Striatal selection in context

A year in research · 21 selected publications · five research threads

In 2014, we connected the microstructure and chemistry of the striatum to the way people select, monitor and adapt actions under changing demands.

The year's findings made action cascading a bridge between computational models, human neurophysiology and clinically informative variation.

01 · STRIATAL MECHANISMS

Action selection depends on microcircuit dynamics

A computational model distinguished transient from steady-state selection in striatal microcircuits and showed how Huntington-like changes could impair one while enhancing the other.[1] Patient data and modelling similarly identified a sensitivity threshold at which striatal dysfunction switches from enhanced to impaired response selection.[2]

Benign hereditary chorea provided a human model of medium-spiny-neuron dysfunction: error-related signals and subsequent behavioural adaptation were selectively reduced.[3] Presaccadic EEG potentials in premanifest Huntington's disease also changed longitudinally, offering a sensitive view of early control alterations.[4]

In plain terms: Striatal disease can produce both gains and losses because transient selection, sustained selection and error adaptation rely on different microcircuit properties.

02 · NEUROCHEMISTRY AND GENES

Biology biases the strategy used for multiple actions

D1- and D2-receptor genotypes shifted action cascading toward more serial or more parallel goal activation.[5] Variation in the neuropeptide Y2 receptor affected response selection and the preferred cascading mode, while a related study linked the same receptor system to the decay of iconic memory.[6,7]

In pilot trainees, efficient cascading was supported by intensified attentional gating and related to striatal GABA and glutamate-related concentrations.[8] These studies joined genetic and neurochemical variation to concrete information-processing strategies.

In plain terms: Neuromodulatory differences change how goals are organized and how long sensory information remains available.

03 · CONTEXT AND STATE

Stress, expectation and immune state target specific stages

Stress increased demands on response selection during action cascading without broadly changing attention or resource allocation.[9] Expectations influenced attentional or inhibitory networks depending on whether consecutive responses were compatible, while leaving conflict monitoring itself unchanged.[10] Binge drinking also produced a specific rather than global change in cascading.[11]

Neurosarcoidosis altered control in relation to inflammatory cytokines without evidence of general cognitive decline.[12] Latent toxoplasmosis delayed attentional allocation in older adults but was associated with faster action cascading in young adults, demonstrating an age- and context-dependent biological effect.[13,14]

In plain terms: State factors act selectively, and the same biological exposure may have different consequences across age and task context.

04 · MONITORING AND MEMORY

Errors and memories are distributed across systems

Cross-modal EEG-fMRI analysis showed that theta oscillations best predicted error-related activity in distinct parts of a distributed monitoring network.[15] Motor efference copies and proprioceptive spatial information were processed asymmetrically and partly independently across hemispheres.[16]

Olfactory memory combined modality-specific frontotemporal encoding with a supramodal maintenance system.[17] These results separated the origin, representation and maintenance of information that later guides action.

In plain terms: Monitoring and memory depend on distributed systems in which different signals preserve different aspects of an event.

05 · INDIVIDUAL TRAJECTORIES

Development and performance reflect multiple routes

Individual overlap between task goals mapped linearly onto frontoparietal electrophysiology.[18] Late-middle-aged adults showed dual-task costs at several processing stages, especially when complexity rose.[19] A review of language lateralization and handedness argued for partly shared but substantially independent developmental influences.[20]

A longitudinal breath test study indicated progressive hepatic mitochondrial dysfunction before Huntington's disease became manifest, widening the biological context in which brain changes develop.[21]

In plain terms: Action-control phenotypes emerge from multiple developmental and biological pathways rather than one continuum of ability.

What 2014 added up to

The 2014 research linked striatal microcircuits, neuromodulators and distributed cortical systems to everyday selection between actions. Its central message was that context determines which biological difference becomes behaviourally relevant.

Selected publications

Curated from PubMed records returned for Beste C[au] in 2014. Citation numbers in the story link to entries below. DOI links open the publisher landing page; PubMed links open the indexed record.

1. Transient and steady-state selection in the striatal microcircuit.

Tomkins A, Vasilaki E, Beste C, Gurney K, Humphries MD. Frontiers in computational neuroscience. 2014;7:192.

DOI: 10.3389/fncom.2013.00192   ·   PubMed

2. Striatal disorders dissociate mechanisms of enhanced and impaired response selection - Evidence from cognitive neurophysiology and computational modelling.

Beste C, Humphries M, Saft C. NeuroImage. Clinical. 2014;4:623-34.

DOI: 10.1016/j.nicl.2014.04.003   ·   PubMed

3. Benign hereditary chorea as an experimental model to investigate the role of medium spiny neurons for response adaptation.

Beste C, Saft C. Neuropsychologia. 2014;59:124-9.

DOI: 10.1016/j.neuropsychologia.2014.05.004   ·   PubMed

4. Changes in cognitive control in pre-manifest Huntington's disease examined using pre-saccadic EEG potentials - a longitudinal study.

Ness V, Bestgen AK, Saft C, Beste C. Journal of Huntington's disease. 2014;3(1):33-43.

DOI: 10.3233/JHD-130086   ·   PubMed

5. DRD1 and DRD2 genotypes modulate processing modes of goal activation processes during action cascading.

Stock AK, Arning L, Epplen JT, Beste C. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2014;34(15):5335-41.

DOI: 10.1523/JNEUROSCI.5140-13.2014   ·   PubMed

6. On the relevance of the NPY2-receptor variation for modes of action cascading processes.

Beste C, Stock AK, Epplen JT, Arning L. NeuroImage. 2014;102 Pt 2:558-64.

DOI: 10.1016/j.neuroimage.2014.08.026   ·   PubMed

7. NPY2-receptor variation modulates iconic memory processes.

Arning L, Stock AK, Kloster E, Epplen JT, Beste C. European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology. 2014;24(8):1298-302.

DOI: 10.1016/j.euroneuro.2014.03.003   ·   PubMed

8. Feeling safe in the plane: neural mechanisms underlying superior action control in airplane pilot trainees--a combined EEG/MRS study.

Yildiz A, Quetscher C, Dharmadhikari S, Chmielewski W, et al.. Human brain mapping. 2014;35(10):5040-5051.

DOI: 10.1002/hbm.22530   ·   PubMed

9. Stress intensifies demands on response selection during action cascading processes.

Yildiz A, Wolf OT, Beste C. Psychoneuroendocrinology. 2014;42:178-87.

DOI: 10.1016/j.psyneuen.2014.01.022   ·   PubMed

10. Expectancy effects during response selection modulate attentional selection and inhibitory control networks.

Chmielewski WX, Mückschel M, Roessner V, Beste C. Behavioural brain research. 2014;274:53-61.

DOI: 10.1016/j.bbr.2014.08.006   ·   PubMed

11. Effects of binge drinking on action cascading processes: an EEG study.

Stock AK, Blaszkewicz M, Beste C. Archives of toxicology. 2014;88(2):475-88.

DOI: 10.1007/s00204-013-1109-2   ·   PubMed

12. Modulatory effects of proinflammatory cytokines for action cascading processes - evidence from neurosarcoidosis.

Beste C, Kneiphof J, Woitalla D. Brain, behavior, and immunity. 2014;41:126-33.

DOI: 10.1016/j.bbi.2014.05.005   ·   PubMed

13. Latent Toxoplasma gondii infection leads to deficits in goal-directed behavior in healthy elderly.

Beste C, Getzmann S, Gajewski PD, Golka K, Falkenstein M. Neurobiology of aging. 2014;35(5):1037-44.

DOI: 10.1016/j.neurobiolaging.2013.11.012   ·   PubMed

14. Latent Toxoplasma gondii infection leads to improved action control.

Stock AK, Heintschel von Heinegg E, Köhling HL, Beste C. Brain, behavior, and immunity. 2014;37:103-8.

DOI: 10.1016/j.bbi.2013.11.004   ·   PubMed

15. Crosslinking EEG time-frequency decomposition and fMRI in error monitoring.

Hoffmann S, Labrenz F, Themann M, Wascher E, Beste C. Brain structure & function. 2014;219(2):595-605.

DOI: 10.1007/s00429-013-0521-y   ·   PubMed

16. Lateralization of spatial information processing in response monitoring.

Stock AK, Beste C. Frontiers in psychology. 2014;5:22.

DOI: 10.3389/fpsyg.2014.00022   ·   PubMed

17. Olfactory short-term memory encoding and maintenance - an event-related potential study.

Lenk S, Bluschke A, Beste C, Iannilli E, Rößner V, Hummel T, Bender S. NeuroImage. 2014;98:475-86.

DOI: 10.1016/j.neuroimage.2014.04.083   ·   PubMed

18. Psychophysiological mechanisms of interindividual differences in goal activation modes during action cascading.

Mückschel M, Stock AK, Beste C. Cerebral cortex (New York, N.Y. : 1991). 2014;24(8):2120-9.

DOI: 10.1093/cercor/bht066   ·   PubMed

19. The neural architecture of age-related dual-task interferences.

Chmielewski WX, Yildiz A, Beste C. Frontiers in aging neuroscience. 2014;6:193.

DOI: 10.3389/fnagi.2014.00193   ·   PubMed

20. The ontogenesis of language lateralization and its relation to handedness.

Ocklenburg S, Beste C, Arning L, Peterburs J, Güntürkün O. Neuroscience and biobehavioral reviews. 2014;43:191-8.

DOI: 10.1016/j.neubiorev.2014.04.008   ·   PubMed

21. Progressive hepatic mitochondrial dysfunction in premanifest Huntington's disease.

Hoffmann R, Stüwe SH, Goetze O, Banasch M, et al.. Movement disorders : official journal of the Movement Disorder Society. 2014;29(6):831-4.

DOI: 10.1002/mds.25862   ·   PubMed