Document Detail


Mossy fibers are the primary source of afferent input to ectopic granule cells that are born after pilocarpine-induced seizures.
MedLine Citation:
PMID:  16342370     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Granule cell (GC) neurogenesis increases following seizures, and some newborn GCs develop in abnormal locations within the hilus. These ectopic GCs (EGCs) display robust spontaneous and evoked excitatory activity. However, the pattern of afferent input they receive has not been fully defined. This study used electron microscopic immunolabeling to quantitatively evaluate mossy fiber (MF) input to EGCs since MFs densely innervate the hilus normally and undergo sprouting in many animal models of epilepsy. EGC dendrites were examined in tissue from epileptic rats that had initially been treated with pilocarpine to induce status epilepticus and subsequently had spontaneous seizures. MF terminals were labeled with a zinc transporter-3 antibody, and calbindin immunoreactivity was used to label hilar EGCs and GC layer GCs. The pattern of input provided by sprouted MF terminals to EGC dendrites was then compared to the pattern of MF input to GC dendrites in the inner molecular layer (IML), where most sprouted fibers are thought to project. Analysis of EGC dendrites demonstrated that MF terminals represented their predominant source of afferent input: they comprised 63% of all terminals and, on average, occupied 40% and 29% of the dendritic surface in the dorsal and ventral dentate gyrus, respectively, forming frequent synapses. These measures of connectivity were significantly greater than comparable values for MF innervation of GC dendrites located in the IML of the same tissue sections. Thus, EGCs develop a pattern of synaptic connections that could help explain their previously identified predisposition to discharge in epileptiform bursts and suggest that they play an important role in the generation of seizure activity in the dentate gyrus.
Authors:
Joseph P Pierce; Jay Melton; Michael Punsoni; Daniel P McCloskey; Helen E Scharfman
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Experimental neurology     Volume:  196     ISSN:  0014-4886     ISO Abbreviation:  Exp. Neurol.     Publication Date:  2005 Dec 
Date Detail:
Created Date:  2005-12-08     Completed Date:  2006-01-25     Revised Date:  2013-06-07    
Medline Journal Info:
Nlm Unique ID:  0370712     Medline TA:  Exp Neurol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  316-31     Citation Subset:  IM    
Affiliation:
Department of Neurology and Neuroscience, Weill Medical College of Cornell University, NY 10021, USA. jppierc@med.cornell.edu
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MeSH Terms
Descriptor/Qualifier:
Afferent Pathways / metabolism,  pathology*,  ultrastructure
Animals
Calcium-Binding Protein, Vitamin D-Dependent / metabolism
Cation Transport Proteins / metabolism
Cell Count / methods
Disease Models, Animal
Immunohistochemistry / methods
Male
Microscopy, Electron, Transmission / methods
Microscopy, Immunoelectron / methods
Mossy Fibers, Hippocampal / metabolism,  pathology*,  ultrastructure
Neurons / metabolism,  pathology*,  ultrastructure
Pilocarpine*
Rats
Rats, Sprague-Dawley
Seizures / chemically induced,  pathology*,  physiopathology
Synapses / metabolism,  pathology,  ultrastructure
Grant Support
ID/Acronym/Agency:
NS 41490/NS/NINDS NIH HHS; R01 NS041490-03/NS/NINDS NIH HHS; R01 NS041490-04/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Calcium-Binding Protein, Vitamin D-Dependent; 0/Cation Transport Proteins; 0/calbindin; 0/zinc transporter 3, rat; 92-13-7/Pilocarpine
Comments/Corrections

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