Tickle fetishism: pleasure beyond playfulness.

Tickling is commonly perceived as juvenile play associated with laughter. However, its potential connection to adult sexual behavior has largely remained unexplored. Our online survey, primarily distributed among individuals interested in tickle fetishism, explored tickling and its association with sexual behavior. Ticklishness types, tools, preferred body parts, and partner preferences, were examined. Results revealed diverse patterns of ticklishness changes over time and distinct body-part preferences for different types of tickling. Childhood experiences and exposure to tickling content in television were found to shape individuals' affinity for tickle fetishism. A quarter of respondents reported experiencing orgasms exclusively from tickling, while around 88% expressed sexual satisfaction through tickling alone, indicating its sufficiency as a sexual stimulus among fetishists. Tickling desire decreased after orgasm, indicating an association between tickling and sexual activity. Moreover, ticklishness degree predicted preferences for being tickled rather than tickling others. Exploratory factor analysis identified three factors underlying tickling and sexual experiences: enjoyment and frequency of tickling during sexual activity; preference for intense sexual experiences; age of becoming sexually active. In conclusion, this study provides unique insights into tickling and its connections to sexual context, enhancing our understanding of diverse human sexual behavior and tickle fetishism as a distinct preference.

Protocol for precise signal synchronization of electrophysiology, videography, and audio recordings using a custom-made pulse generator.

Precise signal synchronization is vital for accurate analysis in systems neuroscience. Here, we present a protocol for synchronizing electrophysiology, videography, and audio recordings using a custom-made pulse generator. We describe steps for building the pulse generator, installing software, connecting devices, and running experimental sessions. We then detail signal analysis, temporal alignment, and duration normalization. This protocol offers flexibility and cost-effectiveness, addressing limited shared knowledge and providing a solution for signal synchronization in various experimental setups.

Tickle contagion in the rat somatosensory cortex.

The cellular mechanisms of emotional contagion are unknown. We investigated tickle contagion and the underlying neuronal representations in playful rats. We recorded trunk somatosensory cortex activity of observer rats while they received tickling and audiovisual playback of tickling footage and while they witnessed tickling of demonstrator rats. Observers vocalized and showed "Freudensprünge" ("joy jumps") during witnessing live tickling, while they showed little behavioral responses to playbacks. Deep layers in the trunk somatosensory neurons showed a larger correlation between direct and witnessed tickling responses compared to superficial layers. Trunk somatosensory neurons discharged upon emission of own and demonstrator's vocalizations and might drive contagious "laughter". We conclude that trunk somatosensory cortex might represent ticklishness contagion.

The human tickle response and mechanisms of self-tickle suppression.

A tickle is a complex sensation: it occurs in response to touch but not unequivocally so, and makes us laugh albeit not when we self-tickle. We quantified human ticklishness by means of physiological, visual and acoustic measures alongside subjective reports, and assessed mechanisms of self-tickle suppression. Tickle responses arose faster than previously reported as changes in thoracic circumference and joyous facial expressions co-emerge approximately 300 ms after tickle onset and are followed by vocalizations starting after an additional 200 ms. The timing and acoustic properties of vocalizations tightly correlated with subjective reports: the faster, louder and higher-pitched participants laughed, the stronger they rated the experienced ticklishness. Externally evoked ticklishness is reduced by simultaneous self-tickling, whereby self-touch evokes stronger suppression than sole self-tickle movement without touch. We suggest that self-tickle suppression can be understood as broad attenuation of sensory temporally coincident inputs. Our study provides new insight on the nature of human ticklishness and the attenuating effects of self-tickling. This article is part of the theme issue 'Cracking the laugh code: laughter through the lens of biology, psychology and neuroscience'.

Behavioral and Cortical Correlates of Self-Suppression, Anticipation, and Ambivalence in Rat Tickling.

The relationship between tickling, sensation, and laughter is complex. Tickling or its mere anticipation makes us laugh, but not when we self-tickle. We previously showed rat somatosensory cortex drives tickling-evoked vocalizations and now investigated self-tickle suppression and tickle anticipation. We recorded somatosensory cortex activity while tickling and touching rats and while rats touched themselves. Allo-touch and tickling evoked somatotopic cortical excitation and vocalizations. Self-touch induced wide-ranging inhibition and vocalization suppression. Self-touch also suppressed vocalizations and cortical responses evoked by allo-touch or cortical microstimulation. We suggest a global-inhibition model of self-tickle suppression, which operates without the classically assumed self versus other distinction. Consistent with this inhibition hypothesis, blocking cortical inhibition with gabazine abolished self-tickle suppression. We studied anticipation in a nose-poke-for-tickling paradigm. Although rats nose poked for tickling, they also showed escaping, freezing, and alarm calls. Such ambivalence ("Nervenkitzel") resembles tickle behaviors in children. We conclude that self-touch-induced GABAergic cortical inhibition prevents self-tickle, whereas anticipatory layer 5 activity drives anticipatory laughter. VIDEO ABSTRACT.

Rab27a GTPase modulates L-type Ca2+ channel function via interaction with the II-III linker of CaV1.3 subunit.

In a variety of cells, secretory processes require the activation of both Rab27a and L-type channels of the Ca(V)1.3 subtype. In the retinal pigment epithelium (RPE), Rab27a and Ca(V)1.3 channels regulate growth-factor secretion towards its basolateral side. Analysis of murine retina sections revealed a co-localization of both Rab27a and Ca(V)1.3 at the basolateral membrane of the RPE. Heterologously expressed Ca(V)1.3/ß3/α2δ1 channels showed negatively shifted voltage-dependence and decreased current density of about 70% when co-expressed with Rab27a. However, co-localization analysis using α(5)ß(1) integrin as a membrane marker revealed that Rab27a co-expression reduced the surface expression of Ca(V)1.3 only about 10%. Physical binding of heterologously expressed Rab27a with Ca(V)1.3 channels was shown by co-localization in immunocytochemistry as well as co-immunoprecipitation which was abolished after deletion of a MyRIP-homologous amino acid sequence at the II-III linker of the Ca(V)1.3 subunit. Rab27a over-expression in ARPE-19 cells positively shifted the voltage dependence, decreased current density of endogenous Ca(V)1.3 channels and reduced VEGF-A secretion. We show the first evidence of a direct functional modulation of an ion channel by Rab27a suggesting a new mechanism of Rab and ion channel interaction in the control of VEGF-A secretion in the RPE.

Munc13-3 superprimes synaptic vesicles at granule cell-to-basket cell synapses in the mouse cerebellum.

Munc13-3 is a presynaptic protein implicated in vesicle priming that is strongly expressed in cerebellar granule cells (GCs). Mice deficient of Munc13-3 (Munc13-3(-/-)) show an increased paired-pulse ratio (PPR), which led to the hypothesis that Munc13-3 increases the release probability (pr) of vesicles. In the present study, we analyzed unitary synaptic connections between GCs and basket cells in acute cerebellar slices from wild-type and Munc13-3(-/-) mice. Unitary EPSCs recorded from Munc13-3(-/-) GCs showed normal kinetics and synaptic latency but a significantly increased PPR and fraction of synaptic failures. A quantal analysis revealed that neither the charge of single quanta nor the binominal parameter N were affected by loss of Munc13-3 but that pr was almost halved in Munc13-3(-/-). Neither presynaptic Ca(2+) influx was affected by deletion of Munc13-3 nor replenishment of the readily releasable vesicle pool. However, a high concentration of EGTA led to a reduction in EPSCs that was significantly stronger in Munc13-3(-/-). We conclude that Munc13-3 is responsible for an additional step of molecular and/or positional "superpriming" that substantially increases the efficacy of Ca(2+)-triggered release.

Nanodomain coupling at an excitatory cortical synapse.

The coupling distance between presynaptic Ca(2+) influx and the sensor for vesicular transmitter release determines speed and reliability of synaptic transmission. Nanodomain coupling (<100 nm) favors fidelity and is employed by synapses specialized for escape reflexes and by inhibitory synapses involved in synchronizing fast network oscillations. Cortical glutamatergic synapses seem to forgo the benefits of tight coupling, yet quantitative detail is lacking. The reduced transmission fidelity of loose coupling, however, raises the question whether it is indeed a general characteristic of cortical synapses. Here we analyzed excitatory parallel fiber to Purkinje cell synapses, major processing sites for sensory information and well suited for analysis because they typically harbor only a single active zone. We quantified the coupling distance by combining multiprobability fluctuation analyses, presynaptic Ca(2+) imaging, and reaction-diffusion simulations in wild-type and calretinin-deficient mice. We found a coupling distance of <30 nm at these synapses, much shorter than at any other glutamatergic cortical synapse investigated to date. Our results suggest that nanodomain coupling is a general characteristic of conventional cortical synapses involved in high-frequency transmission, allowing for dense gray matter packing and cost-effective neurotransmission.