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Cited by 219Neuroscience and Neuropharmacology ResearchNeural dynamics and brain functionEpilepsy research and treatment

Parvalbumin-Deficiency Facilitates Repetitive IPSCs and Gamma Oscillations in the Hippocampus

Vreugdenhil, Martin, Jefferys, John G. R., Celio, Marco R., Schwaller, Beat·2003·Journal of Neurophysiology
DOI 10.1152/jn.00576.2002
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Abstract

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 Ca 2+ -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 μV 2 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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Authors
Vreugdenhil, M., Jefferys, J. G. R., Celio, M. R., & Schwaller, B.
Affiliations
  • University of Birmingham (GB)
  • University of Fribourg (CH)
ORCID
Venue
Journal of Neurophysiology
Publisher
American Physiological Society
Published
2003-03-01
Volume
89
Issue
3
Pages
1414-1422
ISSN
  • 0022-3077 (ISSN-L)
  • 1522-1598
DOI
10.1152/jn.00576.2002
OpenAlex
W2019983560
Cited by
219
References
54
Citations by year
2026: 3 · 2025: 3 · 2024: 3 · 2023: 4 · 2022: 5 · 2021: 12 · 2020: 14 · 2019: 11 · 2018: 4 · 2017: 4 · 2016: 12 · 2015: 9 · 2014: 9 · 2013: 12 · 2012: 9
FWCI
3.81
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Neurophysiology (publishedVersion)
  • PubMed (publishedVersion)
  • University of Birmingham Research Portal (University of Birmingham) (submittedVersion)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
  • Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
Keywords
parvalbumin, gamma oscillations, inhibitory postsynaptic currents, paired-pulse facilitation, GABA release, hippocampus, CA1 pyramidal neurons, interneurons, high-frequency oscillations, CA3, short-term synaptic facilitation
MeSH terms
Animals, Chimera, Female, gamma-Aminobutyric Acid, Hippocampus, Kainic Acid, Male, Mice, Inbred C57BL, Neural Inhibition, Neurons, Parvalbumins, Periodicity, Pregnancy, Presynaptic Terminals, Excitatory Amino Acid Agonists, Mice

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