Mycosporine glycine protects biological systems against photodynamic damage by quenching singlet oxygen with a high efficiency.

This report concerns physiological function of mycosporine-like amino acids (MAA) as an active defense against the photooxidative effects of sunlight in marine organisms. Mycosporine glycine (MG) is a representative member of MAA family and was found to effectively suppress various detrimental effects of the Type-II photosensitization in biological systems, such as inactivation of mitochondrial electron transport, lipid peroxidation of microsomes, hemolysis of erythrocytes and growth inhibition of Escherichia coli. The presence of MG in solutions of eosin Y or methylene blue resulted in a marked decrease in the level of singlet oxygen (1O2) produced by the sensitizers under illumination. The rate constant of 1O2 quenching by MG was determined to be 5.6 x 10(7) M(-1) s(-1) by the time-resolved 1O2 luminescence decay method, which is higher than, or at least comparable to, the values for 1O2 reaction of well-known quenchers such as 1,4-diazabicyclo[2,2,2]octane and furfuryl alcohol. The results suggest that MG probably together with some other active MAA may play an important role in protecting marine organisms against sunlight damage by eliminating 1O2 generated from certain endogenous photosensitizers.

Ionizing radiation-induced alterations in the electrophysiological properties of Aplysia sensory neurons.

It is clear that ionizing radiation can alter neuronal function. Recently it has been suggested that radiation can directly influence neurons and/or the neuronal microenvironment. We have developed a simple in vitro model system utilizing the marine mollusc Aplysia californica to test this hypothesis. We show that ionizing radiation at doses of 5, 10 or 15 Gy produces complex effects on the electrophysiological properties of a population of Aplysia nociceptive sensory neurons at 24 and 48 h post irradiation. These results add support to the notion that ionizing radiation can directly influence neurons and/or the neuronal microenvironment. Furthermore, they demonstrate that Aplysia may be used as a useful model system to study radiation-induced neuronal plasticity.

Operant conditioning of head waving in Aplysia.

Head waving is a naturally occurring behavior that Aplysia use to explore their environment. Aplysia can be operantly trained to modify their head-waving response, increasing the amount of head waving on one side of their body in order to terminate the presentation of an aversive strong light. Acquisition of the operant response is rapid, within 10 min. Two observations indicate that the operant conditioning is under the control of the contingencies of reinforcement: (i) contingent reinforcement significantly elevates operant responding, reversing the contingencies significantly reduces operant performance, and reinstating the contingencies significantly reinstates operant responding; and (ii) yoked controls do not acquire the operant response, yet these same animals readily learn when reinforcement is made contingent upon their responses. Finally, internally derived cues (e.g., proprioceptive or reafferent) appear to play a predominant role in acquiring the operant response. Since progress has been made in understanding the cellular basis of classical conditioning in Aplysia, this demonstration of operant conditioning in a response system that is well-suited for a cellular analysis provides a preparation in which it is possible both to analyze the cellular mechanisms of operant conditioning and to address the theoretical question of the relationship between classical and operant conditioning on a mechanistic level.

The differential effects of ionizing radiation on the circadian oscillator and other functions in the eye of Aplysia.

Ionizing radiation has been used to selectively separate the circadian oscillator function of the eye of Aplysia from some of its other functions--synchronous compound action potential (CAP) generation, the light response, synaptic transmission between photoreceptors and output neurons, and the bursting pacemaker mechanism. Doses of 4-krad (50 kV peak) x-rays have a minimal effect on the circadian rhythm of CAP frequency, measured from the otpic nerve, whereas irradiation with a 40-krad dose abolishes the rhythm without affecting any of the four other functions of this eye (1 rad = 0.01 J/kg = 0.01/Gy). We estimate a 50% survival of the oscillator function at doses of about 6 krad. The oscillators of irradiated eyes are not merely desynchronized when the rhythm is abolished, because in vitro light-dark entrainment does not restore free-running rhythmicity. The results, including those from selective irradiation of the anterior or posterior poles of the eye, suggest that there are a number of circadian oscillators in the eye--most of them in the posterior portion near the optic nerve. An approximate target size has been obtained from target theory approximately equal to 10(8) A3, which is somewhat larger than the target size for viral infectivity function, as one example. There are reservations about estimating target size in a complex organ such as the eye. However, this approximate target size and the fact that recovery or repair can occur in vivo suggest that the oscillator may involve nucleic acid molecules.