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J Neurophysiol (March 1, 2003). 10.1152/jn.00576.2002
Submitted on Submitted 19 July 2002; accepted in final form 19 November 2002
1Department of Neurophysiology, Division of Neuroscience, Medical School, University of Birmingham, B15 2TT, Birmingham, United Kingdom; and 2Institute of Histology and General Embryology, University of Fribourg, CH-1705, Fribourg, Switzerland
Vreugdenhil, Martin,
John G. R. Jefferys,
Marco
R. Celio, and
Beat Schwaller.
Parvalbumin-Deficiency Facilitates Repetitive IPSCs and Gamma
Oscillations in the Hippocampus. J. Neurophysiol. 89: 1414-1422, 2003. In the hippocampus, the
calcium-binding protein parvalbumin (PV) is expressed in interneurons
that innervate perisomatic regions. PV in GABAergic synaptic terminals
was proposed to limit repetitive GABA release by buffering of
"residual calcium." We assessed the role of presynaptic PV in
Ca2+-dependent GABA release in the hippocampus of
PV-deficient (PV
/) mice and wild-type (PV+/+) littermates.
Pharmacologically isolated inhibitory postsynaptic currents (IPSCs)
were evoked by low-intensity stimulation of the stratum pyramidale and
recorded from voltage-clamped CA1 pyramidal neurons. The amplitude and
decay time constant of single IPSCs were similar for both genotypes.
Under our experimental conditions of reduced release probability and
minimal presynaptic suppression, paired-pulse facilitation of IPSCs
occurred at intervals from 2 to 50 ms, irrespective of the presence of
PV. The facilitation of IPSCs induced by trains of 10 stimuli at
frequencies >20 Hz was enhanced in cells from PV/ mice, the
largest difference between PV/ and PV+/+ animals (220%) being
observed at 33 Hz. The effect of IPSC facilitation at sustained gamma
frequencies was assessed on kainate-induced rhythmic IPSC-paced
neuronal oscillations at gamma frequencies, recorded with dual field
potential recordings in area CA3. The maximum power of the oscillation
was 138 µV2 at 36 Hz in slices from PV+/+ mice
and was trebled in slices from PV/ mice. PV deficiency caused a
similar increase in gamma power under conditions used to study IPSC
facilitation and can be explained by an increased facilitation of GABA
release at sustained high frequencies. The dominant frequency and
coherence were not affected by PV deficiency. These observations
suggest that PV deficiency, due to an increased short-term facilitation
of GABA release, enhances inhibition by high-frequency burst-firing
PV-expressing interneurons and may affect the higher cognitive
functions associated with gamma oscillations.
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