Long-term memory formation in the chick requires mobilization of ryanodine-sensitive intracellular calcium stores

Training chicks (Gallus domesticus) on a one-trial passive avoidance task results in transient and time-dependent enhanced increases in N-methyl-d-aspartate- or alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate-stimulated intracellular calcium concentration in synaptoneurosomes isolated from a specific forebrain region, the intermediate medial hyperstriatum ventrale. This increase could result from either calcium entry from the extracellular medium or from mobilization of intracellular calcium stores. We have therefore examined the effects of dantrolene, an inhibitor of calcium release from the intracellular ryanodine-sensitive store, on these processes. Dantrolene, 50 nmol per hemisphere injected intracerebrally 30 min pre- or 30 min posttraining, blocked longer term memory for the passive avoidance task, whereas memory for the task was unaffected when dantrolene was injected at earlier or later times. Preincubation of synaptoneurosomes, isolated from the intermediate hyperstriatum ventrale 10 min after training, with 100 nM dantrolene abolished the enhanced training-induced increase in intracellular calcium concentration elicited by 0.5 mM N-methyl-d-aspartate. By contrast, the training-induced enhancement of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate-stimulated increase in intracellular calcium concentration in synaptoneurosomes prepared 6 h posttraining was unaffected by preincubation with dantrolene, which was not amnestic at this time. Calcium release from ryanodine-sensitive intracellular stores may thus be a necessary stage in the early phase of the molecular cascade leading to the synaptic modulation required for long-term memory storage.     

Differential involvement of mGluR1 and mGluR5 in memory reconsolidation and retrieval in a passive avoidance task in 1-day old chicks

Group I metabotropic glutamate receptors (mGluRs) are involved in memory formation. The Ca2+ signal derived from stimulation of IP3 receptors (IP3Rs) via mGluRs, initiates protein synthesis that is required for memory consolidation and reconsolidation. However it has been suggested that different mechanisms are triggered by mGluR1/5 activation in these two processes. It is also not clear whether the transient amnesia observed after blockade of group I mGluRs after a reminder, results from disturbance of memory reconsolidation or temporal impairment of recall. The aim of this study was to examine more closely the role of mGluR1 in memory consolidation and reconsolidation and to detect differences in the participation of mGluR1 and mGluR5 in memory retrieval after initial training and after the remainder of the task. Our results demonstrate, that in chicks performing a one-trial passive avoidance task, antagonists of mGluR1, mGluR5 and IP3R significantly disturb memory consolidation and reconsolidation. Inhibition of mGluR5 and IP3R also impairs memory recall, whereas mGluR1 do not seem to participate in this process. The presented data suggest that activation of mGluR1 and mGluR5 is necessary for the correct course of memory consolidation and reconsolidation, whereas mGluR5 are additionally involved in retrieval processes dependent on Ca2+ release from IP3 activated intracellular stores.