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Electroporation of the Hindbrain to Trace Axonal Trajectories and Synaptic Targets in the Chick Embryo
Published on: May 29, 2013
Calbindin D-28K and parvalbumin expression in embryonic chick hippocampus is enhanced by prenatal auditory
Sraboni Chaudhury1, Tapas Chandra Nag, Shashi Wadhwa
1Department of Anatomy, All India Institute of Medical Sciences, Ansari Nagar, New Delhi 110029, India.
Insights
Prenatal auditory stimulation, including music and species-specific sounds, significantly increased calcium-binding protein (CaBP) neurons in developing chick hippocampi. This suggests sound exposure enhances neuronal development and survival.
Area of Science:
- Neuroscience
- Developmental Biology
- Auditory Neuroscience
Background:
- Calcium-binding proteins (CaBPs) regulate cytosolic calcium (Ca2+), crucial for neuronal activity.
- Prenatal auditory stimulation impacts auditory pathway maturation and chick behavior.
- Understanding CaBP roles in early development is vital for neuroprotection.
Purpose of the Study:
- To investigate the effects of prenatal auditory stimulation on CaBP expression in the developing chick hippocampus.
- To determine changes in hippocampal volume, neuron count, and CaBP-positive neuron proportions.
- To correlate auditory input with neuronal development and CaBP expression levels.
Main Methods:
- Fertilized chick eggs were exposed to species-specific calls or sitar music from embryonic day 10 until hatching.
- Hippocampi were analyzed at embryonic days 12, 16, and 20.
- Measurements included hippocampal volume, total neuron count, and immunopositive neurons for calbindin D-28K and parvalbumin.
Main Results:
- Auditory stimulation significantly increased the proportion of calbindin D-28K and parvalbumin-positive neurons at all developmental stages compared to controls.
- Music-stimulated chicks showed a significant increase in hippocampal volume at E20.
- Both stimulation groups exhibited enhanced CaBP expression, suggesting activity-dependent calcium influx.
Conclusions:
- Prenatal auditory stimulation positively influences the development of CaBP-expressing neurons in the chick hippocampus.
- Increased CaBP expression may confer neuroprotection against excitotoxicity during development.
- Enhanced CaBP levels could play a role in synaptic plasticity mechanisms like long-term potentiation.
Abstract:
Calcium-binding proteins (CaBPs) buffer excess of cytosolic Ca(2+), which accompanies neuronal activity following external stimuli. Prenatal auditory stimulation by species-specific sound and music influences early maturation of the auditory pathway and the behavioral responses in chicks. In this study, we determined the volume, total number of neurons, proportion of calbindin D-28K and parvalbumin-positive neurons along with their levels of expression in the developing chick hippocampus following prenatal auditory stimulation. Fertilized eggs of domestic chicks were exposed to sounds of either species-specific calls or sitar music at 65 dB for 15 min/h round the clock from embryonic day (E) 10 until hatching. Hippocampi of developmental stages (E12, E16 and E20) were examined. With an increase in embryonic age during normal development, the hippocampus showed an increase in its volume, total number of neurons as well as in the neuron proportions and levels of expression of calbindin D-28K and parvalbumin. A significant increase of volume at E20 was noted only in the music-stimulated group compared to that of their age-matched control (p<0.05). On the other hand, both auditory-stimulated groups showed a significant increase in the proportion of immunopositive neurons and the levels of expression of calbindin D-28K and parvalbumin as compared to the control at all developmental stages studied (p<0.003). The increase in proportions of CaBP neurons during development and in the sound-enriched groups suggests an activity-dependent increase in Ca(2+) influx. The enhanced expression of CaBPs may help in cell survival by preventing excitotoxic death of neurons during development and may also be involved in long-term potentiation.

