title: Calcium-dependent PKC isoforms have specialized roles in short-term synaptic plasticity.
abstract: Posttetanic potentiation (PTP) is a widely observed form of short-term plasticity lasting for tens of seconds after high-frequency stimulation. Here we show that although protein kinase C (PKC) mediates PTP at the calyx of Held synapse in the auditory brainstem before and after hearing onset, PTP is produced primarily by an increased probability of release (p) before hearing onset, and by an increased readily releasable pool of vesicles (RRP) thereafter. We find that these mechanistic differences, which have distinct functional consequences, reflect unexpected differential actions of closely related calcium-dependent PKC isoforms. Prior to hearing onset, when PKCγ and PKCβ are both present, PKCγ mediates PTP by increasing p and partially suppressing PKCβ actions. After hearing onset, PKCγ is absent and PKCβ produces PTP by increasing RRP. In hearing animals, virally expressed PKCγ overrides PKCβ to produce PTP by increasing p. Thus, two similar PKC isoforms mediate PTP in distinctly different ways.
authors.affiliation: Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA.
authors.forename: YunXiang
authors.initials: Y
authors.lastname: Chu
authors.affiliation: Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA.
authors.forename: Diasynou
authors.initials: D
authors.lastname: Fioravante
authors.affiliation: The Biotechnology Centre of Oslo, University of Oslo, Forskningsparken, Gaustadalléen 21, 0349 Oslo, Norway.
authors.forename: Michael
authors.initials: M
authors.lastname: Leitges
authors.affiliation: Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA. Electronic address: wade_regehr@hms.harvard.edu.
authors.forename: Wade G
authors.initials: WG
authors.lastname: Regehr
mesh_terms: D000367:Age Factors; D000818:Animals; D000831:Animals, Newborn; D001581:Benzothiadiazines / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018507:Gene Expression Regulation, Developmental / Q000235:genetics; D066298:In Vitro Techniques; D007736:Kynurenic Acid / Q000494:pharmacology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009473:Neuronal Plasticity / Q000235:genetics / Q000502:physiology; D009474:Neurons / Q000502:physiology*; D011149:Pons / Q000166:cytology*; D017729:Presynaptic Terminals / Q000378:metabolism; D020033:Protein Isoforms / Q000172:deficiency / Q000378:metabolism*; D011493:Protein Kinase C / Q000172:deficiency / Q000378:metabolism*; D013569:Synapses / Q000502:physiology*; D050598:Vesicular Glutamate Transport Protein 1 / Q000378:metabolism
chemical_list: D001581:Benzothiadiazines; D004791:Enzyme Inhibitors; D018691:Excitatory Amino Acid Antagonists; D020033:Protein Isoforms; D050598:Vesicular Glutamate Transport Protein 1; D011493:Protein Kinase C; D007736:Kynurenic Acid; C004639:cyclothiazide; D002118:Calcium