Abstract:
:In the early postnatal period, energy metabolism in the suckling rodent brain relies to a large extent on metabolic pathways alternate to glucose such as the utilization of ketone bodies (KBs). However, how KBs affect neuronal excitability is not known. Using recordings of single NMDA and GABA-activated channels in neocortical pyramidal cells we studied the effects of KBs on the resting membrane potential (E(m)) and reversal potential of GABA-induced anionic currents (E(GABA)), respectively. We show that during postnatal development (P3-P19) if neocortical brain slices are adequately supplied with KBs, E(m) and E(GABA) are both maintained at negative levels of about -83 and -80 mV, respectively. Conversely, a KB deficiency causes a significant depolarization of both E(m) (>5 mV) and E(GABA) (>15 mV). The KB-mediated shift in E(GABA) is largely determined by the interaction of the NKCC1 cotransporter and Cl(-)/HCO3 transporter(s). Therefore, by inducing a hyperpolarizing shift in E(m) and modulating GABA signaling mode, KBs can efficiently control the excitability of neonatal cortical neurons.
journal_name
J Neurochemjournal_title
Journal of neurochemistryauthors
Rheims S,Holmgren CD,Chazal G,Mulder J,Harkany T,Zilberter T,Zilberter Ydoi
10.1111/j.1471-4159.2009.06230.xsubject
Has Abstractpub_date
2009-08-01 00:00:00pages
1330-8issue
4eissn
0022-3042issn
1471-4159pii
JNC6230journal_volume
110pub_type
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