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Training chicks on a passive avoidance task modulates glutamate-stimulated inositol phosphate accumulation
The European Journal of Neuroscience
|January 1, 1993
Summary
Memory formation in chick brains involves NMDA receptor activation in the left hyperstriatum ventrale. This process is linked to synaptic remodeling following passive avoidance learning, with specific timing observed post-training.
Area of Science:
- Neuroscience
- Biochemistry
- Learning and Memory
Background:
- The intermediate medial hyperstriatum ventrale (IMHV) in chick forebrain is crucial for memory formation.
- Phosphoinositide signaling plays a role in synaptic plasticity and memory consolidation.
Purpose of the Study:
- To investigate the effects of various neurotransmitters and receptor agonists on inositol phosphate (IP) accumulation in the chick IMHV.
- To determine the role of specific glutamate receptors in memory formation after passive avoidance training.
Main Methods:
- Tissue prisms from chick forebrain (IMHV) were used for in vitro studies.
- Measurements of inositol phosphate (IP) accumulation were performed.
- Neurotransmitter effects (glutamate, NMDA, MK801, AMPA, quisqualate) on IP accumulation were assessed.
- Passive avoidance training was conducted, followed by IP accumulation measurements at different time points.
Main Results:
- Quisqualate and AMPA significantly increased IP accumulation in the IMHV, with greater effects in the right hemisphere.
- Glutamate also stimulated IP accumulation, particularly in the left IMHV.
- Passive avoidance training reduced glutamate-stimulated IP accumulation in the left IMHV 30 minutes post-training.
- MK801 abolished this training-induced decrease without affecting basal IP accumulation.
Conclusions:
- Memory formation for passive avoidance tasks in chicks involves NMDA receptor channel activation in the left IMHV.
- The observed changes in IP accumulation are time-dependent and specific to the trained hemisphere.
- These findings suggest a role for NMDA receptor-mediated signaling in the biochemical cascade underlying memory consolidation.