|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
RAPID REPORT |
1 Neuroscience Center and Department of Bio- and Environmental Sciences, PO Box 65 (Viikinkaari 1), 00014 University of Helsinki, Finland
Homeostatic regulation, i.e. the ability of neurons and neuronal networks to adjust their output in response to chronic alterations in electrical activity is a prerequisite for the pronounced functional plasticity in the developing brain. Cellular mechanisms of homeostatic plasticity have mainly been studied in cultured preparations. To understand the developmental time frame and properties of homeostatic plasticity under more physiological conditions, we have here compared the effects of activity deprivation on synaptic transmission in acutely isolated and cultured hippocampal slices at different stages of development. We find that transmission at both glutamatergic and GABAergic synapses is strongly and rapidly (15 h) regulated in the opposite directions in response to inactivity during narrow, separated time windows early in development. Following this critical period of synaptic development, induction of the homeostatic response requires longer periods (40 h) of inactivity. At glutamatergic synapses, activity blockade led to an increase in the amplitude and frequency of mEPSCs, and the threshold for induction of this response was increased during development. In contrast, homeostatic regulation at GABAergic synapses was expressed in a qualitatively distinct manner at different developmental stages. Immature neurons responded rapidly to inactivity by regulating mIPSC frequency, while longer activity blockade led to a decrease in the mIPSC amplitude independent of the neuronal maturation. The susceptibility of immature networks to homeostatic regulation may serve as a safety mechanism against rapid runaway destability during the time of intense remodelling of the synaptic circuitry.
(Received 7 February 2007;
accepted after revision 1 March 2007;
first published online 8 March 2007)
Corresponding author S. E. Lauri: Neuroscience Center and Department of Bio- and Environmental Sciences, PO Box 65 (Viikinkaari 1), 00014 University of Helsinki, Finland. Email: sari.lauri{at}helsinki.fi
This article has been cited by other articles:
![]() |
I. V. Sokolova and I. Mody Silencing-Induced Metaplasticity in Hippocampal Cultured Neurons J Neurophysiol, August 1, 2008; 100(2): 690 - 697. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. S. Saliba, G. Michels, T. C. Jacob, M. N. Pangalos, and S. J. Moss Activity-Dependent Ubiquitination of GABAA Receptors Regulates Their Accumulation at Synaptic Sites J. Neurosci., November 28, 2007; 27(48): 13341 - 13351. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Vesikansa, M. Sallert, T. Taira, and S. E. Lauri Activation of kainate receptors controls the number of functional glutamatergic synapses in the area CA1 of rat hippocampus J. Physiol., August 15, 2007; 583(1): 145 - 157. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |