PubMed Health⌕ Search

PubMed · 528905

Information processing in the cerebral hemispheres: selective hemispheric activation and capacity limitations.

Abstract

Several previous experiments have found that concurrently maintaining verbal information in memory influences visual laterality patterns (e.g., Hellige & Cox, 1976; Kinsbourne, 1975). The present article critically reviews existing experiments and reports five additional experiments designed to identify the mechanisms responsible for such effects. Experiment 1 demonstrates that laterality patterns are not influenced by a concurrent memory task that does not require verbal processing. (The verbal nature of the concurrent task was an important aspect of previous experiments.) Experiments 2 and 3 were designed to determined whether concurrent verbal memory primarily influences very early visuospatial processes or later processes such as those involved in visuospatial memory. In Experiment 2, observers indicated whether two simulteneously presented nonsense forms had the same shape. Observers held 0, 2, 4, or 6 words in memory during each shape judgment trial. Responses were faster when the forms were presented to the left visual field--right hemisphere (LVF-RH) than to the right visual field--left hemisphere (RVF-LH). This effect did not interact with memory set size. In Experiment 3, observers indicated whether either of two simultaneously presented forms was identical to a target form held in memory. Observers held 0, 2, or 6 words in memory on each trial. On same-as-target trials, responses were faster on LVF-RH trials than on RVF-LH trials in the no-word memory condition; this difference was reversed in the two-word and six-word conditions. The combined results of Experiments 2 and 3 suggest that concurrent verbal memory influences stages of processing beyond the initial registration of visuospatial information. Experiments 4 and 5 examined the influence of concurrent verbal memory on verbal laterality tasks. Observers indicated whether two simultaneously presented letters of different cases had the same name. In Experiment 4, different groups of observers held 0, 2, 4, or 6 words in memory on each letter-pair trial. In Experiment 5, memory set size was manipulated within subjects. On the same-pair trials of Experiment 4 and the first session of Experiment 5, responses in the no-memory condition were faster on RVF-LH trials than on LVF-RH trials; this difference was reversed in all of the work memory conditions. This shift is opposite to that found when the laterality task does not require verbal processing and further indicates that concurrent verbal memory influences processing stages beyond those that are common to the form-pair and letter-pair tasks. Neither directness-of-pathway nor attention-gradient laterality models can explain the entire pattern of results from the present experiments. Rather, the results suggest that the left hemisphere functions as a typical limited-capacity information processing system that can be influenced somewhat separately from the right hemisphere system.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J B Hellige, P J Cox, L Litvac. 1979. Information processing in the cerebral hemispheres: selective hemispheric activation and capacity limitations.. https://doi.org/10.1037/%2F0096-3445.108.2.251

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Histone H3K9 methyltransferases regulate cortical growth by coordinating heterochromatin formation and neural progenitor dynamics.

DNA packaging into heterochromatin is a fundamental mechanism of transcriptional silencing, yet its role in regulating neural progenitor behavior during brain development remains poorly understood. Trimethylation of histone H3 lysine 9 (H3K9me3), catalyzed by the methyltransferases SETDB1, SUV39H1, and SUV39H2, is a defining feature of heterochromatin, but functional redundancy among these enzymes has obscured their developmental roles. Here, we generated a cortex-specific triple knockout mouse model lacking Setdb1, Suv39h1, and Suv39h2 to directly interrogate H3K9me3 function during corticogenesis. Combined loss of H3K9 methyltransferases caused genome-wide depletion of H3K9me3, disruption of neural progenitor cell-cycle progression, and impaired cortical neurogenesis, resulting in microcephaly. H3K9 methyltransferases preserve neural progenitor identity and function by silencing clustered protocadherins, meiosis-associated genes, and a cell-cycle restraint program through H3K9me3 deposition. Loss of H3K9me3 promoted local chromatin opening and increased transcription factor occupancy, enabling transposable elements to acquire cryptic enhancer activity and modulate proximal gene expression. Together, these findings establish H3K9me3 heterochromatin as an active regulator of neural progenitor dynamics and lineage fidelity, revealing a central epigenetic mechanism that restricts aberrant transcriptional programs to ensure cortical growth.

Cerebral Cortex↗

Prosopagnosia.

Explore the source record for details and available documents.

Cerebral Cortex↗

Prenatal diagnosis of malformations of cortical development by dedicated neurosonography.

OBJECTIVE: Malformations of cortical development (MCD) are rarely diagnosed in utero. We describe and compare the ultrasonographic and pathology findings in a cohort of fetuses with MCD. METHODS: Fetuses with MCD were identified among all fetuses evaluated for suspected brain anomalies at the Fetal Neurology Clinic, and the ultrasonographic findings were compared with the results of the pathology examination. RESULTS: We suspected the presence of MCD by ultrasonography in 23 fetuses. The mean gestational age at the time of ultrasound diagnosis was 26.2 (range, 18-40) weeks. The ultrasonographic findings leading to the diagnosis of MCD were abnormally overdeveloped gyri and sulci for gestational age (n = 7), delay in sulcation (n = 5), abnormally thin cortex (n = 5) abnormally wide and broad sulci (n = 3), bulging into the lateral ventricle (n = 1), cortical cleft (n = 1), and multiple intraparenchymal echogenic nodules (n = 1). All fetuses had associated central nervous system (CNS) and/or non-CNS anomalies. Pathology examination (performed in 17 fetuses) confirmed MCD in 16. CONCLUSIONS: Cortical malformations can be diagnosed in utero by ultrasonography based on the presence of specific deviations from the normal pattern of development. The identified cases may represent the more severe forms in the MCD spectrum. The pathology findings do not always conform to the current classification systems of MCD but help in differentiating between possible genetic and acquired etiologies and in some cases provide a definitive syndromic diagnosis.

Cerebral Cortex↗