Neural Activity in Primate Caudate Nucleus Associated With Pro- and Antisaccades

2009 ◽  
Vol 102 (4) ◽  
pp. 2334-2341 ◽  
Author(s):  
Kristen A. Ford ◽  
Stefan Everling
Keyword(s):  
Caudate Nucleus ◽  
Discharge Rate ◽  
Indirect Pathway ◽  
Behavioral Context ◽  
Firing Rates ◽  
Neuronal Populations ◽  
Input Structure ◽  
Flexible Behavior ◽  
Two Populations

The basal ganglia (BG) play a central role in movement and it has been demonstrated that the discharge rate of neurons in these structures are modulated by the behavioral context of a given task. Here we used the antisaccade task, in which a saccade toward a flashed visual stimulus must be inhibited in favor of a saccade to the opposite location, to investigate the role of the caudate nucleus, a major input structure of the BG, in flexible behavior. In this study, we recorded extracellular neuronal activity while monkeys performed pro- and antisaccade trials. We identified two populations of neurons: those that preferred contralateral saccades (CSNs) and those that preferred ipsilateral saccades (ISNs). CSNs increased their firing rates for prosaccades, but not for antisaccades, and ISNs increased their firing rates for antisaccades, but not for prosaccades. We propose a model in which CSNs project to the direct BG pathway, facilitating saccades, and ISNs project to the indirect pathway, suppressing saccades. This model suggests one possible mechanism by which these neuronal populations could be modulating activity in the superior colliculus.

scholarly journals Delays in activity-based neural networks

2009 ◽  
Vol 367 (1891) ◽  
pp. 1117-1129 ◽  
Author(s):  
Stephen Coombes ◽  
Carlo Laing
Keyword(s):  
Network Architecture ◽  
Linear Stability Theory ◽  
Oscillatory Behaviour ◽  
Firing Rates ◽  
Neuronal Populations ◽  
Natural Extensions ◽  
Discrete Delays ◽  
Numerical Bifurcation ◽  
Numerical Bifurcation Analysis

In this paper, we study the effect of two distinct discrete delays on the dynamics of a Wilson–Cowan neural network. This activity-based model describes the dynamics of synaptically interacting excitatory and inhibitory neuronal populations. We discuss the interpretation of the delays in the language of neurobiology and show how they can contribute to the generation of network rhythms. First, we focus on the use of linear stability theory to show how to destabilize a fixed point, leading to the onset of oscillatory behaviour. Next, we show for the choice of a Heaviside nonlinearity for the firing rate that such emergent oscillations can be either synchronous or anti-synchronous, depending on whether inhibition or excitation dominates the network architecture. To probe the behaviour of smooth (sigmoidal) nonlinear firing rates, we use a mixture of numerical bifurcation analysis and direct simulations, and uncover parameter windows that support chaotic behaviour. Finally, we comment on the role of delays in the generation of bursting oscillations, and discuss natural extensions of the work in this paper.

scholarly journals Striatal Control of Movement: A Role for New Neuronal (Sub-) Populations?

2021 ◽  
Vol 15 ◽  
Author(s):  
Tim Fieblinger
Keyword(s):  
Brain Area ◽  
Projection Neurons ◽  
Anatomical Location ◽  
Striatal Neurons ◽  
Indirect Pathway ◽  
Transcriptional Profiles ◽  
Transcriptional Signature ◽  
Neuronal Populations ◽  
Abnormal Movements ◽  
Two Populations

The striatum is a very heterogenous brain area, composed of different domains and compartments, albeit lacking visible anatomical demarcations. Two populations of striatal spiny projection neurons (SPNs) build the so-called direct and indirect pathway of the basal ganglia, whose coordinated activity is essential to control locomotion. Dysfunction of striatal SPNs is part of many movement disorders, such as Parkinson’s disease (PD) and L-DOPA-induced dyskinesia. In this mini review article, I will highlight recent studies utilizing single-cell RNA sequencing to investigate the transcriptional profiles of striatal neurons. These studies discover that SPNs carry a transcriptional signature, indicating both their anatomical location and compartmental identity. Furthermore, the transcriptional profiles reveal the existence of additional distinct neuronal populations and previously unknown SPN sub-populations. In a parallel development, studies in rodent models of PD and L-DOPA-induced dyskinesia (LID) report that direct pathway SPNs do not react uniformly to L-DOPA therapy, and that only a subset of these neurons is underlying the development of abnormal movements. Together, these studies demonstrate a new level of cellular complexity for striatal (dys-) function and locomotor control.

scholarly journals Microtubule–microtubule sliding by kinesin-1 is essential for normal cytoplasmic streaming in Drosophila oocytes

2016 ◽  
Vol 113 (34) ◽  
pp. E4995-E5004 ◽  
Author(s):  
Wen Lu ◽  
Michael Winding ◽  
Margot Lakonishok ◽  
Jill Wildonger ◽  
Vladimir I. Gelfand
Keyword(s):  
Cytoplasmic Streaming ◽  
Cell Types ◽  
Nurse Cells ◽  
Wild Type ◽  
Actin Cortex ◽  
Microtubule Motor ◽  
Multiple Cell ◽  
Cytoplasmic Microtubules ◽  
Two Populations

Cytoplasmic streaming in Drosophila oocytes is a microtubule-based bulk cytoplasmic movement. Streaming efficiently circulates and localizes mRNAs and proteins deposited by the nurse cells across the oocyte. This movement is driven by kinesin-1, a major microtubule motor. Recently, we have shown that kinesin-1 heavy chain (KHC) can transport one microtubule on another microtubule, thus driving microtubule–microtubule sliding in multiple cell types. To study the role of microtubule sliding in oocyte cytoplasmic streaming, we used a Khc mutant that is deficient in microtubule sliding but able to transport a majority of cargoes. We demonstrated that streaming is reduced by genomic replacement of wild-type Khc with this sliding-deficient mutant. Streaming can be fully rescued by wild-type KHC and partially rescued by a chimeric motor that cannot move organelles but is active in microtubule sliding. Consistent with these data, we identified two populations of microtubules in fast-streaming oocytes: a network of stable microtubules anchored to the actin cortex and free cytoplasmic microtubules that moved in the ooplasm. We further demonstrated that the reduced streaming in sliding-deficient oocytes resulted in posterior determination defects. Together, we propose that kinesin-1 slides free cytoplasmic microtubules against cortically immobilized microtubules, generating forces that contribute to cytoplasmic streaming and are essential for the refinement of posterior determinants.

scholarly journals Private specificities of H-2K and H-2D loci as possible selective targets for effector lymphocytes in cell-mediated immunity.

1975 ◽  
Vol 141 (1) ◽  
pp. 11-26 ◽  
Author(s):  
B D Brondz ◽  
I K Egorov ◽  
G I Drizlikh
Keyword(s):  
T Lymphocytes ◽  
Target Cells ◽  
Cell Mediated Immunity ◽  
Skin Grafts ◽  
Immune Lymphocytes ◽  
Direct Cytotoxicity ◽  
Cross Absorption ◽  
Private Specificity ◽  
Two Populations

Receptors of effector T lymphocytes of congeneic strains of mice do not recognize public H-2 specificities and react to private H-2 specificities only. This has been established with the use of three tests: direct cytotoxicity assay of immune lymphocytes upon target cells, specific absorption of the lymphocytes on the target cells, and rejection of skin grafts at an accelerated fashion. Immunization with two private H-2 specificities in the system C57BL/10ScSn leads to B10.D2 induces formation of two corresponding populations of effector lymphocytes in unequal proportion: a greater part of them is directed against the private specificity H-2.33 (Kb), while the smaller part is towards H-2.2 (Db) private specificity. These two populations of effector lymphocytes do not overlap, as demonstrated by experiments on their cross-absorption on B10.D2 (R107), B10.D2 (R101), B10.A(2R), and B10.A(5R) target cells, as well as on mixtures of R107 and R101 targets. Following removal of lymphocytes reacting with one of the private H-2 specificities, lymphocytes specific to the other specificity are fully maintained. A mixture of target cells, each bearing one of the two immunizing private specificities, absorbs 100% of the immune lymphocytes and is totally destroyed by them. It is suggested that H-2 antigens are natural complexes of hapten-carrier type, in which the role of hapten is played by public H-2 specifities and that of the carrier determinant by either private H-2 specificities or structures closely linked to them. Various models of steric arrangement of MHC determinants recognized by receptors of effector T lymphocytes are discussed.

scholarly journals Estrogen binding by leukocytes during phagocytosis,.

1977 ◽  
Vol 145 (4) ◽  
pp. 983-998 ◽  
Author(s):  
S J Klebanoff
Keyword(s):  
Chronic Granulomatous Disease ◽  
Reaction Mechanisms ◽  
Dehydrogenase Deficiency ◽  
Cell Types ◽  
Neutrophil Function ◽  
Granulomatous Disease ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Estrogen Binding ◽  
Two Populations

Estradiol binds covalently to normal leukocytes during phagocytosis. The binding involves three cell types, neutrophils, eosinophils, and monocytes and at least two reaction mechanisms, one involving the peroxidase of neutrophils and monocytes (myeloperoxidase [MPO]) and possibly the eosinophil peroxidase, and the second involving catalase. Binding is markedly reduced when leukocytes from patients with chronic granulomatous disease (CGD), severe leukocytic glucose 6-phosphate dehydrogenase deficiency, and familial lipochrome histiocytosis are employed and two populations of neutrophils, one which binds estradiol and one which does not, can be demonstrated in the blood of a CGD carrier. Leukocytes from patients with hereditary MPO deficiency also bind estradiol poorly although the defect is not as severe as in CGD. These findings are discussed in relation to the inactivation of estrogens during infection and the possible role of estrogens in neutrophil function.

From Victims to Perpetrators of Bullying: The Role of Irrational Cognitions, Externalizing Problems, and Parental Attachment

2021 ◽  
pp. 088626052110435
Author(s):  
Raluca Balan ◽  
Anca Dobrean ◽  
Robert Balazsi
Keyword(s):  
Public Schools ◽  
Path Analysis ◽  
Indirect Effects ◽  
Externalizing Problems ◽  
Parental Attachment ◽  
Bullying Victimization ◽  
Indirect Pathway ◽  
Bullying Perpetration ◽  
Interaction Terms

The transition from bullying victimization to bullying perpetration is well documented in the literature. However, the mechanisms linking bullying victimization to perpetration are not fully understood. The main aim of the current study was to conduct a preliminary research investigating the indirect effects of youths bullying victimization on bullying perpetration through irrational cognitions and externalizing problems. The second aim of the study was to explore the moderating role of the type of parental attachment (secure vs. insecure) in the proposed model in explaining the association of bullying victimization and bullying perpetration. Data were collected from 269 adolescents (11-15 years; M = 11.98, SD = .68), enrolled in middle public schools from Romania. Path analysis and moderated path analysis were conducted to explore the direct and indirect effects and moderating effects, respectively. Study findings indicate that bullying victimization was indirectly related to bullying perpetration separately through youths’ irrational cognition as well as through externalizing problems. The serial indirect pathway from victimization to perpetration through irrational cognitions leading further to externalizing problems was also significant. However, the type of attachment that adolescents reported having toward their parents failed to moderate the indirect pathways, since all the interaction terms were nonsignificant. These findings advance the field prevention and intervention by identifying irrational cognitions and externalizing problems as important targets that anti-bullying programs should address to stop the transition from victims of bullying to perpetrators.

Changes in gamma-aminobutyric acid and somatostatin in epileptic cortex associated with low-grade gliomas

1992 ◽  
Vol 77 (2) ◽  
pp. 209-216 ◽  
Author(s):  
Michael M. Haglund ◽  
Mitchel S. Berger ◽  
Dennis D. Kunkel ◽  
JoAnn E. Franck ◽  
Saadi Ghatan ◽  
...  
Keyword(s):  
Epileptiform Activity ◽  
Aminobutyric Acid ◽  
Low Grade ◽  
Tumor Infiltration ◽  
Gamma Aminobutyric Acid ◽  
Content Type ◽  
Low Grade Gliomas ◽  
Neuronal Populations ◽  
Significant Difference

✓ The role of specific neuronal populations in epileptic foci was studied by comparing epileptic and nonepileptic cortex removed from patients with low-grade gliomas. Epileptic and nearby (within 1 to 2 cm) nonepileptic temporal lobe neocortex was identified using electrocorticography. Cortical specimens taken from four patients identified as epileptic and nonepileptic were all void of tumor infiltration. Somatostatin- and γ-aminobutyric acid (GABAergic)-immunoreactive neurons were identified and counted. Although there was no significant difference in the overall cell count, the authors found a significant decrease in both somatostatin- and GABAergic-immunoreactive neurons (74% and 51 %, respectively) in the epileptic cortex compared to that in nonepileptic cortex from the same patient. It is suggested that these findings demonstrate changes in neuronal subpopulations that may account for the onset and propagation of epileptiform activity in patients with low-grade gliomas.

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