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Dependency on the brain function of arginine vasopressin system of the development to and recovery from analgesic tolerance to morphine.

Concomitant intracerebroventricular (i.c.v.) injection of anti-arginine vasopressin (AVP) antiserum dose-dependently suppressed the development of analgesic tolerance to daily morphine, 10 mg/kg, s.c., in mice. This suppressive effect of the antiserum was reduced by incubating the antiserum with AVP in vitro, before i.c.v. injection, suggesting that the antiserum inactivates brain AVP to result in the suppression of the development of tolerance in vivo. Similar to the antiserum, both AVP V1 and V2 antagonists given i.c.v., 10 ng and 20 ng/mouse, respectively, suppressed the development of morphine tolerance. Meanwhile, the administration of antiserum dose-dependently recovered morphine analgesia in morphine-tolerant mice and a complete recovery of analgesia was observed at the highest dose of antiserum following the second injection, and the effect of antiserum was maintained for 3 days after its withdrawal. Likewise, 10-100 ng/mouse of AVP V1 receptor antagonist given i.c.v. recovered morphine analgesia partially but significantly in a dose-dependent manner; however, AVP V2 receptor antagonist at the same doses partially recovered analgesic effect but the effect was neither significant nor dose-dependent. These findings suggest that the tolerance developed to morphine can be reversible when disturbing the function of brain AVP, but in addition to the different mechanisms of antiserum, V1 and V2 receptor antagonists, the V1 receptor-mediated mechanism may be more closely concerned in this phenomenon.

Angiotensin Receptor Antagonists

Two biological rhythms of perception distinguishing between intact and relatively damaged brain function in man.

A simple test of perception, the Critical Flicker Fusion threshold (CFF) was given successively for 20 mins. to 69 healthy subjects aged 7-63 and to 53 comparable neuropsychiatric patients. The latter could be divided into a functionally sick group and a group with brain damage. Auto-correlation analysis revealed significant sine-wave cycles of amplitude and ultradian frequency for the CFF mean scores and the CFF "Scatter* scores. Both cycles of recurrence showed frequencies which distinguished significantly between the total healthy subjects and the patients. Further analysis showed no difference between controls and emotionally sick patients (i.e. those with sociopathy, schizophrenia and manic depressive psychosis) but there was a highly significant difference between these three groups and patients with relatively damaged C.N.S. (i.e. those with mental deficiency, organic brain syndrome and organic dementia). Even among the control group a progressive increase in frequency of these perceptual cycles occurred with advancing age. These CFF results point to the existence of a cycle of perceptual acuity and another of vigilance in the organism. Both appear to relate to the neural integrity of the C.N.S.

Adolescent

Changes in brain functional connectivity in Alzheimer-type and multi-infarct dementia.

Clinical and neuropathological evaluation of elderly subjects with dementia has traditionally concentrated upon the focal distribution of brain disease, ignoring changes in the complex connections that link brain areas and that are crucial for cognition. We examined subjects with the two most common forms of dementia in the elderly (dementia of the Alzheimer type or DAT, and multi-infarct dementia or MID); and used electroencephalographic (EEG) coherence to examine the effects of these illnesses on the functional connections between brain areas. We studied coherence between brain areas known to be linked by two different types of connections: (i) dense narrow bands of long corticocortical fibres; (ii) broad complex networks of corticocortical and corticosubcortical fibres. Areas that were linked by dense narrow bands of long corticocortical fibres showed greatly diminished coherence in subjects with DAT; among MID subjects, this coherence was not significantly affected. Areas that were linked by broad connective networks showed the largest decreases in coherence among MID subjects. These findings are consistent with neuropathological evidence that Alzheimer's disease is a neocortical 'disconnection syndrome' in which there is a loss of structural and functional integrity of long corticocortical tracts. The findings further suggest that the vascular disease of MID most prominently affects broad fibre networks that may be more vulnerable to diffuse subcortical vascular damage. A ratio of coherence from complex corticocortical-corticosubcortical networks divided by coherence from long corticocortical tracts correctly classified 76% of subjects into DAT and MID categories. Overall, these results indicate that EEG coherence detects basic pathophysiological differences between subjects with DAT and MID, and that these differences may be clinically useful.

Aged

[Features of using the second principle of thermodynamics for describing brain function].

It has been shown that negative production of information entropy at the expense of its normalization change under the influence of neuromediators is specific for the nervous systems and brain. Chemical synapses are calculation elements with a diffusion input to control information entropy normalization. Reproduction stability of the nervous system and brain, and their functioning as well, are determined due to Lyapunov criteria by the maximum of entropy production in combination with minimum for the entropy itself. As far as information in nervous systems is connected with an element of energy normalization that is much greater than the scales of molecular energy of single atoms, physical and information self-organization can simultaneously either correlate or be sufficiently independent, because entropy corresponds to statically unstable point, with its output being natural in different ways. In particular, the brain potentialities are the more, the further it is advanced in its evolution in the sense of entropy increase of its structure, i.e. evolution perfection of mind results from the elementary meaning of the second principle of thermodynamics but in combination of the biochemical peculiarity--the growth of brain is controlled by adrenogens and because of this correlates with productivity.

Brain

Brain function in epilepsy: midbrain, medullary, and cerebellar interaction with the rostral forebrain.

Against the background previous findings in epileptic patients, in whom electroencephalographic recordings were obtained from numerous deep and surface brain sites during seizures, rhesus monkeys with electrodes implanted into specific brain sites were used to demonstrate anatomical connections by evoked potential techniques and to serve as models of experimental epilepsy. In the animals, many monosynaptic connections were revealed between forebrain sites consistently involved in seizures in patients and more caudal brain sites subserving functions of sensory perception, eye movement, synaptic chemical transmission, and motor coordination. Further, the participation of these interrelated sites during seizures was demonstrated. The findings provide an anatomical-physiological explanation for many of the clinical phenomena observed in epileptic patients and a rationale for the use of cerebellar stimulation as a treatment.

Animals

[The effect of a high-intensity radiation exposure on the brain function of monkeys. The postradiation changes in the EEG response to rhythmic photostimulation].

In experiments with monkeys (Macaca fascicularis) it has been shown that whole-body irradiation with a dose of 45 Gy (6.5 Gy/s) causes considerable changes in the EEG response to rhythmic photostimulation (PS). These changes are: reduction of the desynchronizing effect of PS with regard to a background rhythmicity; decrease in the reception rate of the rhythms of light flashes (RLF); narrowing of the RLF frequency range; and increase in the reaction momentum. The postirradiation changes in the EEG response to PS are considered as a manifestation of inhibition of the cortex functional activity and impairment of sensory information processing in the brain.

Animals