Developmentally regulated expression of c‐Fos and c‐Jun in the brainstem auditory nuclei of Gallus domesticus is modified by prenatal auditory enrichment

Abstract

Recognition of mother's voice by human neonates and behavioral responses of birds and animals to sounds experienced prenatally emphasize the role of sensory inputs in auditory system development. Spontaneous and experience driven neural activity influence the neural circuits' refinement in developing brain. However, cellular mechanisms endowing plasticity for such structural refinement during critical developmental periods are less understood. Sensory stimulation induces fluctuating expression of transcription factors (TFs) of Fos, Jun, and Krox families in the related brain nuclei to activate genes to synthesize proteins such as those needed for cytoskeletal structures, ion channels, and regeneration. To understand the cellular mechanism of response to prenatal auditory stimulation, we studied the expression of c-Fos and c-Jun in brainstem auditory nuclei, nucleus magnocellularis, and nucleus laminaris of the domestic chick. The chick brainstems, five each of E8 (embryonic day 8), E12, E16, E20, and posthatch day 1 were processed for immunohistochemistry as well as Western blotting and quantified using image analysis systems. In controls, c-Fos and c-Jun expression in both the nuclei was developmentally up-regulated. Reduced c-Fos expression and increase in c-Jun was temporarily observed between E12-16. In the stimulated groups, c-Fos expression was elevated while c-Jun showed a reduction matched to controls. This diametrically opposing pattern of c-Fos and c-Jun expression in response to stimulation is indicative of cell survival. Thus the expression of TFs in the auditory nuclei shows a relationship beyond a simple stimulation-activity-expression. While developmental signals control the expression of TFs, extra sensory stimulation modulates their expression to possibly support neuronal survival and enhance synthesis of other proteins.

The Activity of Spontaneous Action Potentials in Developing Hair Cells Is Regulated by Ca2+-Dependence of a Transient K+ Current

“…Moreover, phasic alterations of Ca 2+ i mediate the expression of K + channels that modulate SAPs, or influence the gene expression that may refine neuronal connections [26]–[30]. 4-AP-sensitive currents, presumably of A-type K + currents (I A ) regulate spike timing and firing frequency in neurons [31]–[33] and cardiac myocytes [34].…”

Prenatal auditory enrichment with species‐specific calls and sitar music modulates expression of Bcl‐2 and Bax to alter programmed cell death in developing chick auditory nuclei

“…Since developing neurons with more contacts succeed in engaging an axon to the soma to ultimately survive (Jhaveri and Morest, 1982), it is likely that more number of postsynaptic neurons survive following auditory stimulation. We also showed that extra‐sensory stimulation modulated the developmental expression of transcription factors, c‐Fos and c‐Jun; c‐Fos protein showed a gradual age‐ and stimulus‐dependent increase in expression, parallel to the enhanced syntaxin1 expression (Alladi et al, 2005).…”

Prenatal acoustic stimulation influences neuronal size and the expression of calcium-binding proteins (calbindin D-28K and parvalbumin) in chick hippocampus

“…The enhanced sound stimulation favors the survival of neurons by reducing physiological cell death and increasing the relative amounts of Bcl-2, a anti-apoptotic protein (Alladi et al, 2005a). Prenatal patterned acoustic stimulation enhances synaptic protein synthesis (Alladi et al, 2002) and modulates the expression of the immediate early gene products, c-Fos and c-Jun, in NM and NL (Alladi et al, 2005b). Furthermore, the sound-stimulated groups show an increase in neuronal size and the proportion of neurons containing calcium-binding proteins (CaBPs)-calbindin D-28K (CALB) and parvalbumin (PV) in the mediorostral nidopallium hyperpallium ventrale (MNH), which is an auditory imprinting area of chick forebrain (Panicker et al, 2002).…”