title: Developmental switch in spike timing-dependent plasticity at layers 4-2/3 in the rodent barrel cortex.
abstract: Sensory deprivation during the critical period induces long-lasting changes in cortical maps. In the rodent somatosensory cortex (S1), its precise initiation mechanism is not known, yet spike timing-dependent plasticity (STDP) at layer 4 (L4)-L2/3 synapses are thought to be crucial. Whisker stimulation causes "L4 followed by L2/3" cell firings, while acute single whisker deprivation suddenly reverses the sequential order in L4 and L2/3 neurons in the deprived column (Celikel et al., 2004). Reversed spike sequence then leads to long-term depression through an STDP mechanism (timing-dependent long-term depression), known as deprivation-induced suppression at L4-L2/3 synapses (Bender et al., 2006a), an important first step in the map reorganization. Here we show that STDP properties change dramatically on postnatal day 13-15 (P13-P15) in mice S1. Before P13, timing-dependent long-term potentiation (t-LTP) was predominantly induced regardless of spiking order. The induction of t-LTP required postsynaptic influx of Ca(2+), an activation of protein kinase A, but not calcium/calmodulin-dependent protein kinase II. Consistent with the strong bias toward t-LTP, whisker deprivation (all whiskers in Row "D") from P7-P12 failed to induce synaptic depression at L4-L2/3 synapses in the deprived column, but clear depression was seen if deprivation occurred after P14. Random activation of L4, L2/3 cells, as may occur in response to whisker stimulation before P13 during network formation, led to potentiation under the immature STDP rule, as predicted from the bias toward t-LTP regardless of spiking order. These findings describe a developmental switch in the STDP rule that may underlie the transition from synapse formation to circuit reorganization at L4-L2/3 synapses, both in distinct activity-dependent manners.
authors.affiliation: Department of Physiology, Faculty of Medicine, Saitama Medical University, Moroyama, Saitama 350-0495, Japan. chiaki@saitama-med.ac.jp
authors.forename: Chiaki
authors.initials: C
authors.lastname: Itami
authors.forename: Fumitaka
authors.initials: F
authors.lastname: Kimura
mesh_terms: D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000344:Afferent Pathways / Q000502:physiology; D000367:Age Factors; D000818:Animals; D000831:Animals, Newborn; D001703:Biophysics; D002118:Calcium / Q000378:metabolism; D002614:Chelating Agents / Q000494:pharmacology; D000242:Cyclic AMP / Q000031:analogs & derivatives / Q000494:pharmacology; D004533:Egtazic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D004558:Electric Stimulation; D003576:Electron Transport Complex IV / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials; D005260:Female; D066298:In Vitro Techniques; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D018408:Patch-Clamp Techniques; D010455:Peptides / Q000494:pharmacology; D012683:Sensory Deprivation; D013003:Somatosensory Cortex / Q000166:cytology* / Q000254:growth & development*; D013873:Thionucleotides / Q000494:pharmacology; D014738:Vibrissae / Q000294:innervation
chemical_list: D002614:Chelating Agents; D004791:Enzyme Inhibitors; D018691:Excitatory Amino Acid Antagonists; D010455:Peptides; D013873:Thionucleotides; C514527:autocamptide-2-related inhibitory peptide II; C016957:adenosine-3',5'-cyclic phosphorothioate; D004533:Egtazic Acid; D015763:2-Amino-5-phosphonovalerate; D000242:Cyclic AMP; D003576:Electron Transport Complex IV; C025603:1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid; D002118:Calcium