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

Abstract

The thyroid hormone 3,5,3′-triiodothyronine (T3) is considered to act acutely in the chick forebrain because focal infusion of T3 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 T3 action, we examined synaptic responses of IMM neurons in slice preparations in vitro. 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 T3 (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 T3 suppressed the bursting frequency. Pretreatment of slices with T3 failed to influence the synaptic potentiation caused by tetanic stimulation. Intracellular whole-cell recording using a patch electrode confirmed the T3 actions on the GABA-A and NMDA components. T3 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, T3 suppressed the synaptic drives of IMM neurons, and did not influence activity-dependent synaptic potentiation. Imprinting-associated T3 influx may act as an acute suppressor of the IMM network.

Thyroid hormone as a temporal switch in mouse development

“…It would be of interest to address if these conclusions also apply to the filial imprinting of birds. Similarly, this phenomenon is restricted to a sensitive period defined by T3 (46) and involves GABAergic neurons (47).…”

“…Similarly, the oligodendrocyte precursor cells, responsible for the initial postnatal myelination of axons, are not sensitive to the restricted expression of TRα1 L400R ( 50 , 51 ). Therefore, T3-responsive cells amplify the influence of T3, secreting growth factors and neurotrophins that influence their microenvironment ( 52 , 53 , 54 ).…”

The domestic chick as an animal model of autism spectrum disorder: building adaptive social perceptions through prenatally formed predispositions

“…The mTOR-GABA cascade may mediate the acute facilitatory effects of THs in chicks ( Yamaguchi et al, 2012 ; Batista et al, 2018 ; Lorenzi et al, 2021 ). T 3 acutely enhances GABAergic transmission in slice preparations of the chick pallium ( Saheki et al, 2022 ), although its functional link to the behavioral effects remains elusive.…”