Human neurobiologyPub Date : 1986-01-01DOI: 10.1016/S0166-4115(08)61770-7
M. Cohen, S. Grossberg
{"title":"Neural dynamics of speech and language coding: developmental programs, perceptual grouping, and competition for short-term memory.","authors":"M. Cohen, S. Grossberg","doi":"10.1016/S0166-4115(08)61770-7","DOIUrl":"https://doi.org/10.1016/S0166-4115(08)61770-7","url":null,"abstract":"","PeriodicalId":77724,"journal":{"name":"Human neurobiology","volume":"5 1 1","pages":"1-22"},"PeriodicalIF":0.0,"publicationDate":"1986-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0166-4115(08)61770-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"55913811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Estimation of empty time.","authors":"S S Campbell","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Nine subjects maintained for 60 h in an environment characterized by \"unfilled\" time were requested to estimate the time of day throughout the period. Actual intervals to be estimated ranged from 5.2 to 23.5 h. Subjects tended to underestimate elapsed time, with the mean subjective hour continuing for 1.12 h in real time. Only 21% of all estimates of time of day were accurate. The state in which an interval was spent (sleep or wakefulness) influenced time estimation, as did the degree to which the sleep/wake cycle was disrupted. The data are interpreted as indicating that the degree to which an interval is \"filled\" or \"unfilled\" does not directly affect the manner in which the interval is perceived.</p>","PeriodicalId":77724,"journal":{"name":"Human neurobiology","volume":"5 3","pages":"205-7"},"PeriodicalIF":0.0,"publicationDate":"1986-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14889057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Alterations of visual contrast sensitivity in Parkinson's disease.","authors":"W Skrandies, I Gottlob","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Contrast sensitivity functions were determined in a population of 18 patients suffering from Parkinson's disease, and compared with the data obtained in an age-matched group of healthy controls. The controls were more sensitive at all spatial frequencies tested than the patients. The statistical comparisons were highly significant, indicating general differences between the PD patients and the controls not related to individual spatial frequency channels. When comparing the sensitivity loss between low and high spatial frequencies no significant differences were found suggesting that the decrease in contrast sensitivity is a global effect. We controlled for effects of age and cerebral atrophy, and our findings cannot be accounted for by these factors. In addition, the amount of contrast sensitivity loss was not correlated with the severity of the disease. These global functional alterations appear to be related to the reduction of dopamine at various sites of the visual system.</p>","PeriodicalId":77724,"journal":{"name":"Human neurobiology","volume":"5 4","pages":"255-9"},"PeriodicalIF":0.0,"publicationDate":"1986-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14161964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Transmitter systems in the primate dentate gyrus.","authors":"D G Amaral, M J Campbell","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>While the dentate gyrus is clearly the simplest of the cortical fields that constitute the hippocampal formation, it nonetheless occupies a pivotal position in the flow of information through this region. Though it has been the subject of anatomical study for over a century and its major connections have been known for almost as long, the use of newly developed histochemical and immunohistochemical techniques have demonstrated many new facets of its intrinsic connectivity and afferent innervation. These techniques have established that it is innervated by cholinergic, noradrenergic, serotonergic and dopaminergic fibers. More recent studies have shown that fibers and cell bodies of the dentate gyrus are immunoreactive for variety of neuroactive substances including the excitatory amino acids glutamate and aspartate, the inhibitory transmitter GABA, as well as peptides of many types including the opioid peptides, enkephalin and dynorphin, several forms of somatostatin, neuropeptide Y, cholycystokinin, vasoactive intestinal peptide and substance P. In this review, we will briefly summarize the distribution of each of these putative transmitter systems within the dentate gyrus. The perspective emerges that the plethora of newly identified and chemically specific fiber systems enriches the classical understanding of the organization of this relatively simple cortical structure. Since there is thus far no evidence for the exclusion from the dentate gyrus of any class of transmitter bearing fiber or neuron found in the neocortex, it can be viewed as a relatively simple model system for studying the interactions of specific transmitter systems in a laminated, cortical structure.</p>","PeriodicalId":77724,"journal":{"name":"Human neurobiology","volume":"5 3","pages":"169-80"},"PeriodicalIF":0.0,"publicationDate":"1986-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14012664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Neurotransmitters in the human and nonhuman primate basal ganglia.","authors":"S N Haber","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In recent years, a number of new molecules, particularly peptides, have been identified as putative neurotransmitters. The basal ganglia, is especially rich in a number of classical transmitter molecules, amino acids and neuropeptides considered to function in neurotransmission. These include: the well-described terminal fields in the striatum which originate from the brain stem and contain the monoamines, dopamine and serotonin; amino acid containing axons projecting from the cortex and thalamus; striatal cholinergic and peptide-positive interneurons; and amino acid and peptide containing projection neurons to the globus pallidus and substantia nigra. Two amino acids, glutamate and aspartate, are considered to provide excitatory input to the striatum while gamma aminobutyric acid is thought to mediate inhibitory output. Neuropeptides which are richly concentrated in the basal ganglia include, enkephalin, dynorphin, substance P, somatostatin, neuropeptide Y and cholincystokinease. Changes in many of these peptide levels have recently been associated with a number of basal ganglia disorders.</p>","PeriodicalId":77724,"journal":{"name":"Human neurobiology","volume":"5 3","pages":"159-68"},"PeriodicalIF":0.0,"publicationDate":"1986-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14012663","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The neuropeptide Y-immunoreactive neuronal system: discovery, anatomy and involvement in neurodegenerative disease.","authors":"Y S Allen, S R Bloom, J M Polak","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The discovery of neuropeptides in mammalian nervous tissue has proceeded at an astonishing pace in recent years, encouraged by novel detection techniques which allow peptides to be extracted and sequenced before their biological activity has been determined (Mutt 1983; Sudcliffe et al. 1983). Most of these methods, poached from molecular biology, are nowadays reversing former trends which evolved either as a systematic search for factors known to control pituitary hormone release (vasopressin and oxytocin), for instance, or as an endeavour to find endogenous ligands for newly discovered receptors (the endorphins) (see Krieger 1983 for review). Neuropeptide tyrosine (NPY) has emerged as an important member of this new generation of peptides, not least because it is the most abundant and widely distributed in the mammalian brain. However, despite the considerable attention this peptide has attracted, we are far from understanding its functional significance. The following account traces the history of NPY and appraises some of the literature in an attempt to raise some speculation concerning its function; several reviews on this peptide already exist (Emson and de Quidt 1984; Solomon 1985; Allen and Bloom 1986; Gray and Morley 1986), Particular attention is paid to studies which have recently suggested that NPY might be involved with the pathogenesis of two neurodegenerative disorders, Huntington's chorea and Alzheimer's disease.</p>","PeriodicalId":77724,"journal":{"name":"Human neurobiology","volume":"5 4","pages":"227-34"},"PeriodicalIF":0.0,"publicationDate":"1986-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14085271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Adaptive gain control of saccadic eye movements.","authors":"H Deubel, W Wolf, G Hauske","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Properties of gain adaptivity in the saccadic system were studied. Subjects had to track a target which moved in single or double steps. The first target step which elicited the primary saccade had an amplitude in the range of 8-16 deg. The primary saccade triggered a further target displacement of 4 deg either in the same or--in different experimental sessions--in the opposite direction of the first target step. These consistent intrasaccadic target displacements lead to adaptive changes of saccadic amplitudes. The experimental data show that the saccadic system adapts to the stimulus sequence in a simple, parametric manner, namely by changing its gain. Consequently, it is assumed that a single gain element determines saccade sizes for all target eccentricities. Further, it is shown that adaptation has different time courses for gain increase and decrease, and its performance is close to completeness. The results are discussed with respect to the undershooting behaviour of goal-directed saccades and the functional demands to the saccadic system.</p>","PeriodicalId":77724,"journal":{"name":"Human neurobiology","volume":"5 4","pages":"245-53"},"PeriodicalIF":0.0,"publicationDate":"1986-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14936181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Sexual dimorphism in the human corpus callosum: an extension and replication study.","authors":"R L Holloway, M C de Lacoste","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Using a new sample of 16 human brains (F = 8, M = 8), it was found that the splenial portion of the corpus callosum was larger and more bulbous in females than in males. In addition, the total area of the corpus callosum was both absolutely and relatively larger in females than in males, with the relative measurements (i.e., to brain weight) differing significantly. This was also true when using exponential values of brain weight commensurate with the areas and linear distances of the corpus callosum. These results, which replicate the findings of earlier work, were found by the two authors using different methods, and working independently of each other. We believe these findings provide a partial anatomical basis for purported gender differences in cognitive task behaviour, and are related to early gonadal steroidal influences during prenatal development.</p>","PeriodicalId":77724,"journal":{"name":"Human neurobiology","volume":"5 2","pages":"87-91"},"PeriodicalIF":0.0,"publicationDate":"1986-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14852324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Models for sensation and perception: a selective history.","authors":"C M Bourassa","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>This paper is a historical survey, for nonspecialists, of models used to account for sensation and perception. Emphasis is placed on several crucial ideas that have given rise to major changes in explanatory models: namely, geometrical optics, receptive fields and systems or computational approaches. The nature of sensory coding and neural representation is briefly considered against this background.</p>","PeriodicalId":77724,"journal":{"name":"Human neurobiology","volume":"5 1","pages":"23-36"},"PeriodicalIF":0.0,"publicationDate":"1986-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14640312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Steady-state pattern VEP uncorrelated with suprathreshold contrast perception.","authors":"H Strasburger, I Rentschler, W Scheidler","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Campbell and Maffei (1970) reported a linear relationship between the logarithm of the grating pattern contrast and the amplitude of the visual evoked response (VEP). This enabled them to predict the pattern visibility by extrapolating to zero amplitude. By using a new digital fast sweep technique for acquiring and analysing steady state evoked potentials we show that, at clearly suprathreshold contrast levels, such a linear relationship only exists for certain spatial frequencies. In general, the VEP saturates with increasing contrast in a way that critically depends on stimulus spatial frequency. Such a dependency on spatial frequency is not obtained for suprathreshold contrast perception which is characterized by a remarkable contrast constancy. Thus the amplitude of the pattern VEP does not convey information about visual perception other than contrast detection thresholds.</p>","PeriodicalId":77724,"journal":{"name":"Human neurobiology","volume":"5 3","pages":"209-11"},"PeriodicalIF":0.0,"publicationDate":"1986-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14889696","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}