 |
||||
|
||||
|
||||
|
||||
Previous Article | Next Article
The Journal of Neuroscience, September 15, 2002, 22(18):8052-8062
Distally Directed Dendrotoxicity Induced by Kainic Acid in Hippocampal Interneurons of Green Fluorescent Protein-Expressing Transgenic Mice
Anthony A. Oliva Jr1, 2, Trang T. Lam1, 3, and John W. Swann1, 2, 3 1 The Cain Foundation Laboratories, 2 Division of Neuroscience, and 3 Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030
Excitotoxicity, resulting from the excessive release of glutamate, is thought to contribute to a variety of neurological disorders, including epilepsy. Excitotoxic damage to dendrites, i.e., dendrotoxicity, is often characterized by the formation of large dendritic swellings, or "beads." Here, we show that hippocampal interneurons that express the neuropeptide somatostatin are highly vulnerable to the excitotoxic effects of the ionotropic glutamate receptor agonist kainate. Brief, focal iontophoretic application of kainate rapidly induced bead formation in dendrites of somatostatinergic interneurons that express green fluorescent protein (GFP) from mice of the transgenic line GIN (GFP-expressing inhibitory neurons). Surprisingly, beads often did not form at the site of kainate application or even in the dendritic segment to which kainate was applied; instead, dendritic beading occurred more distally, often encompassing all branches distal to the application site. We have termed this phenomena, "distally directed dendrotoxicity." Distally directed beading was induced regardless of the branch order of the site of application and was found to be dependent on activation of voltage-gated sodium channels. Subsequent to induction, distally directed beading would reverse in most cells; in other cells, however, beading irreversibly invaded proximal dendritic segments and gradually encompassed the entire dendritic tree. These results demonstrate that distal dendritic segments are highly vulnerable to excitotoxic injury and imply that excessive excitatory activity originating in one synaptic pathway can impact synapses at more distal dendritic segments of the same neuron. The discovery of this phenomenon will likely be important in understanding interneuronal dysfunction following excitotoxic injury.
Key words: GABAergic neurons; interneurons; green fluorescent protein; GFP; transgenic mice; hippocampus; somatostatin; explant; organotypic; dendrotoxicity; excitotoxicity; neurotoxicity; kainate; kainic acid; dendrite; sodium; sodium channel; tetrodotoxin; lidocaine; confocal microscopy; fluorescence microscopy; beading; bead
Copyright © 2002 Society for Neuroscience 0270-6474/02/22188052-11$05.00/0
This article has been cited by other articles:
A. F. Bartley, Z. J. Huang, K. M. Huber, and J. R. Gibson
Differential Activity-Dependent, Homeostatic Plasticity of Two Neocortical Inhibitory Circuits
J Neurophysiol, October 1, 2008; 100(4): 1983 - 1994.
[Abstract] [Full Text] [PDF]
T. Mizuno, G. Zhang, H. Takeuchi, J. Kawanokuchi, J. Wang, Y. Sonobe, S. Jin, N. Takada, Y. Komatsu, and A. Suzumura
Interferon-{gamma} directly induces neurotoxicity through a neuron specific, calcium-permeable complex of IFN-{gamma} receptor and AMPA GluR1 receptor
FASEB J, June 1, 2008; 22(6): 1797 - 1806.
[Abstract] [Full Text] [PDF]
C. A. Scott, J. P. Rossiter, R. D. Andrew, and A. C. Jackson
Structural Abnormalities in Neurons Are Sufficient To Explain the Clinical Disease and Fatal Outcome of Experimental Rabies in Yellow Fluorescent Protein-Expressing Transgenic Mice
J. Virol., January 1, 2008; 82(1): 513 - 521.
[Abstract] [Full Text] [PDF]
S. M. Greenwood, S. M. Mizielinska, B. G. Frenguelli, J. Harvey, and C. N. Connolly
Mitochondrial Dysfunction and Dendritic Beading during Neuronal Toxicity
J. Biol. Chem., September 7, 2007; 282(36): 26235 - 26244.
[Abstract] [Full Text] [PDF]
N. R. Glatzer, A. V. Derbenev, B. W. Banfield, and B. N. Smith
Endomorphin-1 Modulates Intrinsic Inhibition in the Dorsal Vagal Complex
J Neurophysiol, September 1, 2007; 98(3): 1591 - 1599.
[Abstract] [Full Text] [PDF]
P. Y. Chang, P. E. Taylor, and M. B. Jackson
Voltage Imaging Reveals the CA1 Region at the CA2 Border as a Focus for Epileptiform Discharges and Long-Term Potentiation in Hippocampal Slices
J Neurophysiol, September 1, 2007; 98(3): 1309 - 1322.
[Abstract] [Full Text] [PDF]
J. Ziburkus, J. R. Cressman, E. Barreto, and S. J. Schiff
Interneuron and Pyramidal Cell Interplay During In Vitro Seizure-Like Events
J Neurophysiol, June 1, 2006; 95(6): 3948 - 3954.
[Abstract] [Full Text] [PDF]
C. Le Duigou, L. Wittner, L. Danglot, and R. Miles
Effects of focal injection of kainic acid into the mouse hippocampus in vitro and ex vivo
J. Physiol., December 15, 2005; 569(3): 833 - 847.
[Abstract] [Full Text] [PDF]
D. W. Verzi, M. B. Rheuben, and S. M. Baer
Impact of Time-Dependent Changes in Spine Density and Spine Shape on the Input-Output Properties of a Dendritic Branch: A Computational Study
J Neurophysiol, April 1, 2005; 93(4): 2073 - 2089.
[Abstract] [Full Text] [PDF]
H. Takeuchi, T. Mizuno, G. Zhang, J. Wang, J. Kawanokuchi, R. Kuno, and A. Suzumura
Neuritic Beading Induced by Activated Microglia Is an Early Feature of Neuronal Dysfunction Toward Neuronal Death by Inhibition of Mitochondrial Respiration and Axonal Transport
J. Biol. Chem., March 18, 2005; 280(11): 10444 - 10454.
[Abstract] [Full Text] [PDF]
|
|
|
|
 |
|