Effects of L‐proline and some of its analogs on retinal spreading depression

Harreveld, A. Van

doi:10.1002/neu.480100403

Cited by 14 publications

(25 citation statements)

References 26 publications

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“…The effect of L-proline on SD in the chick retina has been described previously (Cherkin and Van Harreveld, 1978;Van Harreveld, 1979). Figure 1 (points) shows the biphasic effect of proline in various concentrations on the incidence of SD.…”

Section: L-prolinementioning

confidence: 98%

The nature of the chick's magnesium‐sensitive retinal spreading depression

Harreveld

1984

J. Neurobiol.

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Spreading depression (SD) in the chick retina is completely suppressed by 10 mM MgCl2 in the bathing solution (Mg-sensitive SD). However, after increasing the KCl concentration in the Mg solution to values between 10 and 20 mM the retina can again exhibit SDs (Mg-insensitive SD). It has been postulated that the Mg-sensitive SD is a glutamatergic phenomenon. This is supported by the effect of four gl(utamate)-antagonists--L-proline, glutamic acid diethyl ester (GDEE), D-alpha-aminoadipate (D-AA), and 2-amino-4-phosphonobutyrate (APB)--which all suppressed this type of SD. It was suggested that this effect is due to competitive binding of glutamate involved in the Mg-sensitive SD and the gl-antagonist to glutamate receptors. The suppression of SD could be reversed by washing the preparation in a physiologic salt solution. The gl-antagonists in relatively high concentrations had a cytotoxic effect which, when severe, suppressed SD and prevented the recovery of this phenomenon by washing the compound out of the tissue. The compounds examined had, in addition to their gl-antagonistic properties, a gl-agonistic effect, which was postulated to enhance the Na+ permeability of neural membranes resulting in a release of K+ into the extracellular space. In preparations bathed in 10 mM MgCl2 (which suppresses Mg-sensitive SDs) the four compounds investigated promoted Mg-insensitive SDs supposedly when the extracellular K+ concentration reached values between 10 and 20 mequiv.

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Section: L-prolinementioning

confidence: 98%

The nature of the chick's magnesium‐sensitive retinal spreading depression

Harreveld

1984

J. Neurobiol.

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“…In an alternate mechanism both the excitatory and inhibitory compounds are bound by receptors for the excitatory compound in the postsynaptic membrane. However, whereas the binding of the excitatory compound results in depolarization of the subsynaptic membrane, the inhibitory (Van Harreveld, 1979). Whether a sufficient number of receptors bind with the excitatory compound to cause the necessary depolarization to produce a visible muscle contraction will then depend on the affinity of the receptors for the excitatory and inhibitory compounds and the concentrations of these substances.…”

Section: Discussionmentioning

confidence: 97%

“…This is of interest in view of the finding of Shank and Freeman (1976) that L-proline in 10-mM concentration has a similar effect on the membrane potential and resistance, and on the excitatory and inhibitory junctional potentials of lobster muscle as an excitatory transmitter. There is some evidence for such an agonistic action in the effect of L-proline on spreading depression in the chicken retina (Van Harreveld, 1979). However, this excitatory effect is unable to cause muscle contraction in Procambarus clarhii even in 50-mM concentration and does not interfere with the inhibitory effect of Lproline on the contractions caused by nervous stimulation or glutamate perfusion.…”

Section: E F F E C T O N Glutamate Induced Contractionsmentioning

confidence: 96%

L‐Proline as a glutamate antagonist at a crustacean neuromuscular junction

Harreveld

1980

J. Neurobiol.

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The fast as well as the slow contractions of the adductor muscle in the claw of Procambarus clarkii are inhibited by L-proline. This inhibition is dose dependent and decreases with increasing frequency of stimulation of the "slow" fiber. Contractions caused by perfusing the adductor muscle with L-glutamate solutions are also inhibited by L-proline. The inhibiting potency of L-proline is small; the effective concentration of this amino acid is 50--100 times that of the L-glutamate applied. It was postulated that the inhibitory effect of L-proline is based on competition for excitatory receptor sites of L-glutamate, which causes depolarization and contraction, and L-proline, which lacks these actions. Theoretical considerations suggested a linear relationship between the stimulating L-glutamate and the just-inhibiting L-proline concentrations. Experimental evidence supported this model.

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“…It is thus likely that L-Pro acted, at least in part, directly upon motoneurones. It has been proposed that proline interacts with glutamate receptors as an antagonist (Van Harreveld & Fifkova, 1973), partial agonist (Shank & Freeman, 1976;Van Harreveld, 1979;Van Harreveld & Strumwasser, 1981) or agonist (Ault & Nadler, 1984). Our data are consistent with the latter proposal since antagonists of gluatamate-sensitive receptors depressed the responses to L-Pro, while combined application of L-Pro and L-Glu provided no evidence of a partial agonist action.…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, an interaction with L-glutamate (L-Glu) receptors has been suggested in other studies. Evidence for antagonism of glutamate receptors was provided by Van Harreveld (1980) and Segal (1976) while a partial agonist action of L-Pro appeared to underlie antagonism of glutamate in chick retina (Van Harreveld, 1979;Van Harreveld & Reuter, 1981) and hippocampal neurones (Van Harreveld & Strumwasser, 1981). However, Ault & Nadler (1984) proposed only an excitatory (depolarizing) action of L-Pro on hippocampal pyramidal cells, sensitivity to y-D-glutamylglycine suggesting a stimulation of excitatory amino acid receptors.…”

Section: Introductionmentioning

confidence: 99%

l‐Proline depolarizes rat spinal motoneurones by an excitatory amino acid antagonist‐sensitive mechanism

Ault

Wang

Yawn

1987

British J Pharmacology

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Isolated spinal cords prepared from neonatal rats were used to examine the effects of l‐proline (l‐Pro). l‐Pro (1–8 mm) depolarized ventral and dorsal roots in a dose‐dependent manner with one sixth of the potency of l‐glutamate (l‐Glu). l‐Pro was four times more potent than d‐Pro. Prolonged application of l‐Pro produced a plateau depolarization of motoneurones with no apparent fade. Omission of calcium ions from the medium potentiated the depolarizing actions of l‐Pro, l‐Glu and quisqualate. L‐Pro was antagonized by concentrations of 2‐amino‐5‐phosphonovalerate (25 μm), γ‐d‐glutamylglycine (100 μm) and Mg2+ ions (1 mm) that depressed responses to N‐methyl‐d‐aspartate (NMDA). The NMDA receptor‐mediated component of the response to l‐Pro was estimated to be 60–70%. These data suggest that l‐Pro should be considered as a possible excitatory neurotransmitter and that, because l‐Pro is a neutral compound, excitatory amino acid receptors may not require an agonist to possess two anionic groups and one cationic group.

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Effects of L‐proline and some of its analogs on retinal spreading depression

Cited by 14 publications

References 26 publications

The nature of the chick's magnesium‐sensitive retinal spreading depression

The nature of the chick's magnesium‐sensitive retinal spreading depression

L‐Proline as a glutamate antagonist at a crustacean neuromuscular junction

l‐Proline depolarizes rat spinal motoneurones by an excitatory amino acid antagonist‐sensitive mechanism

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