Memory of inhibitory avoidance in the rat is regulated by glutamate metabotropic receptors in the hippocampus

Bianchin, Marino Muxfeldt; Rc, Da Silva; Pk, Schmitz; Jh, Medina; Izquierdo, Iván

doi:10.1097/00008877-199406000-00014

Cited by 58 publications

(25 citation statements)

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“…Cold Spring Harbor Laboratory Press on May 11, 2018 -Published by learnmem.cshlp.org Downloaded from (Riedel et al 1994a), olfactory learning (Kaba et al 1994), and inhibitory avoidance (Bianchin et al 1994). Similarly, amnesic effects have been reported after blockade of mGluR in passive avoidance in chicks (H61scher 1994; Rickard and Ng 1995).…”

Section: Mglurs In Brightness Discriminationmentioning

confidence: 91%

“…In contrast, Bianchin and co-workers (1994) reported that post-training intrahippocampal injection of MCPG blocks and of ACPD facilitates retention of a step-down inhibitory avoidance task, indicating that there may be differences in drug effects depending on the time point of application. This hypothesis was further supported by the observation that MCPG effectively blocks only when given immediately after, not 180 min after, training (Bianchin et al 1994). Drug infusion into the olfactory bulb has indicated that, whereas MCPG does not affect pheromonal memory formation in female mice, ACPD and other agonists effectively facilitate the formation of a specific olfactory memory (Kaba et al 1994).…”

Section: Introductionmentioning

confidence: 86%

“…In agreement with the hypothesis that LTP may be a substrate for learning and memory, MCPG has been shown to block both spatial learning and LTP (Richter-Levin et al 1994;Riedel et al 1994a). Recent investigations have provided evidence that the mGluR agonists ACPD and L-CCG I improve memory of inhibitory avoidance learning in rats (Bianchin et al 1994) and formation of an olfactory memory block in female mice (Kaba et al 1994). This series of experiments therefore examined the effect of the mGluR agonist tADA in a spatial alternation paradigm, to see whether tADA might facilitate learning.…”

Section: Methodsmentioning

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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Section: Mglurs In Brightness Discriminationmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 86%

Section: Methodsmentioning

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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“…Two to 24 h after the end of the behavioral procedures, the animals were sacrified by decapitation. Anatomical verification of cannula placements was carried out and only behavioral results for animals with correct cannula placement (i.e., within 1 mm 2 of the intended sites) were considered (13).…”

Section: Bevilaqua Et Almentioning

confidence: 99%

Agents that affect cAMP levels or protein kinase A activity modulate memory consolidation when injected into rat hippocampus but not amygdala

Bevilaqua

Ardenghi

Schröder

et al. 1997

Braz J Med Biol Res

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Male Wistar rats were trained in one-trial step-down inhibitory avoidance using a 0.4-mA footshock. At various times after training (0, 1.5, 3, 6 and 9 h for the animals implanted into the CA1 region of the hippocampus; 0 and 3 h for those implanted into the amygdala), these animals received microinfusions of SKF38393 (7.5 µg/side), SCH23390 (0.5 µg/side), norepinephrine (0.3 µg/side), timolol (0.3 µg/side), 8-OH-DPAT (2.5 µg/side), NAN-190 (2.5 µg/side), forskolin (0.5 µg/side), KT5720 (0.5 µg/side) or 8-Br-cAMP (1.25 µg/side). Rats were tested for retention 24 h after training. When given into the hippocampus 0 h post-training, norepinephrine enhanced memory whereas KT5720 was amnestic. When given 1.5 h after training, all treatments were ineffective. When given 3 or 6 h post-training, 8-BrcAMP, forskolin, SKF38393, norepinephrine and NAN-190 caused memory facilitation, while KT5720, SCH23390, timolol and 8-OH-DPAT caused retrograde amnesia. Again, at 9 h after training, all treatments were ineffective. When given into the amygdala, norepinephrine caused retrograde facilitation at 0 h after training. The other drugs infused into the amygdala did not cause any significant effect. These data suggest that in the hippocampus, but not in the amygdala, a cAMP/protein kinase A pathway is involved in memory consolidation at 3 and 6 h after training, which is regulated by D 1 , ß, and 5HT1A receptors. This correlates with data on increased post-training cAMP levels and a dual peak of protein kinase A activity and CREB-P levels (at 0 and 3-6 h) in rat hippocampus after training in this task. These results suggest that the hippocampus, but not the amygdala, is involved in long-term storage of step-down inhibitory avoidance in the rat.Correspondence

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“…Posttraining infusion of the NMDA receptor antagonist aminophosphonopentanoic acid impairs retention of inhibitory avoidance in rats when given into the hippocampus immediately after training (2,3), or when given into the posterior parietal cortex 180 min after training (4). Intrahippocampal infusion of the mGluR antagonist methyl-carboxyphenyl glycine immediately after training (5) or of the AMPA receptor antagonist cyanonitroquinoxaline-dione (CNQX) up to 3 h after training (6) impairs inhibitory avoidance retention, while infusions of glutamate or of the mGluR agonist aminocyclopentane dicarboxylate enhance retention (5). Infusions of CNQX into the hippocampus (4,7) or parietal cortex (4,8) prior to test impair inhibitory avoidance expression.…”

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confidence: 99%

Effect of inhibitory avoidance training on [3H]-glutamate binding in the hippocampus and parietal cortex of rats

Schröder

de‐Paris

Roesler

et al. 2000

Braz J Med Biol Res

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Glutamate receptors have been implicated in memory formation. The aim of the present study was to determine the effect of inhibitory avoidance training on specific [ 3 H]-glutamate binding to membranes obtained from the hippocampus or parietal cortex of rats. Adult male Wistar rats were trained (0.5-mA footshock) in a step-down inhibitory avoidance task and were sacrificed 0, 5, 15 or 60 min after training. Hippocampus and parietal cortex were dissected and membranes were prepared and incubated with 350 nM [ 3 H]-glutamate (N = 4-6 per group). Inhibitory avoidance training induced a 29% increase in glutamate binding in hippocampal membranes obtained from rats sacrificed at 5 min (P<0.01), but not at 0, 15, or 60 min after training, and did not affect glutamate binding in membranes obtained from the parietal cortex. These results are consistent with previous evidence for the involvement of glutamatergic synaptic modification in the hippocampus in the early steps of memory formation. It has been postulated that long-term potentiation (LTP) of glutamatergic synapses is a cellular mechanism underlying learning and memory. Glutamate receptors are involved in both the induction and the expression of LTP. LTP induction depends on activation of the N-methyl-D-aspartate (NMDA) type of glutamate receptor channel and the metabotropic glutamate receptor (mGluR), whereas its maintenance and expression depend on a-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptor channels (1).As with LTP, glutamate receptors play a role in both the formation and the expression of memory for the step-down inhibitory avoidance task. Memory formation for this task depends on glutamate receptor activation in several brain areas. Among other structures, the hippocampus is particularly important in the early phase of memory formation, while the posterior parietal cortex plays a late role in consolidation (4). Posttraining infusion of the NMDA receptor antagonist aminophosphonopentanoic acid impairs retention of inhibitory avoidance in rats when given into the hippocampus immediately after training (2,3), or when given into the posterior parietal cortex 180 min after training (4). Intrahippocampal infusion of the mGluR antagonist methyl-carboxyphenyl glycine immediately after training (5) or of the AMPA receptor antagonist cyanonitroquinoxaline-dione (CNQX) up to 3 h after

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Memory of inhibitory avoidance in the rat is regulated by glutamate metabotropic receptors in the hippocampus

Cited by 58 publications

References 0 publications

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

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

Agents that affect cAMP levels or protein kinase A activity modulate memory consolidation when injected into rat hippocampus but not amygdala

Effect of inhibitory avoidance training on [3H]-glutamate binding in the hippocampus and parietal cortex of rats

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