Developmental plasticity
[2][3] Synaptic plasticity depends on numerous factors including the threshold of the presynaptic stimulus in addition to the relative concentrations of neurotransmitter molecules.
[11] Experimentally, this can be seen when rats are raised in an environment that allows ample social interaction, resulting in increased brain weight and cortical thickness.
The differentiation of stem cell precursors into specialized neurons gives rise to the formation of synapses and neural circuits, which is key to the principle of plasticity.
[14] During this pivotal point in development, consequent developmental processes like the differentiation and specialization of neurons are highly sensitive to exogenous and endogenous factors.
[15] For example, in utero exposure to nicotine has been linked to adverse effects, such as severe physical and cognitive deficits, due to the impediment of the normal acetylcholine receptor activation.
It was determined that nicotine exposure in early development can have a lasting and encompassing effect on neuronal structures, underlying the behavioral and cognitive defects observed in exposed humans and animals.
Additionally, when proper synaptic function is disrupted through nicotine exposure, the overall circuit may become less sensitive and responsive to stimuli, resulting in compensatory developmental plasticity.
[19] The young neurons have complete potential of changing morphology during a time span classified as the critical period to achieve strengthened and refined synaptic connections.
[23] These mechanisms can malfunction with the introduction of toxins, which bind to sodium channels and suppress action potentials and consequently electrical activity between synapses.
[26] This method of tracing employs the migration of a neurotropic virus through tightly interconnected neurons and specific site labeling of distinct connections.
[27] Patch-clamping experiments and calcium imaging are often conducted based on preliminary results from this assay in order to detect spontaneous neuronal activity.
[29] The concept of critical periods is a widely accepted and prominent theme in development, with strong implications for developmental plasticity.
At birth, the development of respiratory control neural circuits is incomplete, requiring complex interactions from both the environment and intrinsic factors.
Experimentally exposing two-week-old kittens and rats to hyperoxic conditions completely eliminates the carotid chemoreceptor response to hypoxia, resulting in respiratory impairment.
This has remarkable clinical significance, as newborn infants are often supplemented with considerable amounts of oxygen, which could detrimentally affect the way in which neural circuits for respiratory control develop during the critical period.
For example, prior to birth, neural circuits in the retina undergo spontaneous network activity, which has been found to elicit the formation of retinogeniculate connections.
[43] For example, in Daphnia, neonates exposed to predator cues displayed higher expression of genes related to digestion, reproductive function, and defense.
Subsequent generations exhibited a similar pattern, despite not being exposed to any predator cues, suggesting an inheritance of epigenetic expression factors.
