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Recent explorations of the morphology of retinal neurones, combined with neurophysiological recordings have made it possible to link specific anatomical types with particular physiological classes. At the same time, the relatively complete anatomical mapping of the retina has revealed some bias in the sampling of neurones by electrophysiological techniques.
Freud built his model of the mind and his hypotheses about dreaming directly on the structure of his neurobiological model of the brain, which was developed in the "Project for a Scientific Psychology", written in 1895. Among the concepts modeled in this work were ego, somatic drives as motivationally critical, cathexes of psychic energy, wish fulfillment, and primary and secondary process. From the vantage point of more than 80 years later, the authors indicate the areas in which many of Freud's neurobiological assumptions are inacurrate. Revisions are needed in the neurobiologically derived psychoanalytic concepts, especially those of Freud's wish fulfillment-disguise theory of dreams.
Recent research in the neurobiology of dreaming sleep provides new evidence for possible structural and functional substrates of formal aspects of the dream process. The data suggest that dreaming sleep is physiologically determined and shaped by a brain stem neuronal mechanism that can be modeled physiologically and mathematically. Formal features of the generator processes with strong implications for dream theory include periodicity and automaticity of forebrain activation, suggesting a preprogrammed neural basis for dream mentation in sleep; intense and sporadic activation of brain stem sensorimotor circuits including reticular, oculomotor, and vestibular neurons, possibly determining spatiotemporal aspects of dream imagery; and shifts in transmitter ratios, possibly accounting for dream amnesia. The authors suggest that the automatically activated forebrain synthesizes the dream by comparing information generated in specific brain stem circuits with information stored in memory.
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The performance of a group of stutters (N = 14) and a group of nonstutterers (N = 14) was compared on the Synthetic Sentence Identification Test (Speaks and Jerger, 1965). The test is designed to assess central auditory function. It was hypothesized that because of subtle neurologically based differences in perceptual processing, the performance of the two groups would differ significantly on one or more of the subtests. An analysis of variance revealed that the performance of the stuttering group was significantly poorer (0.01 level of confidence) than that of the nonstutteres on the Ipsilateral Competing Message Subtest. The results of the investigation were compatible with other studies that suggest a neurological dysfunction within the central auditory apparatus as at least one of the underlying causes of disfluency. It was concluded that further investigations of the central auditory processes in stutterers are warranted to make a more definitive statement about the etiology of stuttering.
This review considers carbohydrate metabolism in the developing brain, in particular the proportion of glucose metabolized via the pentose phosphate pathway. Although small in amount, this fraction serves a vital rôle in some aspects of brain function. Evidence is presented that the pentose phosphate pathway subserves different functions as the developing brain progresses through the stages of growth and myelination to full neurological competence. The general aspects considered are the changing patterns of brain enzymes during development; the flux of glucose through the alternative pathways of glucose metabolism in the developing brain; the functional significance of the pentose phosphate pathway; and the regional and functional association of the pentose phosphate pathway activity and the detoxication of biogenic amínes.
Induced pluripotent stem cells (iPSCs) have revolutionized neuroscience, providing an approach to generate patient-specific neurons for modeling of neurological diseases. However, it remains unclear how closely iPSC-derived neurons replicate the chromatin architecture of authentic brain neurons. Here, we uniformly processed newly generated Hi-C data from iPSC-derived neurons and neurons isolated from the human postmortem brain, together with previously published data sets comprising 228 human and 89 mouse Hi-C and snm3C-seq samples from different cell subtypes. These data were merged into 96 high-coverage contact maps used to examine chromatin features ranging from chromatin compartments and topologically associating domains (TADs) to chromatin loops, Polycomb-mediated contacts, and frequently interacting regions (FIREs). We find that iPSC-derived neurons largely retain the chromatin state of undifferentiated cells and resemble fetal rather than mature neurons. iPSC-derived neurons exhibit unusually strong compartmentalization, an enrichment of developmental genes at TAD borders, and a marked reduction of long-range repressive Polycomb-mediated contacts that typically silence early fetal programs. Although immature, iPSC-derived neurons offer advantages for modeling interactions between disease-associated SNPs and target genes, as many psychiatric disorders have neurodevelopmental origins. Integrating iPSC-derived and postmortem neuronal data sets therefore provides complementary insights into the chromatin landscape underlying disease-associated interactions. Our study offers a valuable Hi-C resource for the community and provides a detailed comparison of chromatin architecture throughout neuronal maturation, underscoring its importance for validating neuronal models and providing a robust framework for future studies.
The neurological base of biological space and of spatial perception is discussed. The nervous system is viewed as a system controlling behaviour. Movements as elements of behaviour are guided movements: goal-directed, programmed and ordered in space. Perceptual space is derived from directional properties of behaviour. The sense organs are not 'doors of perception', transparent to the alleged properties of the environment. Rather they are used in a centrifugal sense--outward from the organism. They are instrumental in updating a 'map' of the outside world and of the organisms as part of that world. The map is, in essence, a projection of the organism's own behaviour modified by the regularities, constraints and supports encountered in the world. The role of the periphery varies from moment to moment with the organisational level of behaviour. Thus, the sensomotor system is operated for updating the map and also for calibrating movements. At a peripheral level it helps to level out irregularities encountered in the execution of simple movements. All these functions may take place at the same time. Taken together, these considerations serve as an explanation of the fact that we are able to determine the spatial properties of objects although the shape as such is not presented to the sensory surface of the body, nor are the various scanpaths of our exploratory movements a replica of the geometrical properties of the object.
The role of zinc in central nervous system metabolism remains obscure but it has been shown in animals that diphenylthiocarbazone (Dithizone) selectively colors intravitally the hippocampus and adnexa, parts affected in human temporal lobe epilepsy. To examine the effect of experimental cerebral lesions on zinc storage in that region, 80 mice were divided into two operative and two control groups. The operative groups had unilateral lesions placed in the hippocampus or frontal lobe. One control group and both lesion groups were injected subcutaneously with zinc lactate daily for ten days before intravenous injection of diphenylthiocarbazone. The other control group was used to determine if zinc storage occurs as a result of its increased systemic availability. Hippocampal lesion mice showed more extensive staining of lethal amygdala and associated cortex on the side of the lesion. Frontal lesions remained unstained and frontal lesions did not alter the staining of hippocampus and related parts. Lack of difference between controls shows that greater availability of systemic zinc does not increase its content in the hippocampal-lateral amygdalar region. Increased zinc uptake in this instance appears to be a local phenomenon.
Simple mathematical equations can be used to estimate the probability of posttraumatic seizures. Risk factors and time since the injury are taken into consideration in the calculations. The equations are based on a constant probability model derived from published data. When these formulae are applied to data from a variety of published studies, the predicted incidence of posttraumatic epilepsy based on the mathematical model agrees well with the incidence observed in the study groups.
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The anatomy, physiology, and pharmacology of an intrinsic neural network that monitors and modulates the activity of pain-transmitting neurons is reviewed. This system can be activated by opiate administration or by electrical stimulation of discrete brainstem sites. Evidence is presented that its pain-suppressing action is mediated in part by endogenous opiatelike compounds (endorphins). This pain suppression system is organized at three levels of the neuraxis: midbrain, medulla, and spinal cord. Activation of neurons in the midbrain periaqueductal gray matter (by electrical stimulation, opiates, and possibly psychological factors) excites neurons of the rostral medulla, some of which contain serotonin. The medullary neurons, in turn, project to and specifically inhibit the firing of trigeminal and spinal pain-transmission neurons. As part of a negative feedback loop, the output of the pain transmission neurons, i.e., pain itself, is an important factor in activating the pain-suppression system. A neural model which incorporates the experimental findings is proposed, and the clinical implications of the model are discussed.
Eye movements in a patient with saccadic oscillations (ocular flutter) were recorded and analyzed. Findings were related to recent microelectrode studies in the monkey pontine reticular formation which have identified three types of premotor neurons related to saccadic eye movements: burst, tonic, and pause cells. We incorporated these cell types into a hypothetical circuit that generates saccades by rapidly driving the eye to a designated orbital position rather than preprogramming a distance for movement. Physiological measurements suggest that this neural network is unstable and that the burst neurons must be tonically inhibited to prevent saccadic oscillations during periods of fixation. Pause cells, which discharge tonically except during saccades, when they pause, appear to inhibit burst cells and prevent such saccadic oscillations. Analysis of our patient's behavior indicates that many types of saccadic oscillations can be explained and classified by assuming an abnormality of pause cell control over saccadic burst neurons.
A number of chemically unrelated neurotoxic compounds and several types of metabolic abnormalities cause strikingly similar patterns of distal symmetrical polyneuropathy in humans and animals. Experimental studies with laboratory species have demonstrated that many toxic polyneuropathies are associated with distal and retrograde axonal degeneration occurring in vulnerable nerve fiber tracts in the central as well as the peripheral nervous system. This has been termed central-peripheral distal axonopathy. Recent observations from the authors' laboratories regarding (1) the spatial-temporal evolution of nerve fiber degeneration in experimental toxic neuropathies and (2) the inhibition of glycolytic enzymes by chemically unrelated neurotoxic compounds point to a common metabolic basis for many distal axonopathies. It is postulated that neurotoxic compounds deplete energy supplies in the axon by inhibiting nerve fiber enzymes required for the maintenance of energy synthesis. Resupply of enzymes from the neuronal soma fails to meet the increased demand for enzyme replacement in the axon, causing the concentration of enzymes to drop in distal regions. This leads to a local blockade of energy-dependent axonal transport, which produces a series of pathological changes culminating in distal nerve fiber degeneration. The idea provides a working hypothesis with which to study the cause of inherited and acquired human and animal polyneuropathies.
This paper presents a theory for the input-output transformation involved in diffuse monosynaptic activation in a neural tissue or organ system of one population of neurons by another. Main findings are: (1) highly diffuse monosynaptic linkages act very much like filters, selectively sensitive to synchronized clusters of action potentials among the fibers of the input population; (2) partially diffuse monosynaptic linkages are capable of effecting either an amplification or diminution of the number of pulses involved in a single synchronized cluster, depending on parameters of the system; and (3) partially diffuse and spatially organized monosynaptic linkages are capable of effecting a spatial inversion of fine-grained spatial patterns. Theoretical predictions are clarified by mathematical analysis and computer simulation.
The dendritic patterns of cells in the optic tectum of the tegu lizard, Tupinambis nigropunctatus, were analyzed with the Ramon-Moliner modification of the Golgi-Cox technique. Cell types were compared with those described by other authors in the tectum of other reptiles; particular comparisons of our results were made with the description of cell types in the chameleon (Ramń, 1896), as the latter is the most complete analysis in the literature. The periventricular gray layers 3 and 5 consist primarily of two cell types--piriform or pyramidal shaped cells and horizontal cells. Cells in the medial portion of the tectum, in an area coextensive with the bilateral spinal projection zone, possess dendrites that extend across the midline. The latter cells have either fusiform or pyramidal shaped somas. The central white zone, layer 6, contains fibers, large fusiform or pyramidal shaped cells, fusiform cells, and small horizontal cells. The central gray zone, layer 7, is composed predominately of fusiform cells which have dendrites extending to the superficial optic layers, large polygonal cells, and horizontal cells. The superficial gray and white layers, layers 8-13, contain polygonal, fusiform, stellate, and horizontal elements. Layer 14 is composed solely of afferent optic tract fibers. Several differences in the occurrence and distribution of cell types between the tegu and the other reptiles studied are noted. Additionally, the laminar distribution of retinal, tectotectal, telencephalic, and spinal projections in the tegutectum can be related to the distribution of cell types, and those cells which may be postsynaptic to specific inputs can be identified. The highly differentiated laminar structure of the reptilian optic tectum, both in regard to cell type and to afferent and efferent connections, may serve as a model for studying some functional properties of lamination common to cortical structures.