Figure 2 | Translational Psychiatry

Figure 2

From: Lack of parvalbumin in mice leads to behavioral deficits relevant to all human autism core symptoms and related neural morphofunctional abnormalities

Figure 2

Impairments in communication: PV−/− null mutant and PV+/− heterozygous mice display ultrasonic vocalization deficits during reciprocal social interactions as juveniles. (a) Total number of ultrasonic vocalizations emitted during the 5-min social interaction period (genotype: F2,21=9.240, P=0.001; sex: NS; genotype × sex: NS). (b) Time course for the number of ultrasonic vocalizations emitted for each 1-min time bin across the 5-min social interaction period, plus 1 min habitation (dashed line indicates introduction of partner mouse). (c) Duration of calls (genotype: F2,21=3.870, P=0.037; sex: NS; genotype × sex: NS), (d) peak frequency (genotype: NS; sex: NS; genotype × sex: NS) and (e) frequency modulation of calls (genotype: NS; sex: NS; genotype × sex: NS) emitted during the 5-min social interaction period. Black bar: PV+/+ wild-type littermate control mice; striped bar: PV+/− heterozygous mice; white bar: PV−/− null mutant mice. Data are presented as means±s.e.m., bars denoting the s.e.m. *P<0.050 vs PV+/+. (fh) Representative spectrograms of ultrasonic vocalizations emitted during juvenile reciprocal social interactions by (f) a PV+/+ wild-type littermate control mouse, (g) a PV+/− heterozygous mouse and (h) a PV−/− null mutant mouse. NS, not significant; PV, parvalbumin.

Back to article page