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PubMed1991

Regional expression of c-fos mRNA in rat brain during the evolution of amygdala kindled seizures.

The biochemical alterations eliciting the growth and spread of afterdischarge and accompanying the evolution of behavioral seizure stages in electrical kindling are not known. In situ hybridization for c-fos mRNA was used to map potential brain structures recruited during the evolution of major seizures from electrical kindling of the amygdala in rats. Two different patterns of c-fos induction were observed in the earliest stages of kindling (stages 1 and 2). A unilateral cortical distribution included the insular, temporal, perirhinal and parietal cortices and the amygdala. No changes in the hippocampus were noted in this group. The second distribution pattern was limited to the hippocampus (either unilateral or bilateral) and amygdala (unilateral) with no changes in the cortical areas. The afterdischarge durations were significantly (2 fold) longer in the 'hippocampal' group as compared to the 'cortical' group. In the later stages of kindling (stages 4 and 5) the distribution of c-fos mRNA was uniformly bilateral and involved a combination of the hippocampal and cortical distributions observed in the earlier stages and including the amygdala bilaterally as well. The induction of c-fos mRNA appears to provide a map of two different routes in the sequential pathways involved in the evolution of kindled seizures; it may also ultimately prove to be an important component of the kindling process itself. Additionally, c-fos mRNA was elevated bilaterally in the inferior colliculus of animals exhibiting running fits with their seizures. The inferior colliculus was previously shown by others to be involved in running fits accompanying convulsions.

Amygdala↗
PubMed1988

Epigenesis and the evolution of the human brain.

This article proposes an hypothesis for the evolution of the human brain. It is based on the concepts of (i) regulation of nerve cell proliferation, and (ii) selective stabilisation of synapses during development. The former process is supposed to be rigidly regulated by the genome, while the latter (selective stabilisation) is proposed as developing in a more plastic manner. It is suggested here that genetic alterations of the regulation of neuroblast proliferation led to epigenetic rearrangements in selective synapse stabilisation, thus producing significant changes in cerebral connectivity. This view is in agreement with the punctuationalist theory of human evolution, and differs from other approaches to human nature, such as structuralist grammar and sociobiology.

Biological Evolution↗
PubMed2000

On the design of neural networks in the brain by genetic evolution.

Hypotheses are presented of what could be specified by genes to enable the different functional architectures of the neural networks found in the brain to be built during ontogenesis. It is suggested that for each class of neuron (e.g., hippocampal CA3 pyramidal cells) a small number of genes specify the generic properties of that neuron class (e.g., the number of neurons in the class, and the firing threshold), while a larger number of genes specify the properties of the synapses onto that class of neuron from each of the other classes that makes synapses with it. These properties include not only which other neuron classes the synapses come from, but whether they are excitatory or inhibitory, the nature of the learning rule implemented at the synapse, and the initial strength of such synapses. In a demonstration of the feasibility of the hypotheses to specify the architecture of different types of neuronal network, a genetic algorithm is used to allow the evolution of genotypes which are capable of specifying neural networks that can learn to solve particular computational tasks, including pattern association, autoassociation, and competitive learning. This overall approach allows such hypotheses to be further tested, improved, and extended with the help of neuronal network simulations with genetically specified architectures in order to develop further our understanding of how the architecture and operation of different parts of brains are specified by genes, and how different parts of our brains have evolved to perform particular functions.

Algorithms↗
PubMed1985

Oxygen deficiency and brain damage: localization, evolution in time, and mechanisms of damage.

Observations on some patients with CO intoxication have revealed a delayed type of brain injury, with symptoms appearing days after the initial insult. Possible mechanisms are discussed, with reference to recent experimental results on ischemic brain damage. These results have shown that brief periods of ischemia can cause necrosis of selectively vulnerable neurons, sometimes after a delay of 1-3 days. In at least one affected cell type (CAI pyramids in the hippocampus) delayed neuronal death was preceded by cellular hyperactivity. Recent neurochemical research offers tentative explanations. For example, several reactions triggered by increased calcium concentrations are long-lasting enough to cause sustained alteration of cell function and/or delayed neuronal death. These encompass physical interruption of the cytoskeleton by disassembly of microtubuli and degradation of neurofilaments, protein phosphorylation, and proteolytic degradation of dendritic structures. Reactions interrupting the cytoskeleton could cause cell death by impeding axonal transport, while phosphorylation-proteolysis could induce increased synaptic efficacy, with harmful overactivity.

Acidosis↗
PubMed1986

Experimental brain abscess development in the chronically immunosuppressed host. Computerized tomographic and neuropathological correlations.

The neuropathological progression of brain abscess formation was studied experimentally in paired immunosuppressed and control dogs. The immunosuppressed animals received azathioprine and prednisone beginning 7 days prior to intracerebral inoculation with alpha streptococcus. Histological findings were correlated with computerized tomography (CT) brain scans. The evolution of brain abscess in the immunosuppressed animals could be divided into three stages based on histological evaluation: cerebritis stage (1 to 11 days), early-capsule stage (12 to 17 days), and late-capsule stage (18 days and later). There was a significant delay in the evolution of alpha streptococcus brain abscess compared to the authors' previous studies. Histologically, abscesses in immunosuppressed dogs were characterized by a decrease and delay in collagen formation, a reduction in polymorphonuclear leukocytes and macrophages, longer persistence of bacterial organisms, and an increase in gliosis. During the cerebritis stage, abscesses in control animals were consistently larger and more edematous than those in immunosuppressed animals and reached their maximum size by Day 8, whereas abscesses in immunocompromised animals reached their maximum size around Day 12. In the late-capsule stage, abscesses in immunosuppressed animals remained larger than those of control animals and continued to show signs of delayed development. This was evidenced by diffusion of contrast medium into the lucent center of ring-enhancing lesions on delayed CT scans. The results suggest that the decreased inflammatory response and edema formation in the immunosuppressed host resulted in less initial mass effect from brain abscess, but that the eventual size and area of the abscess may have become larger due to the less effective host response.

Animals↗
PubMed1985

Conservative features of neocortical evolution in dolphin brain.

A Golgi survey of the convexity cortex in the brain of the dolphin, Tursiops truncatus, has revealed many cellular characteristics which may be indicative of conservative cortical evolution. These include a high degree of pyramidalization, and an accentuation of layer II. The presence of an accentuated layer II in convexity cortex is a protoneocortical characteristic found in more 'primitive' cortical arrangements. The growth ring concepts of cortical development outward in concentric waves from archicortical and paleocortical origins are discussed. In that context we have not been able to identify cores of hyperspecialization in the dolphin cortex corresponding to koniocortex and gigantopyramidal areas. This leads us to suggest that the cortex of the dolphin reflects a condition of the paralimbic-parinsular stage of evolutionary development. Thus, the dolphin brain may serve as a model of the theoretical mammalian archetype brain and its study may shed light on the organization of the brains of the initial ancestors of modern mammals.

Animals↗
PubMed1975

Allometry in primates, with emphasis on scaling and the evolution of the brain.

Allometry should be defined broadly as the study of size and its consequences, not narrowly as the application of power functions to the data of growth. Variation in size may be ontogenetic, static or phyletic. Errors of omission and treatment have plagued the study of allometry in primates. Standard texts often treat brain size as an independent measure, ignoring its allometric relation with body size - on this basis, gracile australopithecines have been accorded the mental status of gorillas. Intrinsic allometries of the brain/body are likewise neglected: many authors cite cerebral folding as evidence of man's mental superiority, but folding is a mechanical correlate of brain size itself. Confusion among types of scaling heads errors of treatment in both historical primacy [Dubois' ontogenetic inferences from interspecific curves] and current frequency. The predicted parameters of brain-body plots differ greatly for ontogenetic, intrapopulational, interspecific and phyletic allometries. I then discuss basic trends in bivariate allometry at the ordinal level for internal organ weights, skeletal dimensions, lifespan and fetal weight. In considering the causes of basic bivariate allometries, I examine the reason for differences among types of scaling in brain-body relationships. The interspecific exponent of 0.66 strongly suggests a relationship to body surfaces, but we have no satisfactory explanation for why this should be so. The tripartite ontogenetic plot is a consequence of patterns in neuronal differentiation. We do not know why intraspecific exponents fall between 0.2 and 0.4; several partial explanations have been offered. Multivariate techniques have transcended the pictorial representation of transformed coordinates and offer new, powerful approaches to total allometric patterns. Allometry is most often used as a 'criterion for subtraction'. In order to assess the nature and purpose of an adaptation, we must be able to identify and isolate the aspect of its form that depends both upon its size and the size of the body within which it resides. Cranial indices and limb lengths are misinterpreted when authors apply no correction for body size. The search for a criterion of subtraction has been most diligently pursued in studies of the brain. Clearly, brain size must be assessed by comparison with a 'standard' animal of the same body size. But how shall size be measured, especially in fossils; and how shall a standard animal be construed. I discuss and criticize three methods recently used: RADINSKY'S foramen magnum criterion; Jerison's minimum convex polygons and cephalization quotients; and the indices of progression in comparison with 'basal' insectivores' of BAUCHOT, Stephan and their colleagues.

Animals↗
PubMed1985

The temporal evolution of hypoglycemic brain damage. III. Light and electron microscopic findings in the rat caudoputamen.

The caudate nucleus and putamen belong to the selectively vulnerable brain regions which incur neuronal damage in clinical and experimental settings of both hypoglycemia and ischemia. We have previously documented the density and distribution of the hypoglycemic damage in rat caudoputamen, but the evolution of the injury, i.e., the sequence of structural changes, has not been assessed. Therefore, in the present study we analyze the light and electron microscopic alterations in the caudoputamen of rats exposed to standardized, pure insults of severe hypoglycemia with isoelectric EEG for 10-60 min, or in rats which, following insults of 30 or 60 min, were allowed to recover for periods from 5 min to 6 months. The hypoglycemic insult produced severe nerve cell injury in the dorsolateral caudoputamen. Immediately after the insult abnormal light neurons with clearing of the peripheral cytoplasm were present. These cells disappeared early in the recovery period, as they do in the cerebral cortex. Dark neurons were also present, but unlike those in the cerebral cortex they did not appear until recovery was instituted. Their number increased for a couple of hours and they became acidophilic within 4-6 h. At this stage, electron microscopy revealed severe clumping of the nuclear chromatin and cytoplasm as well as incipient fragmentation of cell membranes, all these changes indicating an irreversible injury. Within 24 h flocculent densities appeared in the mitochondria and by day 2-3 of recovery the great majority of the medium-sized neurons had undergone karyorrhexis and cytorrhexis, their remnants being subsequently removed by macrophages. After some weeks only large and a few medium-sized neurons remained amidst reactive astrocytes and numerous macrophages. The delay in the appearance of dark, lethally injured medium-sized neurons until the recovery was instituted suggests an effect that does not become apparent until the substrate supply and energy production are restored. Furthermore, it points out again the selectivity of the hypoglycemic nerve cell injury with respect to the type (metabolic characteristics?) and topographic location of the neurons.

Animals↗
PubMed1995

Relationship between diffusion-weighted MR images, cerebral blood flow, and energy state in experimental brain infarction.

The regional evolution of brain infarction was studied in Wistar rats submitted to remotely controlled thread occlusion of the middle cerebral artery. Occlusion was performed in the magnet of an NMR tomography system to allow continuous recording of diffusion-weighted images. After 30 min (n = 6) or 2 h (n = 9), cerebral blood flow was measured by [14C] iodoantipyrine autoradiography while the regional distribution of ATP, glucose, lactate, and pH was imaged using pictorial bioluminescence and fluoroscopic methods. In diffusion-weighted images, the hemispheric lesion area (HLA) at the level of caudate-putamen amounted to 54.2 +/- 10.9% after 30 min and to 67.0 +/- 5.9% after 2 h vascular occlusion. These areas corresponded to the regions exhibiting tissue acidosis (60.8 +/- 9.3% and 70.4 +/- 4.5%), but were clearly larger than those in which ATP was depleted (22.3 +/- 20.8% and 49.6 +/- 12.9% after 30 min and 2 h, respectively). The threshold of blood flow for the increase of signal intensity in diffusion-weighted images increased between 30 min and 2 h occlusion from 34 to 41 ml/100 g per minute, the threshold of acidosis from 40 to 47 ml/100 g per minute, and the threshold for ATP depletion from 13 to 19 ml/100 g per minute. Our study demonstrates that diffusion-weighted imaging detects both the core and the penumbra of the evolving infarction but is not able to differentiate between the two parts. It further shows that the ischemic lesion grows during the initial 2 h of vascular occlusion, and that the size of the infarct core increases more rapidly than that of the penumbra.

Adenosine Triphosphate↗