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The Journal of Neuroscience, September 30, 2009, 29(39):12131-12144; doi:10.1523/JNEUROSCI.1333-09.2009

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Development/Plasticity/Repair
Spontaneous Bursting Activity in the Developing Entorhinal Cortex

Maxim G. Sheroziya,^1,2 Oliver von Bohlen und Halbach,^1,3 Klaus Unsicker,^1,4 and Alexei V. Egorov^1,2,4

¹Interdisciplinary Center for Neurosciences, Department of Neuroanatomy, University of Heidelberg, D-69120 Heidelberg, Germany, ²Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, 117485 Moscow, Russia, ³Institute of Anatomy and Cell Biology, University of Greifswald, D-17487 Greifswald, Germany, and ⁴Department of Molecular Embryology, Institute of Anatomy and Cell Biology, University of Freiburg, D-79104 Freiburg, Germany

Correspondence should be addressed to Dr. Alexei V. Egorov, Interdisciplinary Center for Neurosciences, Department of Neuroanatomy, University of Heidelberg, Im Neuenheimer Feld 307, D-69120 Heidelberg, Germany. Email: alexei.egorov{at}urz.uni-heidelberg.de

Periodic spontaneous activity represents an important attribute of the developing nervous system. The entorhinal cortex (EC) is a crucial component of the medial temporal lobe memory system. Yet, little is known about spontaneous activity in the immature EC. Here, we investigated spontaneous field potential (fp) activity and intrinsic firing patterns of medial EC layer III principal neurons in brain slices obtained from rats at the first two postnatal weeks. A fraction of immature layer III neurons spontaneously generated prolonged (2–20 s) voltage-dependent intrinsic bursting activity. Prolonged bursts were dependent on the extracellular concentration of Ca²⁺ ([Ca²⁺]_o). Thus, reduction of [Ca²⁺]_o increased the fraction of neurons with prolonged bursting by inducing intrinsic bursts in regularly firing neurons. In 1 mM [Ca²⁺]_o, the percentages of neurons showing prolonged bursts were 53%, 81%, and 29% at postnatal day 5 (P5)–P7, P8–P10, and P11–P13, respectively. Prolonged intrinsic bursting activity was blocked by buffering intracellular Ca²⁺ with BAPTA, and by Cd²⁺, flufenamic acid (FFA), or TTX, and was suppressed by nifedipine and riluzole, suggesting that the Ca²⁺-sensitive nonspecific cationic current (I_CAN) and the persistent Na⁺ current (I_Nap) underlie this effect. Indeed, a 0.2–1 s suprathreshold current step stimulus elicited a terminated plateau potential in these neurons. fp recordings at P5–P7 showed periodic spontaneous glutamate receptor-mediated events (sharp fp events or prolonged fp bursts) which were blocked by FFA. Slow-wave network oscillations become a dominant pattern at P11–P13. We conclude that prolonged intrinsic bursting activity is a characteristic feature of developing medial EC layer III neurons that might be involved in neuronal and network maturation.

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Received March 19, 2009; revised Aug. 11, 2009; accepted Aug. 17, 2009.

Correspondence should be addressed to Dr. Alexei V. Egorov, Interdisciplinary Center for Neurosciences, Department of Neuroanatomy, University of Heidelberg, Im Neuenheimer Feld 307, D-69120 Heidelberg, Germany. Email: alexei.egorov{at}urz.uni-heidelberg.de

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