Abstract:
:While the activity-dependent mechanisms guiding functional maturation of synaptic transmission postsynaptically are well characterized, less is known about the corresponding presynaptic mechanisms. Here we show that during the first postnatal week, a subset of CA3-CA1 synapses express postsynaptically induced LTP that is tightly associated with a robust decrease in synaptic facilitation, consistent with an increase in release probability (P(r)). The loss of facilitation is readily induced by physiologically relevant pairing protocols at immature synapses and is dependent on activation of NMDA-receptors but not L-type calcium channels. The putative pre- and postsynaptic components of neonatal LTP were distinguished in their downstream signaling requirements, PKC activity being selectively needed for the decrease in facilitation but not for synaptic potentiation per se. These data suggest that maturation of glutamatergic synapses involves a critical period during which presynaptic function is highly susceptible to activity-dependent regulation via a PKC-dependent mechanism.
journal_name
Neuropharmacologyjournal_title
Neuropharmacologyauthors
Luchkina NV,Sallert M,Clarke VR,Taira T,Lauri SEdoi
10.1016/j.neuropharm.2012.11.019subject
Has Abstractpub_date
2013-04-01 00:00:00pages
494-502eissn
0028-3908issn
1873-7064pii
S0028-3908(12)00566-7journal_volume
67pub_type
杂志文章abstract::The role of dopamine in spinal motor transmission was investigated using spinal reflexes in acutely spinalized rats. Intravenous administration of a relatively high dose of the dopamine receptor agonist apomorphine-HCl (3 mg/kg) or the D2 receptor agonist bromocriptine mesylate (1 mg/kg) reduced the amplitude of the m...
journal_title:Neuropharmacology
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abstract::Phosphodiesterases (PDE) are the only enzymes that degrade cAMP and cGMP which are second messengers crucial to memory consolidation. Different PDE inhibitors have been developed and tested for their memory-enhancing potential, but the occurrence of side effects has hampered clinical progression. As separate inhibitio...
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
pub_type: 杂志文章
doi:10.1016/j.neuropharm.2017.07.008
更新日期:2017-10-01 00:00:00
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
pub_type: 杂志文章
doi:10.1016/j.neuropharm.2007.06.010
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
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journal_title:Neuropharmacology
pub_type: 杂志文章
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journal_title:Neuropharmacology
pub_type: 杂志文章
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journal_title:Neuropharmacology
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