Maturational effects of single and multiple early-life seizures on AMPA receptors in prepubescent hippocampus.

The effects of single versus multiple episodes of status epilepticus on the expression of AMPA receptors during a critical growth spurt are unknown. To determine whether the pattern of hippocampal AMPA receptor subunit expression depends upon the age of the animal, timing and number of perinatal seizures, we characterized maturational changes in AMPA receptor protein levels of the hippocampus with immunohistochemistry and Western blotting in rats of juvenile ages with and without a history of neonatal seizures. Kainic acid (KA) was used to induce a single episode of status epilepticus (1 x KA) in rats on P20 or P30. Animals with a history of multiple seizures (3 x KA) were given KA on P6, P9, and then on P20 or P30. After 1 x KA, in P20 and P30 rats that are preferentially sensitive to CA1 damage, GluR1 immunoreactivity was depleted remarkably in CA1 stratum pyramidale and stratum lucidum and only morphologically healthy cells were faintly labeled. At P30, GluR2 subunit expression was nearly absent in the healthy cells and increased within the injured CA1 neuronal population. Western blot analysis confirmed that the GluR1/GluR2 ratio was decreased at P20 and further decreased at P30. A history of perinatal seizures (3 x KA) prevented the age-dependent alterations in the CA1. Except for areas of cell loss, NR1 and NR2A/B antibody labeling was relatively stable throughout the hippocampus at both ages and conditions examined. Data suggest that (i) Ca2+ permeable AMPA receptors may not be responsible for neuronal injury or irreversible cell loss and that (ii) the expression of AMPA receptors after status epilepticus depends upon the age of the animal, the timing of the first insult and subsequent formation of AMPA receptor subunit compositions within specific populations of hippocampal neurons.

Onset of oscillopsia after visual maturation in patients with congenital nystagmus.

PURPOSE: To describe the clinical and oculographic characteristics of a cohort of five patients with congenital nystagmus (CN) and late-onset oscillopsia caused by a coincidental decline in other visual and/or ocular motor functions. DESIGN: Retrospective, observational, case series. PARTICIPANTS: Five visually mature patients with CN and recent-onset oscillopsia were evaluated clinically and with motility recordings. INTERVENTION: Eye movement analysis was performed off-line by computer analysis of digitized data. Nystagmus was analyzed for null-zone characteristics, waveforms, frequency, amplitudes, and slow-phase drift velocity during foveation. Surgical and medical treatment of associated ocular conditions in four of five patients. MAIN OUTCOME MEASURES: Presence of symptomatic oscillopsia and average time during foveation periods of slow-phase drift velocity less than 10 degrees /second. RESULTS: One of the five patients had associated rod-cone dystrophy, and another had recurrence of childhood head posturing with return of an eccentric null zone. The remaining three patients had decompensated strabismus associated with their oscillopsia. All five patients complained of oscillopsia in primary position that was relieved in the four who received treatment. Treatment included prismatic correction in one patient and surgery in three. Recordings in primary position after treatment showed increased duration during foveation periods of slow-phase drift velocity less than 10 degrees /second and an overall decreased intensity (amplitude/frequency) of the nystagmus. CONCLUSIONS: Symptomatic oscillopsia in patients with CN is unusual. This visually disturbing symptom can be precipitated by new or changing associated visual sensory conditions (e.g., decompensating strabismus, retinal degeneration). If the associated conditions can be treated, then accompanying oscillopsia may be relieved.