Central nervous system and computation

Computational systems are useful in neuroscience in many ways. For instance, they may be used to construct maps of brain structure and activation, or to describe brain processes mathematically. Furthermore, they inspired a powerful theory of brain function, in which the brain is viewed as a system characterized by intrinsic computational activities or as a "computational information processor. "Although many neuroscientists believe that neural systems really perform computations, some are more cautious about computationalism or reject it. Thus, does the brain really compute? Answering this question requires getting clear on a definition of computation that is able to draw a line between physical systems that compute and systems that do not, so that we can discern on which side of the line the brain (or parts of it) could fall. In order to shed some light on the role of computational processes in brain function, available neurobiological data will be summarized from the standpoint of a recently proposed taxonomy of notions of computation, with the aim of identifying which brain processes can be considered computational. The emerging picture shows the brain as a very peculiar system, in which genuine computational features act in concert with noncomputational dynamical processes, leading to continuous self-organization and remodeling under the action of external stimuli from the environment and from the rest of the organism.     

Central nervous system drug design

A model which suggests that there is a common structural basis for the action of many different classes of CNS drugs is described. It is shown that this general model is consistent with specific models for opioid analgesic and antidepressant activity. The significance of these models is not only that they define specific spatial relationships between the structural requirements in different CNS drug classes, but also that they allow the formulation of three very simple drug design techniques which will be referred to as pruning, splicing and grafting. When combined with available structure-activity information, these techniques may provide a rational approach to the design of drugs with specified CNS activity.     

Central nervous system and mechanisms of hypertension

There are several mechanisms by which the central nervous system participates in the neural and humoral alterations associated with various forms of experimental hypertension. Structures in forebrain with multiple integrative roles in neuroendocrine control of the circulation are involved. Tissue surrounding the anteroventral region of the third cerebral ventricle (AV3V region) is involved physiologically in thirst, sodium homeostasis, osmoreception, secretion of vasopressin and natriuretic factor and sympathetic discharge to blood vessels. Destruction of this tissue prevents or reverses many forms of hypertension. In genetically based spontaneous hypertension, limbic structures such as the central nucleus of the amygdala rather than the AV3V region are the necessary neuroanatomic substrate. Recent evidence suggests that a circumventricular organ in brain stem, the area postrema, is also involved in the mediation of several forms of experimental hypertension. In renin- and nonrenin-dependent forms of renal hypertension, two major factors activate central mechanisms. First, direct central actions of angiotensin, acting through receptors in the subfornical organ and organum vasculosum of the lamina terminalis, increase sympathetic discharge and secretion of vasopressin through mechanisms integrated at the level of the AV3V region. Second, sensory systems originating in the kidney can activate increased sympathetic discharge through complex projection pathways involving forebrain systems. Mineralocorticoid hypertension appears to involve enhanced secretion of vasopressin and central vasopressinergic mechanisms also dependent on the AV3V region. Reciprocal connections between key central areas involved in control of arterial pressure provide the neuroanatomical basis for central nervous system participation in hypertension.     

Central nervous system regulation of adipocyte metabolism

The white adipose tissue was initially largely known only as an energy storage tissue. It is now well recognized that white adipose tissue is a major endocrine and secretory organ, which releases a wide range of protein signals and factors termed adipokines. The regulation of adipocyte metabolism is an important factor for the understanding of obesity, and some mechanisms are still unknown. Many homeostatic processes, including appetite and food intake, are controlled by neuroendocrine circuits involving the central nervous system. There is substantial evidence demonstrating that the central nervous system also directly regulates adipocyte metabolism. In this review, we discuss the central actions of some peptides with an important role in energy balance regulation on adipocyte metabolism and the physiological relevance of these actions.     

Clinical complications of Mycoplasma pneumoniae disease--central nervous system

The mechanism of the neurologic complications associated with primary atypical pneumonia is unknown. To examine the ability of Mycoplasma pneumoniae to enter the brain of experimental animals, the organism was inoculated into adult and suckling mice by various routes. After intranasal infection, M. pneumoniae was isolated from brains and lungs of both groups of mice. After intracerebral inoculation, the high levels of the mycoplasma persisted for two months or more in the brains of suckling mice. In addition, after intravenous infection, the systemic spread of infection occurred in the mice treated with high doses of cyclophosphamide. Our results suggest that M. pneumoniae may be able to reach the brain via blood and it may occur with relative ease in compromised hosts.     

Central nervous system mechanisms for pain modulation

Although a great deal has been learned about the neural basis for stimulation-produced analgesia, it is evident that the 'analgesia systems' are much more complex than was initially thought. Part of the complexity derives from the fact that a number of different pathways, using several different neurotransmitters, can affect nociceptive transmission. Further complexity stems from evidence that nociceptive transmission can be modulated both at a spinal cord level and at higher levels of the nociceptive projection system, such as the thalamus. Hopefully, a greater understanding of the 'analgesia systems' will lead to explanations for a number of puzzling aspects of pain and perhaps to improved therapy.     

Central nervous system injury-induced immune deficiency syndrome

Infections are a leading cause of morbidity and mortality in patients with acute CNS injury. It has recently become clear that CNS injury significantly increases susceptibility to infection by brain-specific mechanisms: CNS injury induces a disturbance of the normally well balanced interplay between the immune system and the CNS. As a result, CNS injury leads to secondary immunodeficiency - CNS injury-induced immunodepression (CIDS) - and infection. CIDS might serve as a model for the study of the mechanisms and mediators of brain control over immunity. More importantly, understanding CIDS will allow us to work on developing effective therapeutic strategies, with which the outcome after CNS damage by a host of diseases could be improved by eliminating a major determinant of poor recovery.     

Central nervous system functions of PAK protein family

Several of the genes currently known to be associated, when mutated, with mental retardation, code for molecules directly involved in Rho guanosine triphosphatase (GTPase) signaling. These include PAK3, a member of the PAK protein kinase family, which are important effectors of small GTPases. In many systems, PAK kinases play crucial roles regulating complex mechanisms such as cell migration, differentiation, or survival. Their precise functions in the central nervous system remain, however, unclear. Although their activity does not seem to be required for normal brain development, several recent studies point to a possible involvement in more subtle mechanisms such as neurite outgrowth, spine morphogenesis or synapse formation, and plasticity. This article reviews this information in the light of the current knowledge available on the molecular characteristics of the different members of this family and discuss the mechanisms through which they might contribute to cognitive functions.     

Central nervous system mechanisms of arterial pressure regulation

This paper provides a review of recent developments in the field of neural and humoral control of the cardiovascular system mediated through the central nervous system. The areas covered include central mechanism of baroreceptor reflex control, sites of origin of tonic vasomotor activity, interactions between forebrain and brain stem, central actions of humoral factors, the role of visceral and somatic afferents, and the potential for central selectivity of vasomotor control.     

Central nervous system fatigue alters autonomic nerve activity

AimsFatigue is a common symptom in modern society. In order to clarify the mechanisms underlying fatigue, we examined the association between central nervous system fatigue and autonomic nerve activity.Main methodsThe study group consisted of 20 healthy subjects. They performed the 2-back test for 30 min to induce fatigue. Just before and after the fatigue-inducing session, they completed the advanced trail making test (ATMT) for 30 min as a fatigue-evaluating task session. In order to measure autonomic nerve activity, electrocardiograms were monitored continuously throughout the experiment.Key findingsAfter the fatigue-inducing task session, impaired task performance was demonstrated based on the total trial number and error counts of the ATMT. During the task session, although task performance as measured using the accuracy and the mean reaction time of the 2-back test was almost unchanged, electrocardiographic R-R wave interval analyses showed a decreased high-frequency component power and an increasing trend in the low-frequency component power/high-frequency component power ratio.SignificanceDecreased vagal nerve activity and increased sympathetic nerve activity are associated with central nervous system fatigue.     

Central nervous system function in systemic lupus erythematosus

Autoantibodies to three eukaryotic 60S ribosomal phosphoproteins P0, P1 and P2 have been found in the sera of 10–20% of patients with systemic lupus erythematosus (SLE). These antibodies inhibit protein synthesis in vitro and when microinjected into cultured human fibroblasts. The three proteins share a common epitope contained within the carboxyl terminal 22 amino acids of each protein. Because a significant number of SLE patients have central nervous system disturbances with major behavioral disorders, the antiribosomal protein autoantibodies were measured in this subset of SLE individuals to determine whether or not there was an association. These antibodies are present in 90% of SLE patients who were diagnosed as having psychosis, secondary to the disease.Special issue dedicated to Dr. Sidney underfriend     

Central nervous system neuropeptides after peripheral nerve deafferentation

Beta-endorphin, Met-enkephalin, substance P, somatostatin and dynorphin concentrations were evaluated in right and left brain areas, and in cervical, thoracic, and lumbosacral spinal cord of rats that underwent section of either the right, the left, both sciatic nerves, the right brachial plexus, the saphenous, or the sural nerve. With all the surgeries, beta-endorphin concentrations decreased significantly in all brain areas with the exception of the striatum where they did not change. By contrast Met-enkephalin increased in all brain areas and in the spinal cord tracts interested by the lesions. The other peptides were always unaffected. The changes in the concentrations of the neuropeptides were observed starting twenty-four hours after surgery and lasted for at least four months. We did not find a lateralization in the brain peptide concentrations of either sham operated or unilaterally deafferentated rats. Moreover, the treatment with serotoninergic agents normalized the concentrations of beta-endorphin, suggesting a role of the serotoninergic system in the decrease of the peptide that follows the lesion of peripheral nerves.     

Central nervous system mediation of pituitary adrenal rhythmicity.

Evidence favoring the view that there is a dissociation between the two aspects of pituitary adrenal operation, the stress and the rhythm modes, is as follows 1) it is possible to abolish rhythmic function by anterior hypothalamic lesions without altering the responses to stress; 2) during maturation of the rat CNS, the stress response appears prior to weaning while pituitary-adrenal rhythm appears after weaning; 3) appropriate neuropharmacologic treatment can block circadian rhythm without altering the stress response; 4) responsiveness to ether or immobilization may be independent of the diurnal rhythm; 5) the stress response to a very strong stimulus, such as immobilization, habituates while the circadian rhythm does not. On the other hand there is some evidence in favor of interdependence between the two modes of operation: 1) input channels for stress and rhythm may overlap since strong synchronizers of rhythm, such as food and water restriction and light can become stress stimuli; 2) steroid feedback can alter the timing of the circadian rhythm; 3) circadian variation has been observed in the responses to certain stimuli; 4) neurotransmitters which are prominently implicated in the circadian rhythm also appear involved in the stress response.