Effects of cocaine on melanophore responses to catecholamines and KCl in the isolated caudal fin of the marine goby, Tridentiger trigonocephalus

Abstract

AbstractEffects of cocaine on melanophore responses to catecholamines and KCl were investigated in the isolated caudal fin of fish to obtain evidence for the neuronal uptake of the catecholamines and the released adrenergic transmitter in the melanophore nerve. In the presence of 10−4M cocaine, pigment aggregation responses of normal melanophores to l‐noradrenaline (NA) and l‐adrenaline (A) were augmented, while aggregation responses to dopamine (D) and isoprenaline (Iso) were partly suppressed. Immediately after the cocaine (10−4M) treatment, the sensitivity of the normal melanophores to NA or A was greatly enhanced and aggregation responses to these catecholamines were greatly augmented. This is probably due to the blocking effect of cocaine on the neuronal uptake of the catecholamines. Such supersensitivity to the catecholamines of the normal melanophores was approximate to that of denervated melanophores. Probably, the supersensitivity of the denervated melanophores to NA and A mainly results from impairment of the neuronal uptake of the catecholamines. The sensitivity of melanophores to D or Iso was somewhat enhanced after denervation. After pretreatment with 10−4M cocaine, the pigment aggregating response to KCl was augmented. In the presence of 10−4M cocaine, pigment dispersion in the physiological solution was slowed down when the pigment had been made to aggregate by KCl or administered NA. It is highly probable that the exogenous NA, A, or the released adrenergic transmitter is taken up by the melanophore nerve endings. D and Iso are also probably taken up but only to a very limited extent.