Intracerebroventricular kainic acid administration in adult rat alters hippocampal calbindin and non-phosphorylated neurofilament expression.
Calbindin and non-phosphorylated neurofilament proteins were assessed in hippocampus following a unilateral intracerebroventricular kainic acid injection at 4, 26, and 60 days post-lesion, using immunocytochemical expression. The density of calbindin-positive non-pyramidal neurons throughout the hippocampus showed no significant alteration at 4 days post-lesion, a significant decrease at 26 days post-lesion, and a partial recovery at 60 days post-lesion. In addition, calbindin immunoreactivity was dramatically reduced at 26 days post-lesion in the CA1 pyramidal and dentate granule cell layers and the mossy fibers, bilaterally. Although not significant statistically, most of these reductions showed signs of reversal at 60 days post-lesion except the CA1 pyramidal cell layer where the dramatic reductions persisted. Neurofilaments were also altered throughout the post-lesion period, particularly in abnormal expression of non-phosphorylated neurofilament proteins in mossy fibers. The apparent return of calbindin immunoreactivity in non-pyramidal neurons by 60 days post-lesion suggests that recovery from the lesion may involve remaining neuronal elements which either become reactivated with time or have the capability to express normal levels of calbindin with re-innervation. On the other hand, prolonged calbindin reductions in superficial CA1 pyramidal cells suggest sustained down-regulation of calbindin expression owing to persistent reductions in the activity of these neurons. The temporal correlation of the expression of non-phosphorylated neurofilaments in mossy fibers with their sprouting response following target loss suggests a potential role for non-phosphorylated neurofilaments in neuronal plasticity involving axonal sprouting. Alternatively, it may also suggest that injury-induced neurofilament modifications are either conducive or permissive for axonal sprouting.
Shetty
A K
AK
Department of Surgery (Neurosurgery), Duke University Medical Center, Durham, North Carolina 27710, USA.
Turner
D A
DA
D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D064026:Calbindins; D018891:Dentate Gyrus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D018690:Excitatory Amino Acid Agonists / Q000008:administration & dosage / Q000494:pharmacology*; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D007150:Immunohistochemistry; D007276:Injections, Intraventricular; D007608:Kainic Acid / Q000008:administration & dosage / Q000494:pharmacology*; D008297:Male; D009412:Nerve Fibers / Q000187:drug effects / Q000378:metabolism; D016900:Neurofilament Proteins / Q000096:biosynthesis*; D009473:Neuronal Plasticity / Q000187:drug effects; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D017966:Pyramidal Cells / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D011916:Rats, Inbred F344; D064030:S100 Calcium Binding Protein G / Q000096:biosynthesis*
D064026:Calbindins; D018690:Excitatory Amino Acid Agonists; D016900:Neurofilament Proteins; D064030:S100 Calcium Binding Protein G; D007608:Kainic Acid