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I consider an autonomous agent to be a physical system able to act on its own behalf, such as a bacterium swimming up a glucose gradient. I tentatively define an autonomous agent to be a system capable of self-reproduction and at least capable of performing one thermodynamic work cycle. I give a hypothetical chemical example. I then explore the increasingly odd implications of this definition.
BACKGROUND: Evolutionary autonomous agents are robots or robot simulations whose controller is a dynamical neural network and whose evolution occurs autonomously under the guidance of a fitness function without the detailed or explicit direction of an external programmer. They are embodied agents with a simple neural network controller and as such they provide the optimal forum by which sensorimotor interactions in a specified environment can be studied without the computational assumptions inherent in standard neuroscience. METHODS: Evolutionary autonomous agents were evolved that were able to perform identical movements under two different contexts, one which represented an automatic movement and one which had a symbolic context. In an attempt to model the automatic-voluntary dissociation frequently seen in ideomotor apraxia, lesions were introduced into the neural network controllers resulting in a behavioral dissociation with loss of the ability to perform the movement which had a symbolic context and preservation of the simpler, automatic movement. RESULTS: Analysis of the changes in the hierarchical organization of the networks in the apractic EAAs demonstrated consistent changes in the network dynamics across all agents with loss of longer duration time scales in the network dynamics. CONCLUSION: The concepts of determinate motor programs and perceptual representations that are implicit in the present day understanding of ideomotor apraxia are assumptions inherent in the computational understanding of brain function. The strength of the present study using EAAs to model one aspect of ideomotor apraxia is the absence of these assumptions and a grounding of all sensorimotor interactions in an embodied, autonomous agent. The consistency of the hierarchical changes in the network dynamics across all apractic agents demonstrates that this technique is tenable and will be a valuable adjunct to a computational formalism in the understanding of the physical basis of neurological disorders.
We have established conditions under which cultured embryonic myocardial cells are highly sensitive to the autonomic agents norepinephrine and acetylcholine and have determined that the most important factors affecting this sensitivity involve the application protocol. Using cells 3-5 days in culture, isolated from ventricles of 13-day chick embryos, the ED50 for noerpinephrine was 800 pM and that for acetylcholine was 370 pM. These cells were more than 2 orders of magnitude more sensitive than 13-day embryonic hearts freshly isolated, but not dispersed. Intracellular recording of the membrane actions of norepinephrine and acetylcholine on these cultured cells showed changes in pacemaker slope similar to those seen in freshly isolated hearts. These data demonstrate that preparation of ventricular muscle as isolated cells in culture does not necessarily result in the loss of sensitivity to autonomic agents. On the contrary, the isolated cells show the highest sensitivity to norepinephrine and acetylcholine that has been reported for the myocardium.
The response of the urinary bladder body and base to autonomic agents was studied in streptozocin (STZ)-diabetic rats. The bladder body region from 6-wk diabetic rats showed no changes in response to acetylcholine, phenylephrine, or isoproterenol. In contrast, the bladder base region showed a 39% increase in contractile response to acetylcholine and a 37% increased response to phenylephrine. In tissues from 47-wk diabetic animals, the bladder body showed a 51% increased contractile response to acetylcholine and a 37% increased relaxation response to isoproterenol. The bladder base showed a 66% increased contraction to acetylcholine. Thus, in the bladder base, enhanced responses to acetylcholine are detected soon after induction of diabetes and continue to increase as the diabetic state progresses. Moreover, in the same bladder region, an increase in responsiveness to alpha-adrenergic stimuli occurs. In the bladder body, enhanced responses to cholinergic and to beta-adrenergic stimuli occur, but are only observed in a more chronic diabetic state. The data suggest that an effect associated with autonomic diabetic neuropathy of the urinary bladder is an increased postsynaptic responsiveness to cholinergic stimuli in both regions.
Mesoscopic level neurodynamics study the collective dynamical behavior of neural populations. Such models are becoming increasingly important in understanding large-scale brain processes. Brains exhibit aperiodic oscillations with a much more rich dynamical behavior than fixed-point and limit-cycle approximation allow. Here we present a discretized model inspired by Freeman's K-set mesoscopic level population model. We show that this version is capable of replicating the important principles of aperiodic/chaotic neurodynamics while being fast enough for use in real-time autonomous agent applications. This simplification of the K model provides many advantages not only in terms of efficiency but in simplicity and its ability to be analyzed in terms of its dynamical properties. We study the discrete version using a multilayer, highly recurrent model of the neural architecture of perceptual brain areas. We use this architecture to develop example action selection mechanisms in an autonomous agent.
The effects of some autonomic agents including adrenaline, noradrenaline, dopamine, 5-hydroxytryptamine (5-HT), histamine, acetylcholine and adenyl nucleotides and nucleosides were examined on atria and ventricles of the trout (Salmo gairdneri). In atria, adrenaline, noradrenaline and dopamine produced positive chronotropic and negative or positive inotropic effects. Acetylcholine and 5-HT produced negative inotropic effects; 5-HT also produced small positive chronotropic effects. Adenosine and ATP produced negative inotropic and positive chronotropic effects; these effects were not antagonized by 8-phenyltheophylline nor were they potentiated by dipyridamole. alpha, beta-Methylene ATP, which is resistant to degradation, was inactive. These results suggest that, unlike all other vertebrate hearts studied, ATP and adenosine do not act via P1- or P2-purinoceptors. In the ventricle, adrenaline and noradrenaline produced positive inotropic effects. Acetylcholine and adenyl compounds had no direct action on contractility.
Experiments were conducted in the freshwater turtle, Pseudemys scripta, to study the effect of autonomic agents on the control of renin in this primitive species. The unique finding in these studies was that, unlike mammals, isoproterenol infusion fails to increase renin activity even though heart rate and arterial pressure patterns indicated that systemic responses were similar to that in mammals. On the other hand, acetylcholine (ACh) infusion resulted in a prompt threefold elevation (P less than 0.01) of renin activity. This response was blocked by propranolol but not atropine. Other experiments demonstrated that ACh elicited a prompt elevation of circulating norepinephrine and epinephrine in these turtles and led to the hypothesis that the renin response to ACh was secondary to the release of endogenous catecholamines. This hypothesis was supported by the fact that, in reserpinized turtles, ACh failed to elicit the usual renin response. Further evidence stemmed from the fact that epinephrine administration led to a prompt fourfold increase (P less than 0.01) in renin, which could be blocked by propranolol. On the other hand, phenoxybenzamine failed to block the response under identical conditions. Taken as a whole, these data suggest that in this primitive species renin activity is elevated by endogenous catecholamines even though isoproterenol, a classical beta-adrenergic agonist, is without effect. These data illustrate again the need for caution when assuming analogy when comparing responses in primitive species with that of mammals.
Active ion transport by the airway epithelium plays an important role in maintaining the effective defense mechanisms of the airway by regulating the volume and composition of the airway fluid. We investigated the abilities of adrenergic agents, cholinergic agents, and chemical mediators to modulate ion transport in canine tracheal epithelium, using Ussing-type chambers. Transepithelial electric potential difference (PD), resistance (R), and short circuit current (SCC) of the tracheal epithelium were measured before and during exposure to a drug or after a change in the perfusate composition. The mean values and S.E. (N = 41) of PD, R, and SCC during the control period were -18 +/- 4 mV (luminal negative to submucosa), 240 +/- 42 omega.cm2, and 50 +/- 5 microA/cm2, respectively. Ouabain (10(-4) M), an inhibitor of Na+-K+-ATPase, in the mucosal bath abolished PD and SCC. Replacement of luminal Na by choline reversibly reduced PD and SCC. These findings suggest that PD and SCC of the tracheal epithelium are maintained by the transcellular transport of luminal Na toward the mucosa. Isoproterenol (10(-5) M), epinephrine (10(-4) M), and norepinephrine (10(-4) M) markedly increased both PD and SCC. Acetylcholine (10(-4) M) and histamine (10(-4) M) did not alter SCC significantly. Prostaglandin E1 (10(-6) M) and F2 alpha (10(-5) M) slightly increased PD and SCC. These results indicate that adrenergic and cholinergic agents induce different patterns of effect on ion transport (adrenergic-dominant) in the tracheal epithelium. Thus, the effects of autonomic agents and chemical mediators on ion transport may explain, in part, the pathogenesis of airway disorders observed in many respiratory diseases.
In this article, I discuss the use of neurally driven evolutionary autonomous agents (EAAs) in neuroscientific investigations. Two fundamental questions are addressed. Can EAA studies shed new light on the structure and function of biological nervous systems? And can these studies lead to the development of new tools for neuroscientific analysis? The value and significant potential of EAA modelling in both respects is demonstrated and discussed. Although the study of EAAs for neuroscience research still faces difficult conceptual and technical challenges, it is a promising and timely endeavour.
The characteristics of the glycoproteins contained in the secretory segments of the three major salivary glands of adult male rats and the secretion of these various glycoproteins in response to autonomic agents were examined by micro-disc electrophoresis. Characterization of the glycoproteins showed that the acinar segments from the three major salivary glands and the segments of the convoluted granular tubules from the submandibular gland each contain characteristic species of glycoproteins. The glycoproteins characteristic of the acinus of the submandibular gland were secreted into saliva in response to carbachol or dobutamine, those characteristic of the parotid gland by carbachol, methoxamine, or dobutamine, and those of the sublingual gland by carbachol, whereas glycoproteins characteristic of the convoluted granular tubules of the submandibular gland were only elicited by methoxamine. The secretory response of carbachol, methoxamine and dobutamine, respectively, were almost completely reduced by pretreatment with atropine, prazosin and metoprolol. The relative proportions of glycoproteins secreted into the oral cavity from secretory cells of the three major glands varied significantly with the nature of the stimulant.
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The purpose of this investigation was to examine the effects of autonomic neurohormones, cyclic nucleotides, and related agents on the immunologic discharge of lysosomal enzymes from, and phagocytosis by, purified human neutrophils. In order to discern the possible intracellular mechanisms by which certain neurohormones influence neutrophil function, the concentrations of cyclic AMP and cyclic GMP in neutrophils were assessed during cell contact with phagocytizable particles and autonomic agents. The model system employed for study was the interaction of purified human neutrophils with rheumatoid arthritic (RA) serum-treated zymosan particles at 37 degrees C in a neutral, balanced salt solution containing glucose. Neutrophils ingested the particles and discharged beta-glucuronidase but not lactate dehydrogenase activity during 30 min of incubation. Treatment of zymosan particles with RA serum was more effective than treatment with normal serum with regard to the extent of both particle uptake and lysosomal enzyme release. During contact of neutrophils with RA serum-treated zymosan particles epinephrine, isoproterenol, and cyclic AMP inhibited both particle ingestion and beta-glucuronidase discharge. These actions of epinephrine were associated with a concomitant elevation of cyclic AMP levels. In contrast to the actions of catecholamines and cyclic AMP, acetylcholine and cyclic GMP accelerated lysosomal enzyme release without affecting particle uptake. The actions of acetylcholine were associated with a concomitant elevation of cyclic GMP levels. Increases in neutrophil levels of cyclic GMP but not of cyclic AMP were associated also with the discharge of beta-glucuronidase provoked by particles in the absence of added cholinergic agents. The data suggest that the immunologic release of lysosomal enzymes from human neutrophils can be regulated by autonomic neurohormones, perhaps via the selective formation of appropriate nucleotides.
Experiments were done to determine if age-related changes occur in autonomic regulation of rat urinary bladder. The maximum contractile responses to acetylcholine were 63% and 15% greater in isolated bladders from 29-month and 17-month animals, respectively, as compared to 7-month animals. The amounts of [3H]quinuclidinyl benzilate bound to membrane preparations were 46% and 7% greater. In contrast, no age-related changes were observed in phenylephrine-induced contraction or in isoproterenol-induced relaxation of bladder. Thus, the urinary bladder of aged rats appears to develop increased sensitivity to cholinergic stimuli because of an increase in the number of muscarinic cholinergic receptors.
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The parasympathetic and sympathetic divisions of the autonomic nervous system are involved in homeostatic control of a wide variety of ocular functions, including accommodation, pupillomotor control, lacrimation, eyelid position, and aqueous humor production. Familiarity with the functional anatomy of the autonomic nervous system is paramount to the understanding and application of the large number of autonomic drugs used in veterinary ophthalmology. The cholinergic and adrenergic agents discussed in this article are commonly employed to facilitate routine ophthalmic examination, in the diagnosis of autonomic dysfunction, and in the treatment of a variety of ocular diseases.
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