In this study, we evaluated the goldfish model
of hemilabyrinthectomy for investigating potential
recovery-promoting drugs. In this lesion model,
the unilateral removal of the labyrinth induces a
postural imbalance in response to light (Dorsal
Light Reflex), from which the animals can
recover over time. The behavioral effects of two
neuropeptides were tested–namely, of substance
P and ACTH4-10, both of which are known to
promote functional recovery in several other
lesion models. Furthermore, the effect of MK-
801, an antagonist of the glutamatergic NMDAreceptor
subtype, was tested because this
substance has also been shown to exert a
neuroprotective effect. After lesion of the right
labyrinth, the animals (n=12)
were treated intraperitoneally
daily either with vehicle (n=12),
substance P (n=11)
, ACTH4-10 (n=12)
, or MK-
801 (n=12)
. Another group (n=11)
, which served
as a non-lesion control, did not receive hemilabyrinthectomy
or systemic injections. The
lesion group, treated post-operatively with vehicle,
did not recover from the postural deviation over
the 24-d testing period. In contrast, all three test
substances accelerated the functional recovery
after unilateral labyrinthectomy. The decrease of
the dorsal light reflex persisted even after
cessation of drug treatment after 20d. The
results indicate that using the dorsal light reflex
in the model of hemilabyrinthectomy in goldfish
provides a useful approach to studying the
ability of potential new neurotrophic or neuroprotective
drugs to promote functional recovery.