Strategies used to combine seriated cups by chimpanzees (Pan troglodytes), bonobos (Pan paniscus), and capuchins (Cebus apella).

The authors investigated strategies used to combine seriated cups by apes (Pan troglodytes and P. paniscus) and monkeys (Cebus apella) using a protocol reported in P. M. Greenfield, K. Nelson, and E. Saltzman's (1972) study with children. It was hypothesized that apes would exhibit more hierarchical combinations of cups than monkeys, given apes' language capacity, and that apes would seriate the cups more efficiently than monkeys. As predicted, apes made many structures with the cups using a variety of strategies, and monkeys rarely combined the cups. After a training phase to orient monkeys to the task, the 2 genera did not differ in the strategies used to combine the cups or in efficiency in seriating the cups. Success in this task suggests that sensorimotor versions of hierarchically organized combinatorial activity are well within apes' and monkeys' abilities.

N-terminal degradation of low molecular weight opioid peptides in human cerebrospinal fluid.

Opioid peptides are present in human cerebrospinal fluid (CSF), and their levels are reported to change in some pathologic conditions. However, less is known about their degradation in CSF. In the present study, human CSF was found to contain aminopeptidase activity which hydrolyzed alanyl-, leucyl- and arginyl-naphthylamides in a ratio of 100:28:27. Twelve CSF samples hydrolyzed alanyl-2-naphthylamide and degraded Met5-enkephalin (N-terminal hydrolysis) at rates of 188 +/- 38 and 420 +/- 79 pmol/min/mL respectively. Further, the distribution of alanyl-naphthylamidase activity in individual samples (39-437 pmol/min/mL) was closely correlated with that of Met5-enkephalin degradation (37-833 pmol/min/mL). Both alanyl-naphthylamidase and enkephalin degradation were optimal at pH 7.0 to 7.5 and were inhibited by aminopeptidase inhibitors amastatin (IC50 = 20 nM), bestatin (4-7 microM) and puromycin (30-35 microM). Conversely, degradation was unaffected by inhibitors of neutral endopeptidase (phosphoramidon), carboxypeptidase N (MERGETPA) or angiotensin converting enzyme (captopril). The Km of Met5-enkephalin for the CSF aminopeptidase activity was 201 +/- 19 microM (N = 4). Rates of hydrolysis of the Tyr1-Gly2 bond of larger opioid peptides decreased with increasing peptide length. Pooled, concentrated CSF hydrolyzed Leu5-enkephalin, dynorphin A fragments [1-7], [1-10] and [1-13] and dynorphin A at rates of 2.05 +/- 0.27, 1.27 +/- 0.18, 0.94 +/- 0.06, 0.55 +/- 0.14 and 0.16 +/- 0.03 nmol/min/mL respectively. When analyzed by rocket-immunoelectrophoresis against antisera to aminopeptidase M (EC 3.4.11.2), the concentrated CSF formed an immunoprecipitate which could be stained histochemically for alanyl-naphthylamidase activity. These data are consistent with a significant role for aminopeptidase M activity in the degradation of low molecular weight opioid peptides in human CSF.

Epinephrine induced myocardial necrosis: effects of aminophylline and adrenergic blockade.

The pathogenesis of myocardial necrosis produced in the albino rat by a single large dose of the potent alpha and beta adrenergic agonist epinephrine was investigated. In confirmation and extension of earlier observations with the alpha adrenergic antagonist tolazoline, it was found that alpha adrenergic blockade with phenoxybenzamine or beta adrenergic blockade with propranolol only partially attenuated the cardiotoxic effect of epinephrine while complete prevention of myocardial injury was achieved with the combined use of the two antagonists. In the presence of alpha adrenergic blockade alone, phosphodiesterase inhibition (aminophylline) caused a dramatic increase of epinephrine cardiotoxicity, demonstrating the importance of unopposed beta adrenergic activation. These results are consistent with the assumption that, in the rat, a cardiotoxic dose of epinephrine produces powerful alpha adrenergic activation which overshadows the effects of the beta adrenergic component of this catecholamine. It is concluded that in epinephrine induced myocardial necrosis, excessive alpha-adrenergic receptor activation in the cardiovascular system is clearly dominant in the initial phases. However, the contribution of the beta-adrenergic component of this catecholamine is of considerable importance for the eventual full development of the injury.