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Spatial learning and synaptic hippocampal plasticity in type 2 somatostatin receptor knock-out mice
P Dutar1, C Vaillend, C Viollet
1Neurobiologie de la Croissance et de la Sénescence, INSERM U 549, Centre Paul Broca, 2 ter rue d'Alésia, F-75014 Paris, France. dutar@broca.inserm.fr
Mice lacking the sst2 receptor showed improved spatial learning and altered synaptic plasticity in the hippocampus, suggesting somatostatin
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Somatostatin influences central nervous system (CNS) functions via five receptor subtypes.
- The sst2 receptor is highly expressed in the cortex and hippocampus, but its specific role is unclear.
Purpose of the Study:
- To investigate the role of the sst2 receptor in hippocampal function using sst2 gene-invalidated (KO) mice.
- To explore the impact of sst2 receptor deletion on learning, memory, and synaptic plasticity.
Main Methods:
- Behavioral tests (radial maze, operant bar-pressing) were used to assess learning and memory.
- Electrophysiological recordings in ex vivo hippocampal slices examined glutamatergic responses and synaptic plasticity (LTP, LTD).
Main Results:
- Sst2 KO mice exhibited enhanced spatial discrimination learning but altered operant learning.
- Enhanced glutamatergic (AMPA, NMDA) responses and increased short-term potentiation and long-term depression were observed in sst2 KO mice.
- Long-term potentiation remained unaffected.
Conclusions:
- Somatostatin acting through hippocampal sst2 receptors may reduce glutamate efficiency.
- This modulation impacts glutamate-dependent plasticity and spatial learning processes.
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