[Simultaneous metastases to brain and scalp during the evolution of a hypernephroma].
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An excessive intracellular accumulation of calcium (Ca2+) in neurons and glia has been proposed to represent a major 'final common pathway' for cell death arising from hypoxia-ischemia. To clarify the role of altered calcium flux into the perinatal brain undergoing hypoxic-ischemic damage, 7-day postnatal rats underwent unilateral common carotid artery ligation followed by systemic hypoxia with 8% oxygen. This insult is known to produce brain damage in the form of selective neuronal death or infarction largely limited to the cerebral hemisphere ipsilateral to the arterial occlusion. Either prior to or following hypoxia-ischemia, the rat pups received a s.c. injection of 45CaCl2, and specimens of blood, cerebrospinal fluid (CSF), and brain were obtained for isotopic measurements and the calculation of the extent of brain intracellular radioactivity. During hypoxia-ischemia, there was a modest increase in intracellular Ca2+ radioactivity (+28-47%) in both cerebral hemispheres only after 2 h of hypoxia-ischemia. During recovery from 2 h of hypoxia-ischemia, intracellular Ca2+ accumulated progressively only in the ipsilateral cerebral hemisphere for up to 24 h, during which interval intracellular Ca2+ decreased in the contralateral hemisphere. No such progressive accumulation was noted during recovery in animals previously exposed to only 1 h of hypoxia-ischemia. The results suggest that a disruption of intracellular Ca2+ homeostasis is a major contributing factor in the evolution of perinatal hypoxic-ischemic brain damage. Ca2+ accumulation is a relatively modest and late event during the hypoxic-ischemic phase, and a progressive overload occurs during the recovery phase only if infarction occurs. The question remains as to whether or not the intracellular Ca2+ overload occurring during recovery is a contributor to or a consequence of the ultimate brain damage.
Evidence for right-left asymmetries in eye use at the individual level in the Siamese fighting fish, Betta splendens, is reported. When faced with their mirror image (in two daily trials of 10 min each), adult male Betta splendens showed consistency in their right or left eye use during threat lateral displays. Moreover, if one side was preferred by an individual to exhibit the lateral displays, then the duration of the displays on that side was longer than the duration of the displays on the other side. Similar findings were obtained when a sample of animals was tested for eye use during courtship displays in the presence of a female. Furthermore, consistency in eye use was observed in fish tested first with the mirror and then, 2 months later, with the female. Results are discussed with respect to the issue of the evolution of brain lateralization.
The dominant frequency of hippocampal rhythmic slow activity (RSA) is known to differ among species, even under similar experimental conditions. The cause of these species differences has not yet been identified. In this paper it is shown that RSA frequency is allometrically related to brain size for the 9 mammalian species for which data are available. It is further shown that the relationship between brain size and RSA frequency is similar to the relationship between brain size and specific brain metabolic rate. Based on these and other relationships, it is suggested that differences in the firing frequencies of the neuronal pacemakers underlying the generation of RSA reflect differences in specific brain metabolic rate, both within and among species.
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Prospective blood samplings from 15 patients admitted with a Glasgow Coma Score of less than 7 were obtained to observe and compare epinephrine, norepinephrine, and dopamine serum levels in patients with brain injury before, after, and in the absence of brain death. Nine of the patients developed or were admitted after brain death. Wide variations in catecholamine blood levels over time were documented, and subgroup analysis precluded useful statistical comparison or inference of the data. The data are presented therefore as descriptive observations only. No apparent differences were noted between similarly injured patients in whom brain death did not develop and patients before brain death or between patients with penetrating versus nonpenetrating brain injury. Brain death was preceded by hypertension and corresponding elevations in serum catecholamine levels in one patient with complete data. Catecholamine levels appeared to fall after brain death in most patients. Only minimal changes in myocardial histology were present in three donor hearts, and the two transplanted hearts functioned satisfactorily. Serum catecholamine measurement or monitoring does not provide a precise method of determining potential injury to the donor heart before or after brain death. Other experimental data and clinical observation indicate that some hearts may be injured in the donor during the evolution of brain death. Pharmacologic intervention may prevent such injury in experimental animals but must be used before brain death is induced. Such interventions should be studied in selected human donors before brain death to determine whether cardiac function is improved in the donor or recipient.
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1. Specific high affinity binding of 2-[125I]iodomelatonin was detected in the brain of the pouch young of a marsupial, Bennett's wallaby. 2. Binding was rapid, stable, saturable and reversible. 3. Scatchard analysis indicated a single class of high affinity binding sites with an equilibrium dissociation constant (Kd) of 68 +/- 13 pM, a maximal number of binding sites (Bmax) of 0.7 +/- 0.1 fmol/mg protein and a Hill coefficient (nH) of 1.12 +/- 0.10. 4. Specific binding was inhibited by GTP (1 mM) indicating that the melatonin receptor is coupled to a guanine nucleotide binding protein, and by melatonin and closely related analogues with a potency order identical to that reported previously in the brain of eutherian mammals, birds and a reptile. 5. These studies suggest that the melatonin receptor is well-conserved through evolution.
The present paper's aim is of to give an overview about the basic knowledge as well as actual topics of olfaction--with a special regard on behavior. We summarize different functions of the nose and the olfactory system in human physiology and psychology. We will first describe the functional anatomy of the olfactory system in man. Afterwards, the function of the olfactory system will be viewed from an evolutionary and phylogenetic perspective. We will further outline the main features of olfactory perception, and will show how olfactory perception is influenced by learning. Olfactory signals are relevant stimuli that affect communication. Consequently, the role of the olfactory system in social interaction and mood will be described and gender differences will be addressed. Finally, the function of the nose as an interface to the brain, including implications for pharmacology, will be discussed.
The evolutionary significance of neurochemical events in the brain has received minimal attention in the field of addiction research. Likewise, the general failure of neuroscientists to postulate how basic brain circuits might mediate emotional urges has retarded the development of scientific perspectives that could inform new inquiries into the underlying dynamics and treatment of addictions. In this paper, we revisit the argument that prototypically abused substances activate or alter specific emotional brain systems that were evolutionarily designed to signal potential increments or decrements in fitness. We then discuss two distinct emotional systems (reward seeking and separation distress) which may track different types of potential changes in fitness. Based on this evolutionarily inspired approach, we illustrate how a mammalian model of emotion (i.e. rodent ultrasonic vocalizations) may enable scientists to predict drug-related phenomena such as abuse potential, anatomical location of mediating neural substrates, and the psychological impact of withdrawal. We conclude by discussing some therapeutic and social implications of examining drug addiction processes with multiple emotional brain systems in mind.
The evolution of monoamine oxidase (MAO) activity towards tryptamine has been studied from birth to 20 days post-natal in the brain and heart of male rats. Hyperthyroidism was induced by thyroxine injections and hypothyroidism by PTU administration. The results are expressed per unit of fresh weight and per unit of protein weight. Cardiac MAO is higher in the hyperthyroid animals than in controls as soon as 5 days following birth; the difference between the 2 groups increases until 20 days. The deficiency in thyroid hormones, on the other hand, was followed by a slight decrease in the cardiac enzyme, this decrease reflecting the general deficit in protein synthesis. Brain MAO is not affected by hyperthyroidism, but a clear deficit follows PTU administration. This deficit is significant beginning at 10 days and the difference between the 2 groups increases up to 20 days. The effects of PTU-induced hypothyroidism can be corrected by thyroxine injections. Except for the decrease in the level of cardiac enzyme in hypothyroid animals, all the effects on MAO activity are independent of the total protein content of both organs.