Physiological and pharmacological profile oftrans-azetidine-2,4-dicarboxylic acid: Metabotropic glutamate receptor agonism and effects on long-term potentiation

Manahan‐Vaughan, Denise; Reiser, Michael; Pin, Jean‐Philippe; Wilsch, Volker W.; Bockaert, Joël; Reymann, Klaus G.; Riedel, Gernot

doi:10.1016/0306-4522(95)00594-3

Cited by 54 publications

(23 citation statements)

References 48 publications

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“…In vivo, 200 Hz tetanic stimulation of perforant path fibers to the dentate gyrus gives rise to robust synaptic plasticity which is abolished by application of the NMDA receptor antagonist, AP5 (Manahan-Vaughan et al, 1996). Pharmacological blockade of NMDA receptors, in concentrations which prevent hippocampal plasticity, disrupt learning and memory in multiple forms, such as, spatial learning (Morris et al, 1986;Whishaw and Auer, 1989;Heale and Harvey, 1990;Shapiro and Caramanos, 1990;Lukoyanov and Paula-Barosa, 2000), conditioned fear (Miserendino et al, 1990;Kim et al, 1991), olfactory memory (Staubli et al, 1989) and gustatory memory (Welzl et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

A single application of MK801 causes symptoms of acute psychosis, deficits in spatial memory, and impairment of synaptic plasticity in rats

et al. 2007

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Schizophrenia is mostly a progressive psychiatric illness. Although cognitive changes in chronic schizophrenia have been investigated, little is known about the consequences of a single psychotic episode on memory mechanisms and formation. We investigated changes in hippocampal long-term potentiation (LTP) and spatial memory in a rat model of an acute psychotic episode. Application of NMDA receptor antagonists, such as MK801 (dizolcilpine) in rats, have been shown to give rise to an acute and short-lasting behavioral state, which mirrors many symptoms of schizophrenia. Furthermore, NMDA antagonist-intake in humans elicits symptoms of schizophrenia such as hallucinations, delusions, and affective blunting. We therefore treated animals with a single systemic injection of MK801 (5 mg/kg). Increased stereotypy, locomotion, and ataxia were evident immediately after MK801-treatment, with effects disappearing within 24 h. MK801-treatment caused a disruption of prepulse inhibition of the acoustic startle reflex, 1 day but not 7 or 28 days after treatment. These effects were consistent with the occurrence of an acute psychotic episode. LTP was profoundly impaired in freely moving rats 7 days after MK801 application. Four weeks after treatment, a slight recovery of LTP was seen, however marked deficits in long-term spatial memory were evident. These data suggest that treatment with MK801 to generate an acute psychotic episode in rats, gives rise to grave disturbances in synaptic plasticity and is associated with lasting impairments with the ability to form spatial memory.

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Section: Discussionmentioning

confidence: 99%

A single application of MK801 causes symptoms of acute psychosis, deficits in spatial memory, and impairment of synaptic plasticity in rats

et al. 2007

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“…On the basis that pretetanus-applied tADA facilitates in vivo LTP (Riedel et al 1994c(Riedel et al , 1995bManahan-Vaughan et al 1996), we predicted that application of tADA prior to training might facilitate learning. The results reported in experiment 4A, however, indicate the opposite.…”

Section: Discussionmentioning

confidence: 99%

“…In this series of experiments, the mGluR agonist tADA (racemic form, Calbiochem, USA) was applied in a concentration that has been shown to facilitate LTP in freely moving rats in vivo (Riedel et al 1994c(Riedel et al , 1995bManahan-Vaughan et al 1996). tADA was dissolved in saline (0.9%) prior to use, and a total volume of 5 txl was injected into the ventricle of test animals within 5 min.…”

Section: Drugs and Drug Applicationmentioning

confidence: 99%

“…Furthermore, tADA has the advantage of distinguishing between mGluR classes, because it stimulates PI hydrolysis but does not depress forskolin-stimulated cAMP formation in either hippocampal slices (Manahan-Vaughan et al 1996) or mixed cortical cell cultures (Bruno et al 1995). However, in cell lines expressing human mGluR2, tADA acted as a weak agonist (Kn0pfel et al 1995).…”

Section: Specificity Of the Drugsmentioning

confidence: 99%

“…In urethane anesthetized rats, however, MCPG failed to block dentate gyrus LTP (Bordi and Ugolini 1995), suggesting changes in sensitivity owing to the anesthetic status of the animals. Furthermore, mGluR agonists like ACPD and tADA facilitate LTP induction both in vitro (Otani and Ben-Ari 1991;Behnisch and Reymann 1993) and in vivo (Riedel et al 1994c(Riedel et al 1995bManahan-Vaughan et al 1996). Given that LTP is suggested to be a substrate for some forms of learning and memory, these data imply that mGluRs may play a pivotal role in behavior and that mGluR antagonists may block memory formation, whereas mGluR agonists might facilitate learning under certain conditions.…”

Section: Introductionmentioning

confidence: 99%

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Metabotropic glutamate receptors in spatial and nonspatial learning in rats studied by means of agonist and antagonist application.

Riedel¹,

Wetzel²,

Reymann³

1995

Learn. Mem.

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We examined the effects of both the metabotropic glutamate receptor (mGluR) antagonist MCPG and the agonist tADA in two behavioral paradigms in rats: (1) brightness discrimination and (2) spatial alternation. Compounds were applied intracerebroventricularly at different times, either 30 min prior to training or immediately after training, and rats were tested for retention 24 hr later in the same paradigms. Both MCPG and tADA caused amnesia in the spatial alternation test, when applied pretraining, but no effect was obtained in the brightness discrimination paradigm. Drug-induced amnesia was shown not to be attributable to state-dependent effects of MCPG or tADA. Moreover, the memory inhibiting effect of MCPG was dose dependent, with a low dose (20 raM/5 ml) having no effect on learning and memory and a 10 times higher concentration (200 mM/5 ml) causing complete amnesia. Application of both saline and MCPG immediately post-training prevented memory formation, which may be attributable to an interference by the injection procedure with the process of memory formation. The mGluR agonist tADA, however, facilitated memory formation in the spatial alternation task, when injected immediately after training. 3Corresponding author. Present address:

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Long-term potentiationin vivo increases rat hippocampal tenascin-C expression

et al. 1998

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Physiological and pharmacological profile oftrans-azetidine-2,4-dicarboxylic acid: Metabotropic glutamate receptor agonism and effects on long-term potentiation

Cited by 54 publications

References 48 publications

A single application of MK801 causes symptoms of acute psychosis, deficits in spatial memory, and impairment of synaptic plasticity in rats

A single application of MK801 causes symptoms of acute psychosis, deficits in spatial memory, and impairment of synaptic plasticity in rats

Metabotropic glutamate receptors in spatial and nonspatial learning in rats studied by means of agonist and antagonist application.

Long-term potentiationin vivo increases rat hippocampal tenascin-C expression

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