Figure 1.
Reduced density of parvalbumin-expressing interneurons in CA1 caused by prenatal immune challenge.
A) Photomicrograph of the CA1 subfield of the hippocampus from pups of dams treated with poly I∶C during pregnancy (bottom) and control (top). Scale bar 200 µm, in green: somatostatin, in red: parvalbumin. B) and C) Comparison of somatostatin- (B) and parvalbumin- (C) positive cell density between the poly I∶C and the saline group, for all the CA1 subfields (total), stratum oriens (Or.) or stratum pyramidale (Pyr.) (saline n = 8, poly I∶C n = 6).
Figure 2.
Prenatal immune challenge decreases the frequency and amplitude of miniIPSCs recorded in CA1 pyramidal cells.
A) Representative miniIPSC recordings from animals prenatally exposed to saline (left) or poly I∶C (right). Scale bar 500 ms (horizontal) and 60 pA (vertical). B) Average cumulative amplitude histogram (± SEM) of miniIPSCs recorded from the saline and poly I∶C group. Inset: average mean IPSC amplitude (100 events averaged for each cell) recorded for each group. C) Average cumulative inter-event interval histogram (± SEM) of miniIPSCs recorded from saline and poly I∶C treated animals. Inset: average frequency of miniIPSCs of all cells recorded for each group. D) Average waveform of 100 mini events from each cell for both groups (± SEM), scale 5 pA (vertical) and 5 ms (horizontal). Inset: Average miniIPSCs time constant. n = 7 for both groups.
Figure 3.
Prenatal immune challenge reduced monosynaptic IPSCs but increased recruitment of local inhibitory feedback interneurons.
A) Recording configuration and diagram showing the two components of the mixed IPSC (composed of the monosynaptic IPSC from direct activation of local interneurons shown in red and the antidromic IPSC from feedback interneurons activated by CA1 recurrent projections shown in blue). B) monosynaptic IPSCs isolated by the addition of DNQX (20 µM) and AP-5 (25 µM). Left: representative recordings from both groups. Right: average monosynaptic IPSC area for both groups (n = 8 for each group). C) Isolation of the antidromic IPSC. Left: representative recording showing the mixed IPSC before the addition of DNQX (20 µM) and AP-5 (25 µM) and the isolated antidromic IPSC (IPSC sensitive to AP-5 and DNQX). Middle: average magnitude of the antidromic IPSC area from both groups. Right: fraction (in percent) of the mixed IPSC contributed by the antidromic IPSC (n = 8 for each group). D) Isolation of the NMDA receptor-dependent antidromic IPSC. Left: representative recording showing the mixed IPSC before the addition of AP-5 (25 µM) and the NMDA receptor-dependent antidromic IPSC. Middle: average magnitude of the NMDA receptor-dependent antidromic IPSC area from both groups. Right: fraction (in percent) of the mixed IPSC contributed by the NMDA receptor-dependent antidromic IPSC (n = 8 for saline and n = 7 for the poly I∶C treated group). Stimulation intensity was 300 µA and each trace displayed corresponds to the average of 5 consecutive responses.
Figure 4.
Reduction of CA1 theta power in the hippocampus after prenatal immune challenge.
A) Photo of the intact hippocampal preparation with CA1 and CA3 outlined. B) Representative recording of spontaneous oscillatory activity in the whole hippocampal preparation in vitro. C) Average power spectrum (± SEM). Notice in both cases the peak power at around 4 Hz, corresponding to theta rhythm. D) The average power and peak frequency of the spontaneous self-generated theta oscillation recorded in the whole hippocampal preparation from poly I∶C- and saline-treated animals. For this experiment n = 6 in the saline and n = 7 in the poly I∶C-treated group.