Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifty-day streptomycin (STP) treatment in guinea pigs causes specific vestibular hair cell (VHC) types I and II (HCI; HCII) degeneration, depletion of glutamate decarboxylase (GAD) and a gradual disappearance of postrotatory nystagmus response (PRNR), which is a sign of vestibular function alteration. In order to look for a possible spontaneous reversibility and its time course guinea pigs receiving 300 mg/kg STP daily were monitored for PRNR and vestibular GAD loss. Once PRNR was lost, STP was interrupted and the animal was allowed to recover; at the time that PRNR was completely reestablished, vestibular GAD was measured. PRNR was lost within 22-25 days of STP treatment. Vestibular GAD showed a loss that, with time of treatment, gave two slopes: a fast decrement (45% in 20 days) and a slow one (40% in the remaining 30). Stopping of the STP treatment after 22-25 days and animal recovery resulted in the return of both PRNR and GAD activity 22 days after STP stoppage. These results suggest two STP-susceptible GAD-containing VHC populations, one more sensitive than the other, possibly HCI followed by hair cell II (HCII). As hypothetic HCI loss and PRNR disappearance is simultaneous, the important role of the former for vestibular function could be inferred. Interruption of STP treatment after PRNR loss results in a long range restoration of both GAD activity and vestibular function, and thus recovery of HCI, the first evidence of its occurrence in a mammalian vestibule, could be suggested. The intimate mechanism of this recovery remains to be seen.
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PMID:Recovery of vestibular function in young guinea pigs after streptomycin treatment. Glutamate decarboxylase activity and nystagmus response assessment. 149 92