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A '''giant depolarizing potential''' ('''GDP''') is a type of patterned spontaneous activity that can be observed in preparations of developing [[brain]] at early stages of development.<ref name=rev2007>{{cite journal |vauthors=Ben-Ari Y, Gaiarsa JL, Tyzio R, Khazipov R |title=GABA: a pioneer transmitter that excites immature neurons and generates primitive oscillations |journal=Physiol. Rev. |volume=87 |issue=4 |pages=1215–84 |date=October 2007 |pmid=17928584 |doi=10.1152/physrev.00017.2006 |url=http://www.hal.inserm.fr/inserm-00483857|url-access=subscription }}</ref> These patterns of activity differ a lot from both the adult brain activity, and [[epileptiform]] activity. In [[human]]s they exist only on [[prenatal]] stages, in [[rat]]s they last for approximately [[postnatal|P6]].

GDPs were postulated to be essential for the establishment and maturation of [[synapse|synaptic]] connections in the immature brain {{citation needed|date=April 2014}}.

One of the main conditions for GDP development (that is met in premature but not adult brain) is that [[GABA]] action on these stages should be [[excitatory]] rather than [[inhibitory]]. This is caused by a much higher concentration of [[chloride|Cl<sup>−</sup>]] concentration in the [[cytoplasm]] of neonatal neurons. Further, the expression of the chloride transporter, KCC2, is less in immature neurons, as a result of which there is the above-mentioned high intracellular chloride. On receiving a GABAergic stimulus, there is an efflux of Chloride from the cell, resulting in depolarization of the cell. This causes the GDPs. Once the KCC2 expression is relatively high, as in the adult, mature neurons, the GDPs almost simultaneously disappear. The increased level of KCC2 expression in adult, mature neurons alone is not the reason for the disappearance of the GDPs, however{{Citation needed|date=November 2012}}.

==References==
{{Reflist}}

[[Category:Developmental neuroscience]]

Giant depolarizing potential - Revision history

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