How to not induce SNAs: The insufficiency of directional force.

People respond faster to smaller numbers in their left space and to larger numbers in their right space. Here we argue that movements in space contribute to the formation of spatial-numerical associations (SNAs). We studied the impact of continuous isometric forces along the horizontal or vertical cardinal axes on SNAs while participants performed random number production and arithmetic verification tasks. Our results suggest that such isometric directional force do not suffice to induce SNAs.

Spatial-numerical associations without a motor response? Grip force says 'Yes'.

In numerical processing, the functional role of Spatial-Numerical Associations (SNAs, such as the association of smaller numbers with left space and larger numbers with right space, the Mental Number Line hypothesis) is debated. Most studies demonstrate SNAs with lateralized responses, and there is little evidence that SNAs appear when no response is required. We recorded passive holding grip forces in no-go trials during number processing. In Experiment 1, participants performed a surface numerical decision task ("Is it a number or a letter?"). In Experiment 2, we used a deeper semantic task ("Is this number larger or smaller than five?"). Despite instruction to keep their grip force constant, participants' spontaneous grip force changed in both experiments: Smaller numbers led to larger force increase in the left than in the right hand in the numerical decision task (500-700 ms after stimulus onset). In the semantic task, smaller numbers again led to larger force increase in the left hand, and larger numbers increased the right-hand holding force. This effect appeared earlier (180 ms) and lasted longer (until 580 ms after stimulus onset). This is the first demonstration of SNAs with passive holding force. Our result suggests that (1) explicit motor response is not a prerequisite for SNAs to appear, and (2) the timing and strength of SNAs are task-dependent. (216 words).

Spatial-numerical associations in the presence of an avatar.

When we interact with other people or avatars, they often provide an alternative spatial frame of reference compared to our own. Previous studies introduced avatars into stimulus-response compatibility tasks and demonstrated compatibility effects as if the participant was viewing the task from the avatar's point of view. However, the origin of this effect of perspective taking remained unclear. To distinguish changes in stimulus coding from changes in response coding, caused by the avatar, two experiments were conducted that combined a SNARC task and a spontaneous visual perspective taking task to specify the role of response coding. We observed compatibility effects that were based on the avatar's perspective rather than the participants' own. Because number magnitude was independent of the avatar's perspective, the observed changes in compatibility caused by different perspectives indicate changes in response coding. These changes in response coding are only significant when they are accompanied by visual action effects.

TRPC1 regulates fMLP-stimulated migration and chemotaxis of neutrophil granulocytes.

Neutrophils form the first line of defense of the innate immune system and are rapidly recruited by chemotactic signals to sites of inflammation. Understanding the mechanisms of neutrophil chemotaxis is therefore of great interest for the potential development of new immunoregulatory therapies. It has been shown that members of the transient receptor potential (TRP) family of cation channels are involved in both cell migration and chemotaxis. In this study, we demonstrate that TRPC1 channels play an important role in fMLP mediated chemotaxis and migration of murine neutrophils. The knock-out of TRPC1 channels leads to an impaired migration, transmigration and chemotaxis of the neutrophils. In contrast, Ca²âº influx but not store release after activation of the TRPC1(-/-) neutrophils with fMLP is strongly enhanced. We show that the enhanced Ca²âº influx in the TRPC1(-/-) neutrophils is associated with a steepened front to rear gradient of the intracellular Ca²âº concentration with higher levels at the cell rear. Taken together, this paper highlights a distinct role of TRPC1 in neutrophil migration and chemotaxis. We propose that TRPC1 controls the activity of further Ca²âº influx channels and thus regulates the maintenance of intracellular Ca²âº gradients which are critical for cell migration. This article is part of a Special Issue entitled: 13th European Symposium on Calcium.

TRP channels and STIM/ORAI proteins: sensors and effectors of cancer and stroma cell migration.

UNLABELLED: Cancer cells are strongly influenced by host cells within the tumour stroma and vice versa. This leads to the development of a tumour microenvironment with distinct physical and chemical properties that are permissive for tumour progression. The ability to migrate plays a central role in this mutual interaction. Migration of cancer cells is considered as a prerequisite for tumour metastasis and the migration of host stromal cells is required for reaching the tumour site. Increasing evidence suggests that transient receptor potential (TRP) channels and STIM/ORAI proteins affect key calcium-dependent mechanisms implicated in both cancer and stroma cell migration. These include, among others, cytoskeletal remodelling, growth factor/cytokine signalling and production, and adaptation to tumour microenvironmental properties such as hypoxia and oxidative stress. In this review, we will summarize the current knowledge regarding TRP channels and STIM/ORAI proteins in cancer and stroma cell migration. We focus on how TRP channel or STIM/ORAI-mediated Ca(2+) signalling directly or indirectly influences cancer and stroma cell migration by affecting the above listed mechanisms. LINKED ARTICLES: This article is part of a themed section on Cytoskeleton, Extracellular Matrix, Cell Migration, Wound Healing and Related Topics. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2014.171.issue-24.