Suppressive Modulation of the Chick Forebrain Network for Imprinting by Thyroid Hormone: An Study.

The thyroid hormone 3,5,3'-triiodothyronine (T) is considered to act acutely in the chick forebrain because focal infusion of T to the intermediate medial mesopallium (IMM) causes 4 to 6-day-old hatchlings to become imprintable approximately 30 min after the infusion. To understand the mechanism of this acute T action, we examined synaptic responses of IMM neurons in slice preparations . Extracellular field potential responses to local electrical stimulation were pharmacologically dissociated to synaptic components mediated by AMPA and NMDA receptors, as well as GABA-A and -B receptors. Bath-applied T (20-40 μM) enhanced the positive peak amplitude of the field potential, which represented the GABA-A component. Bicuculline induced spontaneous epileptic bursts by NMDA receptor activation, and subsequent application of T suppressed the bursting frequency. Pretreatment of slices with T failed to influence the synaptic potentiation caused by tetanic stimulation. Intracellular whole-cell recording using a patch electrode confirmed the T actions on the GABA-A and NMDA components. T enhanced the GABA-A response and suppressed the NMDA plateau potential without changes in the resting membrane potential or the threshold of action potentials. Contrary to our initial expectation, T suppressed the synaptic drives of IMM neurons, and did not influence activity-dependent synaptic potentiation. Imprinting-associated T influx may act as an acute suppressor of the IMM network.