A delayed response enhancement during hippocampal presynaptic plasticity in mice

doi:10.1113/jphysiol.2007.131300

A delayed response enhancement during hippocampal presynaptic plasticity in mice

¹Molecular Neurobiology Research Group (MONERG), PO Box 1104, Faculty of Medicine, University of Oslo, N-0317 Blindern, Oslo, Norway ²Department Physiology, Institute of Basic Medical Science, PO Box 1104, University of Oslo, N-0317 Blindern, Oslo, Norway ³Department Biochemistry, Institute of Basic Medical Science, PO Box 1112, University of Oslo, N-0317 Blindern, Oslo, Norway ⁴CSIC Institute, Instituto Avda de Conocimiento s/n, Armilla (Granada) 18100, Spain ⁵Institute of Neurology, University College London, London WC1N 3BG, UK

Corresponding author Ø. Hvalby: Molecular Neurobiology Research Group (MONERG), PO Box 1104, Faculty of Medicine, University of Oslo, N-0317 Blindern, Oslo, Norway. Email: o.c.hvalby{at}medisin.uio.no

Abstract

High frequency afferent stimulation of chemical synapses often induces short-term increases in synaptic efficacy, due to increased release probability and/or increased supply of readily releasable synaptic vesicles. This may be followed by synaptic depression, often caused by vesicle depletion. We here describe an additional, novel type of delayed and transient response enhancement phase which occurred during prolonged stimulation at 5–20 Hz frequency of excitatory glutamatergic synapses in slices from the adult mouse CA1 hippocampal region. This second enhancement phase, which was most clearly defined at physiological temperatures and essentially absent at 24°C, was dependent on the presence of F-actin filaments and synapsins I and/or II, and could not be ascribed to changes in presynaptic action potentials, inhibitory neurotransmission or glutamate receptor desensitization. Time course studies showed that the delayed response phase interrupted the synaptic decay 3–4 s after stimulus train initiation and continued, when examined at 5–10 Hz frequencies, for approximately 75 stimuli before decay. The novel response enhancement, probably deriving from a restricted pool of synaptic vesicles, may allow maintenance of synaptic efficacy during prolonged periods of excitatory synaptic activity.