scholarly journals Circuits for State-Dependent Modulation of Locomotion

2021 ◽  
Vol 15 ◽  
Author(s):  
Alejandro J. Pernía-Andrade ◽  
Nikolaus Wenger ◽  
Maria S. Esposito ◽  
Philip Tovote
Keyword(s):  
Periaqueductal Gray ◽  
Higher Order ◽  
Postural Adjustment ◽  
Dependent Manner ◽  
Emotional States ◽  
Neural Basis ◽  
Medullary Reticular Formation ◽  
Mesencephalic Locomotor Region ◽  
State Dependent ◽  
Circuit Elements

Brain-wide neural circuits enable bi- and quadrupeds to express adaptive locomotor behaviors in a context- and state-dependent manner, e.g., in response to threats or rewards. These behaviors include dynamic transitions between initiation, maintenance and termination of locomotion. Advances within the last decade have revealed an intricate coordination of these individual locomotion phases by complex interaction of multiple brain circuits. This review provides an overview of the neural basis of state-dependent modulation of locomotion initiation, maintenance and termination, with a focus on insights from circuit-centered studies in rodents. The reviewed evidence indicates that a brain-wide network involving excitatory circuit elements connecting cortex, midbrain and medullary areas appears to be the common substrate for the initiation of locomotion across different higher-order states. Specific network elements within motor cortex and the mesencephalic locomotor region drive the initial postural adjustment and the initiation of locomotion. Microcircuits of the basal ganglia, by implementing action-selection computations, trigger goal-directed locomotion. The initiation of locomotion is regulated by neuromodulatory circuits residing in the basal forebrain, the hypothalamus, and medullary regions such as locus coeruleus. The maintenance of locomotion requires the interaction of an even larger neuronal network involving motor, sensory and associative cortical elements, as well as defined circuits within the superior colliculus, the cerebellum, the periaqueductal gray, the mesencephalic locomotor region and the medullary reticular formation. Finally, locomotor arrest as an important component of defensive emotional states, such as acute anxiety, is mediated via a network of survival circuits involving hypothalamus, amygdala, periaqueductal gray and medullary premotor centers. By moving beyond the organizational principle of functional brain regions, this review promotes a circuit-centered perspective of locomotor regulation by higher-order states, and emphasizes the importance of individual network elements such as cell types and projection pathways. The realization that dysfunction within smaller, identifiable circuit elements can affect the larger network function supports more mechanistic and targeted therapeutic intervention in the treatment of motor network disorders.

Emotional Reactivity to Visual Content as Revealed by ERP Component Clustering

2015 ◽  
Vol 29 (4) ◽  
pp. 135-146 ◽  
Author(s):  
Miroslaw Wyczesany ◽  
Szczepan J. Grzybowski ◽  
Jan Kaiser
Keyword(s):  
Emotional Reactivity ◽  
Brain Activity ◽  
Affective State ◽  
Occipital Lobe ◽  
Stimulus Onset ◽  
Emotional States ◽  
Neural Basis ◽  
Temporoparietal Junction ◽  
The Right ◽  
The Impact

Abstract. In the study, the neural basis of emotional reactivity was investigated. Reactivity was operationalized as the impact of emotional pictures on the self-reported ongoing affective state. It was used to divide the subjects into high- and low-responders groups. Independent sources of brain activity were identified, localized with the DIPFIT method, and clustered across subjects to analyse the visual evoked potentials to affective pictures. Four of the identified clusters revealed effects of reactivity. The earliest two started about 120 ms from the stimulus onset and were located in the occipital lobe and the right temporoparietal junction. Another two with a latency of 200 ms were found in the orbitofrontal and the right dorsolateral cortices. Additionally, differences in pre-stimulus alpha level over the visual cortex were observed between the groups. The attentional modulation of perceptual processes is proposed as an early source of emotional reactivity, which forms an automatic mechanism of affective control. The role of top-down processes in affective appraisal and, finally, the experience of ongoing emotional states is also discussed.

scholarly journals Modulation of High-Voltage Activated Ca2+ Channels in the Rat Periaqueductal Gray Neurons by μ-Type Opioid Agonist

1997 ◽  
Vol 77 (3) ◽  
pp. 1418-1424 ◽  
Author(s):  
Chang-Ju Kim ◽  
Jeong-Seop Rhee ◽  
Norio Akaike
Keyword(s):  
G Proteins ◽  
Opioid Receptor ◽  
High Voltage ◽  
Inhibitory Effect ◽  
Periaqueductal Gray ◽  
Dependent Manner ◽  
Opioid Agonist ◽  
Voltage Clamp Condition ◽  
Voltage Dependent ◽  
Clamp Condition

Kim, Chang-Ju, Jeong-Seop Rhee, and Norio Akaike. Modulation of high-voltage activated Ca2+ channels in the rat periaqueductal gray neurons by μ-type opioid agonist. J. Neurophysiol. 77: 1418–1424, 1997. The effect of μ-type opioid receptor agonist, D-Ala2,N-MePhe4,Gly5-ol-enkephalin (DAMGO), on high-voltage-activated (HVA) Ca2+ channels in the dissociated rat periaqueductal gray (PAG) neurons was investigated by the use of nystatin-perforated patch recording mode under voltage-clamp condition. Among 118 PAG neurons tested, the HVA Ca2+ channels of 38 neurons (32%) were inhibited by DAMGO (DAMGO-sensitive cells), and the other 80 neurons (68%) were not affected by DAMGO (DAMGO-insensitive cells). The N-, P-, L-, Q-, and R-type Ca2+ channel components in DAMGO-insensitive cells shared 26.9, 37.1, 22.3, 7.9, and 5.8%, respectively, of the total Ca2+ channel current. The channel components of DAMGO-sensitive cells were 45.6, 25.7, 21.7, 4.6, and 2.4%, respectively. The HVA Ca2+ current of DAMGO-sensitive neurons was inhibited by DAMGO in a concentration-, time-, and voltage-dependent manner. Application of ω-conotoxin-GVIA occluded the inhibitory effect of DAMGO ∼70%. So, HVA Ca2+ channels inhibited by DAMGO were mainly the N-type Ca2+ channels. The inhibitory effect of DAMGO on HVA Ca2+ channels was prevented almost completely by the pretreatment of pertussis toxin (PTX) for 8–10 h, suggesting that DAMGO modulation on N-type Ca2+ channels in rat PAG neurons is mediated by PTX-sensitive G proteins. These results indicate that μ-type opioid receptor modulates N-type HVA Ca2+ channels via PTX-sensitive G proteins in PAG neurons of rats.

scholarly journals Duality of Complex Systems Built from Higher-Order Elements

Complexity ◽  
2018 ◽  
Vol 2018 ◽  
pp. 1-15 ◽  
Author(s):  
Dalibor Biolek ◽  
Zdeněk Biolek ◽  
Viera Biolková
Keyword(s):  
Nonlinear Systems ◽  
Complex Systems ◽  
Higher Order ◽  
Duality Principle ◽  
Shift Type ◽  
Hardware Emulation ◽  
Classical Duality ◽  
Memristive Circuits ◽  
Circuit Elements

The duality of nonlinear systems built from higher-order two-terminal Chua’s elements and independent voltage and current sources is analyzed. Two different approaches are now being generalized for circuits with higher-order elements: the classical duality principle, hitherto restricted to circuits built from R-C-L elements, and Chua’s duality of memristive circuits. The so-called storeyed structure of fundamental elements is used as an integrating platform of both approaches. It is shown that the combination of associated flip-type and shift-type transformations of the circuit elements can generate dual networks with interesting features. The regularities of the duality can be used for modeling, hardware emulation, or synthesis of systems built from elements that are not commonly available, such as memristors, via classical dual elements.

scholarly journals Neural and genetic degeneracy underlies Caenorhabditis elegans feeding behavior

2014 ◽  
Vol 112 (4) ◽  
pp. 951-961 ◽  
Author(s):  
Nicholas F. Trojanowski ◽  
Olivia Padovan-Merhar ◽  
David M. Raizen ◽  
Christopher Fang-Yen
Keyword(s):  
Caenorhabditis Elegans ◽  
Neural Circuit ◽  
Dependent Manner ◽  
State Dependent ◽  
Excitatory Pathways ◽  
Genetic Mechanisms ◽  
Genetic Level ◽  
Pharyngeal Pumping ◽  
Robust Network

Degenerate networks, in which structurally distinct elements can perform the same function or yield the same output, are ubiquitous in biology. Degeneracy contributes to the robustness and adaptability of networks in varied environmental and evolutionary contexts. However, how degenerate neural networks regulate behavior in vivo is poorly understood, especially at the genetic level. Here, we identify degenerate neural and genetic mechanisms that underlie excitation of the pharynx (feeding organ) in the nematode Caenorhabditis elegans using cell-specific optogenetic excitation and inhibition. We show that the pharyngeal neurons MC, M2, M4, and I1 form multiple direct and indirect excitatory pathways in a robust network for control of pharyngeal pumping. I1 excites pumping via MC and M2 in a state-dependent manner. We identify nicotinic and muscarinic receptors through which the pharyngeal network regulates feeding rate. These results identify two different mechanisms by which degeneracy is manifest in a neural circuit in vivo.

Uncovering Relationships Between Emotional States and Higher-Order Needs

2013 ◽  
Vol 3 (1) ◽  
pp. 31-46 ◽  
Author(s):  
Andrew Pressey ◽  
Laura Salciuviene ◽  
Stuart Barnes
Keyword(s):  
Survey Data ◽  
Virtual Worlds ◽  
Second Life ◽  
Emotional State ◽  
Higher Order ◽  
Emotional States ◽  
Emotional Experiences ◽  
Informed Decisions ◽  
Computer Mediated ◽  
Self Actualization

The purpose of the study is to examine the effects of emotional states on higher-order need attainment in the computer-mediated environment. A survey data were collected from 404 adult visitors within the Second Life of virtual worlds. The findings suggest that the emotional states exert significant effects on attainment of higher-order needs (i.e. belongingness, esteem and self-actualization); the flow emotional state exerts a greater effect on attaining higher-order needs than the remaining emotional states of anxiety, confusion and apathy. Companies with presence in the Second Life of virtual worlds will be able to make more informed decisions when directing their efforts to enhance visitors’ emotional experiences in their virtual islands.

scholarly journals Uncoupling Sensation and Perception in Human Time Processing

2020 ◽  
Vol 32 (7) ◽  
pp. 1369-1380 ◽  
Author(s):  
Nicola Binetti ◽  
Alessandro Tomassini ◽  
Karl Friston ◽  
Sven Bestmann
Keyword(s):  
Constant Velocity ◽  
Subjective Experience ◽  
Brain Activity ◽  
Posterior Cingulate Cortex ◽  
Higher Order ◽  
Neural Basis ◽  
Subjective Duration ◽  
Msec Duration ◽  
Sensory Cortices ◽  
Higher Visual Areas

Timing emerges from a hierarchy of computations ranging from early encoding of physical duration (time sensation) to abstract time representations (time perception) suitable for storage and decisional processes. However, the neural basis of the perceptual experience of time remains elusive. To address this, we dissociate brain activity uniquely related to lower-level sensory and higher-order perceptual timing operations, using event-related fMRI. Participants compared subsecond (500 msec) sinusoidal gratings drifting with constant velocity (standard) against two probe stimuli: (1) control gratings drifting at constant velocity or (2) accelerating gratings, which induced illusory shortening of time. We tested two probe intervals: a 500-msec duration (Short) and a longer duration required for an accelerating probe to be perceived as long as the standard (Long—individually determined). On each trial, participants classified the probe as shorter or longer than the standard. This allowed for comparison of trials with an “Objective” (physical) or “Subjective” (perceived) difference in duration, based on participant classifications. Objective duration revealed responses in bilateral early extrastriate areas, extending to higher visual areas in the fusiform gyrus (at more lenient thresholds). By contrast, Subjective duration was reflected by distributed responses in a cortical/subcortical areas. This comprised the left superior frontal gyrus and the left cerebellum, and a wider set of common timing areas including the BG, parietal cortex, and posterior cingulate cortex. These results suggest two functionally independent timing stages: early extraction of duration information in sensory cortices and Subjective experience of duration in a higher-order cortical–subcortical timing areas.

Inhibition by Imipramine of the Voltage-Dependent K+ Channel in Rabbit Coronary Arterial Smooth Muscle Cells

2020 ◽  
Vol 178 (2) ◽  
pp. 302-310
Author(s):  
Jin Ryeol An ◽  
Mi Seon Seo ◽  
Hee Seok Jung ◽  
Ryeon Heo ◽  
Minji Kang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Dependent Manner ◽  
Arterial Smooth Muscle ◽  
Closed State ◽  
Kv Channels ◽  
State Dependent ◽  
Voltage Dependent ◽  
Arterial Smooth Muscle Cells

Abstract Imipramine, a tricyclic antidepressant, is used in the treatment of depressive disorders. However, the effect of imipramine on vascular ion channels is unclear. Therefore, using a patch-clamp technique we examined the effect of imipramine on voltage-dependent K+ (Kv) channels in freshly isolated rabbit coronary arterial smooth muscle cells. Kv channels were inhibited by imipramine in a concentration-dependent manner, with an IC50 value of 5.55 ± 1.24 µM and a Hill coefficient of 0.73 ± 0.1. Application of imipramine shifted the steady-state activation curve in the positive direction, indicating that imipramine-induced inhibition of Kv channels was mediated by influencing the voltage sensors of the channels. The recovery time constants from Kv-channel inactivation were increased in the presence of imipramine. Furthermore, the application of train pulses (of 1 or 2 Hz) progressively augmented the imipramine-induced inhibition of Kv channels, suggesting that the inhibitory effect of imipramine is use (state) dependent. The magnitude of Kv current inhibition by imipramine was similar during the first, second, and third depolarizing pulses. These results indicate that imipramine-induced inhibition of Kv channels mainly occurs in the closed state. The imipramine-mediated inhibition of Kv channels was associated with the Kv1.5 channel, not the Kv2.1 or Kv7 channel. Inhibition of Kv channels by imipramine caused vasoconstriction. From these results, we conclude that imipramine inhibits vascular Kv channels in a concentration- and use (closed-state)-dependent manner by changing their gating properties regardless of its own function.

scholarly journals Glucose-6-Phosphate Dehydrogenase of Trypanosomatids: Characterization, Target Validation, and Drug Discovery

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Shreedhara Gupta ◽  
Mariana Igoillo-Esteve ◽  
Paul A. M. Michels ◽  
Artur T. Cordeiro
Keyword(s):  
Oxidative Stress ◽  
Enzyme Activity ◽  
Trypanosoma Brucei ◽  
Redox State ◽  
Chemotherapeutic Agents ◽  
Dependent Manner ◽  
Target Validation ◽  
Leishmania Mexicana ◽  
State Dependent ◽  
Glucose 6 Phosphate Dehydrogenase

In trypanosomatids, glucose-6-phosphate dehydrogenase (G6PDH), the first enzyme of the pentosephosphate pathway, is essential for the defense of the parasite against oxidative stress. Trypanosoma brucei, Trypanosoma cruzi, and Leishmania mexicana G6PDHs have been characterized. The parasites' G6PDHs contain a unique 37 amino acid long N-terminal extension that in T. cruzi seems to regulate the enzyme activity in a redox-state-dependent manner. T. brucei and T. cruzi G6PDHs, but not their Leishmania spp. counterpart, are inhibited, in an uncompetitive way, by steroids such as dehydroepiandrosterone and derivatives. The Trypanosoma enzymes are more susceptible to inhibition by these compounds than the human G6PDH. The steroids also effectively kill cultured trypanosomes but not Leishmania and are presently considered as promising leads for the development of new parasite-selective chemotherapeutic agents.

Protriptyline, a tricyclic antidepressant, inhibits voltage-dependent K+ channels in rabbit coronary arterial smooth muscle cells

2020 ◽  
Vol 52 (3) ◽  
pp. 320-327 ◽  
Author(s):  
Jin Ryeol An ◽  
Hojung Kang ◽  
Hongliang Li ◽  
Mi Seon Seo ◽  
Hee Seok Jung ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Steady State ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Tricyclic Antidepressant ◽  
Dependent Manner ◽  
Kv Channels ◽  
State Dependent ◽  
Voltage Dependent ◽  
Arterial Smooth Muscle Cells

Abstract In this study, we explore the inhibitory effects of protriptyline, a tricyclic antidepressant drug, on voltage-dependent K+ (Kv) channels of rabbit coronary arterial smooth muscle cells using a whole-cell patch clamp technique. Protriptyline inhibited the vascular Kv current in a concentration-dependent manner, with an IC50 value of 5.05 ± 0.97 μM and a Hill coefficient of 0.73 ± 0.04. Protriptyline did not affect the steady-state activation kinetics. However, the drug shifted the steady-state inactivation curve to the left, suggesting that protriptyline inhibited the Kv channels by changing their voltage sensitivity. Application of 20 repetitive train pulses (1 or 2 Hz) progressively increased the protriptyline-induced inhibition of the Kv current, suggesting that protriptyline inhibited Kv channels in a use (state)-dependent manner. The extent of Kv current inhibition by protriptyline was similar during the first, second, and third step pulses. These results suggest that protriptyline-induced inhibition of the Kv current mainly occurs principally in the closed state. The increase in the inactivation recovery time constant in the presence of protriptyline also supported use (state)-dependent inhibition of Kv channels by the drug. In the presence of the Kv1.5 inhibitor, protriptyline did not induce further inhibition of the Kv channels. However, pretreatment with a Kv2.1 or Kv7 inhibitor induced further inhibition of Kv current to a similar extent to that observed with protriptyline alone. Thus, we conclude that protriptyline inhibits the vascular Kv channels in a concentration- and use-dependent manner by changing their gating properties. Furthermore, protriptyline-induced inhibition of Kv channels mainly involves the Kv1.5.

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