Protective Effect of Heat Shock Proteins 70.1 and 70.3 on Retinal Photic Injury after Systemic Hyperthermia

PURPOSE: This study aimed to determine the relationship between the heat shock protein 70 from hsps70.1 and 70.3 on retinal photic injury after systemic hyperthermia. METHODS: Eight-week-old female C57BL/6 mice were kept at a constant temperature of 41~42 degrees C for 25~30 minutes. After dark-adaptation for 8 hours, intense light of 11000 lux was maintained for 6 hours. Histology and immunohistochemistry for the inducible heat shock protein 70 (hsp70), the constitutive heat shock protein 70 (hsc70), and western blot analysis, reverse transcriptase-polymerase chain reaction for hsp70.1 and hsp70.3 were performed just before photic injury and after 1, 4, 7, and 14 days. RESULTS: Light-induced retinal degeneration was prevented by thermotolerance. After hyperthermia, hsp70 was densely expressed in the inner segment of the photoreceptor layer on the photic injury. Hsp70 expression increased for 4 days after photic injury and slowly decreased thereafter. mRNA from hsp70.3 was induced earlier than that of hsp70.1. CONCLUSIONS: Retinal photic injury was prevented by hyperthermia-induced hsp70. Hsp70 from hsp70.3 may be a rapid and short-lived responder, and that from hsp70.1 is a slower and more sustained responder. Hsp70 from hsp70.3 may be an initial retinal chaperone while hsp70 from hsp70.1 may be a sustained chaperone.

Delay of Photoreceptor Cell Degeneration in rd Mice by Systemically Administered Phenyl-N-tert-butylnitrone

PURPOSE: To study the effect of systemic administration of phenyl-N-tert-butylnitrone (PBN) on the degeneration of photoreceptor cells in rd mice. METHODS: PBN was injected intraperitoneally into FVB/rd mice on postnatal days (P) 5 to 14 (group A), and P10 to 18 (group B). At days P14, 16, 18, 20 and 27, morphological changes and apoptosis were analyzed by staining with hematoxylin and eosin or DAPI. The effect of PBN on apoptosis was analyzed in retinal pigment epithelial (RPE) cells by the measurement of caspase-3 activity. RESULTS: In control and group B mice, the outer nuclear layer (ONL) of the retina was composed of 8-10 rows at P12, and rapidly decreased to one row at P18. In group A mice, the ONL was preserved with 5-7 rows at P18, and decreased to one row at P22. PBN inhibited caspase-3 activity in cultured RPE cells. CONCLUSIONS: PBN delayed, but did not block, the degeneration of photoreceptor cells in rd mice. PBN may exert its inhibitory effect during the early phase of photoreceptor cell degeneration.

Oculomotor Palsy from Neurocysticercosis Involving the Midbrain

Papilledema, pupillary abnormalities, and nystagmus are common neuro-ophthalmologic signs in neurocysticercosis (NCC). Oculomotor palsy rarely occurs and usually accompanies compression of the midbrain by supratentorial or subarachonoid lesions with or without inflammation and hydrocephalus. Oculomotor palsy from NCC involving the midbrain parenchyme has rarely been described. We report on a patient who presented with oculomotor palsy caused by mesencephalic NCC. The patient showed recurrences of symptoms in association with steroid tapering.

Ocular Contrapulsion in Medial Medullary Infarction

Ocular contrapulsion refers to a syndrome of static ocular deviation and saccadic hypermetria toward the intact side, and saccadic hypometria and impaired smooth pursuit toward the lesion side. It has been reported in patients with lesions in the rostral cerebellum and caudal medullary hemorrhge. We report a 60-year-old man who showed ocular contrapulsion with unilateral upper medial medullary infarction. Ocular contrapulsion may be a sign of medial medullary infarction. In our patient, the climbing fibers may be damaged before crossing the midline in the upper medulla.