fraction with 10 mM L-glutamate for 10 min at 30"C, followed by extensive washings with 0.5 mM HEPEWKOH, pH 7.4 buffer, resulted in no change in subsequent Na+-independent and C1 -/Ca2+-independent or C1-/Ca2+-dependent L-glutamate binding to the fractions (data not shown).…”

Section: Table 2 Lzfkcts Of Apb Ctnd Iariorrs Inns On Binding Of ~-mentioning

confidence: 99%

Binding of L‐[³H]Glutamate to Fresh or Frozen Synaptic Membrane and Postsynaptic Density Fractions Isolated from Cerebral Cortex and Cerebellum of Fresh or Frozen Canine Brain

Carlin

Siekevitz

1986

Journal of Neurochemistry

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Synaptic membrane (SPM) and postsynaptic density (PSD) fractions isolated from cerebral cortex (CTX) and cerebellum (CL) of canine brain, either fresh or frozen and isolated from either fresh or frozen tissue, were found to contain L-[3H]glutamate binding sites. It was found that there was a concentration of L-glutamate binding sites in CTX-PSD and CL-PSD over the respective membrane fractions, and the Bmax value of CL-PSD (92.0 pmol/mg protein) was about three times that of CTX-PSD (28.9 pmol/mg). The results, together with those of others, suggest that the thin CL-PSD are probably derived from the excitatory synapses in the molecular layer. The ion dependency of L-glutamate binding to canine CTX-SPM fraction was found to be similar to that reported for a rat brain SPM fraction: (a) Cl- increased the number of L-glutamate binding sites and the effect was enhanced by Ca2+; Ca2+ alone had no significant effect; (b) the Cl-/Ca2+-sensitive binding sites were abolished by 2-amino-4-phosphonobutyrate (APB) or freezing and thawing; (c) the effect of Na+ ion was biphasic; low concentration of Na+ (less than 5 mM) decreased Cl-/Ca2+-dependent L-glutamate binding sites, whereas at higher concentrations of Na+ the binding of glutamate was found to increase either in the presence or absence of Ca2+ and Cl-. In addition, the K+ ion (50 mM) was found to decrease the Na+-independent and Cl-/Ca2+-independent binding of L-glutamate to fresh CTX-SPM by 18%, but it decreased the Na+-dependent and Cl-/Ca2+-independent L-glutamate binding by 93%; in the presence of Cl-/Ca2+, the K+ ion decreased the Na+-dependent binding by 78%. Freezing and thawing of CTX-SPM resulted in a 50% loss of the Na+-dependent L-glutamate binding sites assayed in the absence of Ca2+ and Cl-. The CL-SPM fraction showed similar ion dependency of L-glutamate binding except for the absence of Na+-dependent glutamate binding sites. The CTX-PSD fraction contained neither Na+-dependent nor APB (or Cl-/Ca2+)-sensitive L-glutamate binding sites and its L-glutamate binding was unaffected by freezing and thawing, in agreement with the reported findings using rat brain PSD preparation. L-Glutamate binding to CTX-SPM or CTX-PSD fraction was not affected by pretreatment with 10 mM L-glutamate, nor by simultaneous incubations with calmodulin.(ABSTRACT TRUNCATED AT 400 WORDS)

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Induction of glutamate binding sites in hippocampal membranes by transient exposure to high concentrations of glutamate or glutamate analogs

Cited by 14 publications

References 18 publications

Long‐term potentiation at nicotinic synapses in the rat superior cervical ganglion.

Long‐term potentiation at nicotinic synapses in the rat superior cervical ganglion.

Long‐term regulation of synaptic acetylcholine release and nicotinic transmission: the role of cyclic AMP

Binding of L‐[³H]Glutamate to Fresh or Frozen Synaptic Membrane and Postsynaptic Density Fractions Isolated from Cerebral Cortex and Cerebellum of Fresh or Frozen Canine Brain

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Induction of glutamate binding sites in hippocampal membranes by transient exposure to high concentrations of glutamate or glutamate analogs

Cited by 14 publications

References 18 publications

Long‐term potentiation at nicotinic synapses in the rat superior cervical ganglion.

Long‐term potentiation at nicotinic synapses in the rat superior cervical ganglion.

Long‐term regulation of synaptic acetylcholine release and nicotinic transmission: the role of cyclic AMP

Binding of L‐[3H]Glutamate to Fresh or Frozen Synaptic Membrane and Postsynaptic Density Fractions Isolated from Cerebral Cortex and Cerebellum of Fresh or Frozen Canine Brain

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Binding of L‐[³H]Glutamate to Fresh or Frozen Synaptic Membrane and Postsynaptic Density Fractions Isolated from Cerebral Cortex and Cerebellum of Fresh or Frozen Canine Brain