Extended Data Fig. 7: PIL inputs to the PVN do not induce postsynaptic spiking or affect the excitability of oxytocin neurons.
From: Neural circuitry for maternal oxytocin release induced by infant cries
a, Schematic showing injection of AAV1-hSyn-hChR2(H134R)-EYFP in PIL of Oxytocin:Cre × Ai9 dams before whole-cell recordings from oxytocin neurons (tdTomato+) in PVN brain slices. PIL, posterior intralaminar nucleus of the thalamus; PVN, paraventricular nucleus of the hypothalamus. b, Whole-cell recordings from tdTomato+ oxytocin neurons in PVN slices, optogenetic stimulation of PIL axons and placement of the extracellular stimulation electrode. c,d, Optogenetic stimulation of PIL axons in PVN does not induce postsynaptic spiking in oxytocin neurons. c, Single pulse of optogenetic stimulation triggered postsynaptic potentials but did not induce spiking in oxytocin cells (n = 8 neurons). d, Repeated optogenetic stimulation of PIL axons (‘PIL opto’) did not trigger depolarization of oxytocin cells (n = 16 neurons; p = 0.10, Wilcoxon matched-pairs signed-rank two-tailed test) and did not induce postsynaptic spiking (n = 16 neurons; p = 0.26, Wilcoxon matched-pairs signed-rank two-tailed test). e,f, No change in the number of spikes in oxytocin neurons in response to 20 pA steps of intracellular current injection before (‘Pre’) or after (‘Post’) PIL opto. Sample traces (e) and summary (f; n = 9 neurons, p > 0.44, Wilcoxon matched-pairs signed-rank two-tailed test). g–i, No change in the intrinsic properties of oxytocin neurons after PIL opto, in terms of rheobase (g; n = 9 neurons; p = 0.38, Wilcoxon matched-pairs signed-rank two-tailed test), resting membrane potential (h; n = 6 neurons; p = 0.16, Wilcoxon matched-pairs signed-rank two-tailed test), or input resistance (i; n = 12 neurons; p = 0.06, Wilcoxon matched-pairs signed-rank two-tailed test). Data reported as mean ± s.e.m.
