Inorganic As speciation and bioavailability in estuarine sediments of Todos os Santos Bay, BA, Brazil.

The spatial distribution of As (total As, As (III) and As (V)) in estuarine sediments from the main tributaries of Todos os Santos Bay, BA, Brazil, was evaluated under high and low flow conditions. The concentrations of As were determined using a slurry sampling procedure with hydride generation atomic absorption spectrometry (HG-AAS). The highest concentrations were observed at estuary mouths, and exceeded conservative lower threshold value (Threshold Effects Level; TEL). Due to the oxic conditions and abundance of Mn and Fe (oxyhydr)oxides in the sediments, most inorganic arsenic in the Subaé and Paraguaçu estuaries was present as As (V). Nevertheless, the concentration of As (III) at several locations along the Jaguaripe River were also above the TEL value, suggesting that As may be toxic to biota. In the Subaé estuary, antropogenic activities are the main source of As. At the Jaguaripe and at Paraguaçu estuaries, nevertheless, natural sources of As need to be considered to explain the distribution patterns.

A mechanism for savings in the cerebellum.

The phenomenon of savings (the ability to relearn faster than the first time) is a familiar property of many learning systems. The utility of savings makes its underlying mechanisms of special interest. We used a combination of computer simulations and reversible lesions to investigate mechanisms of savings that operate in the cerebellum during eyelid conditioning, a well characterized form of motor learning. The results suggest that a site of plasticity outside the cerebellar cortex (possibly in the cerebellar nucleus) can be protected from the full consequences of extinction and that the residual plasticity that remains can later contribute to the savings seen during relearning.

Timing mechanisms in the cerebellum: testing predictions of a large-scale computer simulation.

We used large-scale computer simulations of eyelid conditioning to investigate how the cerebellum generates and makes use of temporal information. In the simulations the adaptive timing displayed by conditioned responses is mediated by two factors: (1) different sets of granule cells are active at different times during the conditioned stimulus (CS), and (2) responding is not only amplified at reinforced times but also suppressed at unreinforced times during the CS. These factors predict an unusual pattern of responding after partial removal of the cerebellar cortex that was confirmed using small, electrolytic lesions of cerebellar cortex. These results are consistent with timing mechanisms in the cerebellum that are similar to Pavlov's "inhibition of delay" hypothesis.

Cerebellar cortex lesions prevent acquisition of conditioned eyelid responses.

We have used aspiration and electrolytic lesions to investigate the contributions of cerebellar cortex to the acquisition and expression of conditioned eyelid responses. We show that lesions of the anterior lobe of rabbit cerebellar cortex disrupt the timing of previously learned conditioned eyelid responses. These short-latency responses were used as an indication that the cerebellar cortex was sufficiently damaged and that the underlying pathways necessary for the expression of responses were sufficiently intact to support responses. Rabbits were subsequently trained for 15 daily sessions using a new conditioned stimulus. Whereas rabbits in which lesions had no significant effect on response timing showed rapid acquisition of appropriately timed eyelid responses to the new conditioned stimulus, animals with lesions that disrupt timing showed no significant increases in either amplitude or probability of responses. Histological analysis suggests that damage to the anterior lobe of the cerebellar cortex is necessary and sufficient to abolish timing and prevent acquisition. These data indicate that the cerebellar cortex is necessary for the acquisition of conditioned eyelid responses and are consistent with the hypotheses that (1) eyelid conditioning results in plasticity in both the anterior lobe of the cerebellar cortex and in the anterior interpositus nucleus and (2) induction of plasticity in the interpositus requires intact input from the cerebellar cortex.

Pharmacological analysis of cerebellar contributions to the timing and expression of conditioned eyelid responses.

Contradictory results have been reported regarding the effects of cerebellar cortex lesions on the expression of conditioned eyelid responses--either no effect, partial to complete abolition of responses, or disruption of response timing. This uncertainty is increased by debates regarding the region(s) of cerebellar cortex that are involved, by the likelihood that cortex lesions can inadvertently include damage to the interpositus nucleus or other pathways necessary for response expression, and by potential confounds from the degeneration of climbing fibers produced by cerebellar cortex lesions. We have addressed these issues by reversibly blocking cerebellar cortex output via infusion of the GABA antagonist picrotoxin into the interpositus nucleus. After picrotoxin infusion, conditioned responses are spared but their timing is disrupted and their amplitude diminished. In the same animals, conditioned responses were abolished by infusion of the GABA agonist muscimol and were unaffected by infusion of saline vehicle. These results are consistent with the hypothesis that (i) plasticity in the interpositus nucleus contributes to the expression of conditioned responses, as suggested by the responses seen with the cortex disconnected, and (ii) plasticity in the cerebellar cortex also contributes to conditioned response expression, as suggested by disruption of response timing.

Information storage in the nervous system of Aplysia: specific proteins affected by serotonin and cAMP.

To identify proteins that may be involved in the induction of long-term changes in the nervous system, we investigated whether specific proteins in pleural sensory neurons of Aplysia were affected by procedures that mimic those used to produce long-term sensitization. Using two-dimensional PAGE, we found that exposure to serotonin (5-hydroxytryptamine, 5-HT) for 2 or 3 hr appeared to increase incorporation of labeled amino acids into one protein (P9) and decrease incorporation into two other proteins (P19 and P20). These effects of 5-HT were observed whether the labeled amino acid was leucine or methionine. The same proteins that were affected by 5-HT were also altered by the adenylate cyclase activator forskolin and by the 8-bromo and 8-benzylthio analogs of cAMP. Addition of Co2+ to 5-HT did not seem to affect the action of 5-HT on P9 and P20, but it did seem to block the effect of 5-HT on P19. However, the effect of analogs of cAMP on P9, P19, and P20 was not altered by inclusion of Co2+. A phorbol ester that activates protein kinase C did not appear to affect the proteins that were modified by 5-HT, but phorbol ester did appear to increase the amount of labeled amino acids incorporated into another protein (P24). To investigate the specificity of these effects for pleural ganglion neurons, we examined the effect of 3- and 6-hr treatments of 5-HT on proteins in the abdominal ganglion. 5-HT affected at least nine proteins in the abdominal ganglion. One of these proteins (P9) appeared to be the same as one altered by 5-HT in the pleural sensory neurons. However, the occurrence of some proteins and some effects of 5-HT were specific for one ganglion or the other. The identified proteins that were affected by both 5-HT and changes in cAMP may be involved in the induction of long-term changes in the nervous system of Aplysia.