Fig. 3

Esr1, esr2a and esr2a mutants do not show habituation deficits after treatment with estradiol. A) Homozygous esr1(−/−) mutants (n = 231 fish) do not show impaired habituation relative to sibling controls (esr1(+/−) = esr1(+/−) and esr1(+/+), n = 490 fish). B) Homozygous esr2a(−/−) mutants (n = 124 fish) do not show impaired habituation relative to sibling controls (esr2a(+/−) = esr2a(+/−) and esr2a(+/+), n = 128 fish). C) Homozygous esr2b(−/−) mutants (n = 205 fish) do not show impaired habituation relative to sibling controls (esr2b(+/−) = esr2b(+/−) and esr2b(+/+), n = 542 fish). i)-vi) For each lettered section: i) Responsiveness to stimuli comparing homozygous mutants to sibling controls (heterozygous or wild-type). Each dot is the probability of response to one stimulus. Lines are smoothed in time with a Savitzky–Golay filter (window = 15 stimuli, order = 2). Suppression of responsiveness is indicated by arrows, potentially reflecting increased habituation. ii)-v) Distributions responsiveness for different epochs of the experiment. Each dot is the per-fish average of the epoch. Statistical significance was calculated using Mann-Whitney U test, * = P < .05, ** = P < .01. ii) the naive response to the first 5 DF stimuli; iii) the mean response to the remaining DF stimuli in the Block 1 (DFs 6:60); iv) the trained response to the last 45 DFs in all 4 training blocks (DFs 16:60,76:120,136:180,196:240); v) the 30 vibration stimuli delivered with a tap from a solenoid on the 300-well plate platform. vi) Cumulative mean difference (CMD) plot quantifying habituation performance of mutants relative to sibling controls.