Author's present address
Miniature synaptic transmission and BDNF modulate dendritic spine growth and form in rat CA1 neurones
Article first published online: 16 JUL 2004
The Journal of Physiology
Volume 553, Issue 2, pages 497–509, December 2003
How to Cite
Tyler, W. J. and Pozzo-Miller, L. (2003), Miniature synaptic transmission and BDNF modulate dendritic spine growth and form in rat CA1 neurones. The Journal of Physiology, 553: 497–509. doi: 10.1113/jphysiol.2003.052639
W. J. Tyler: Department of Molecular and Cellular Biology, Harvard University, Biological Laboratories, RM 2065, 16 Divinity Avenue, Cambridge, MA 02138, USA.
- Issue published online: 16 JUL 2004
- Article first published online: 16 JUL 2004
- (Received 1 August 2003; accepted after revision 12 September 2003; first published online 18 September 2003)
The refinement and plasticity of neuronal connections require synaptic activity and neurotrophin signalling; their specific contributions and interplay are, however, poorly understood. We show here that brain-derived neurotrophic factor (BDNF) increased spine density in apical dendrites of CA1 pyramidal neurones in organotypic slice cultures prepared from postnatal rat hippocampal slices. This effect was observed also in the absence of action potentials, and even when miniature synaptic transmission was inhibited with botulinum neurotoxin C (BoNT/C). There were, however, marked differences in the morphology of individual spines induced by BDNF across these different levels of spontaneous ongoing synaptic activity. During both normal synaptic transmission, and when action potentials were blocked with TTX, BDNF increased the proportion of stubby, type-I spines. However, when SNARE-dependent vesicular release was inhibited with BoNT/C, BDNF increased the proportion of thin, type-III spines. Our results indicate that BDNF increases spine density irrespective of the levels of synaptic transmission. In addition, miniature synaptic transmission provides sufficient activity for the functional translation of BDNF-triggered spinogenesis into clearly defined morphological spine types, favouring those spines potentially responsible for coordinated Ca2+ transients thought to mediate synaptic plasticity. We propose that BDNF/TrkB signalling represents a mechanism of expression of both morphological and physiological homeostatic plasticity in the hippocampus, leading to a more efficient synaptic information transfer across widespread levels of synaptic activity.