Topic
Somatosensory system
About: Somatosensory system is a research topic. Over the lifetime, 6371 publications have been published within this topic receiving 316900 citations.
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TL;DR: Experimental as well as theoretical work in the olfactory cortex and hippocampus suggests that acetylcholine, via the muscarinic receptors, serves to shift the dynamics of the cortical networks into a state where afferent influence predominates over intracortical influence.
101 citations
TL;DR: The ontogeny of 5-HTT and its relationship with serotonin (5-HT) neurons is reported and it is indicated that 5- HTT is associated preferentially with 4-HT neurons in brainstem and expressed in non-5- HT neurons within a specific window, which may affect the development of the systems "borrowing" the 5-ht.
101 citations
TL;DR: It is found that neurons along the lemniscal pathway robustly encode rhythmic whisking on a cycle-by-cycle basis, while encoding along the paralemniscal pathway is relatively poor.
Abstract: Active sensing involves the fusion of internally generated motor events with external sensation. For rodents, active somatosensation includes scanning the immediate environment with the mystacial vibrissae. In doing so, the vibrissae may touch an object at any angle in the whisk cycle. The representation of touch and vibrissa self-motion may in principle be encoded along separate pathways, or share a single pathway, from the periphery to cortex. Past studies established that the spike rates in neurons along the lemniscal pathway from receptors to cortex, which includes the principal trigeminal and ventral-posterior-medial thalamic nuclei, are substantially modulated by touch. In contrast, spike rates along the paralemniscal pathway, which includes the rostral spinal trigeminal interpolaris, posteromedial thalamic, and ventral zona incerta nuclei, are only weakly modulated by touch. Here we find that neurons along the lemniscal pathway robustly encode rhythmic whisking on a cycle-by-cycle basis, while encoding along the paralemniscal pathway is relatively poor. Thus, the representations of both touch and self-motion share one pathway. In fact, some individual neurons carry both signals, so that upstream neurons with a supralinear gain function could, in principle, demodulate these signals to recover the known decoding of touch as a function of vibrissa position in the whisk cycle.
101 citations
TL;DR: It is shown that an internal state of malaise induces plastic reshaping in the GC associated to behavioral shift of the stimulus hedonic value, and it is proposed that the GC not only encodes taste modality, intensity, and memory but extends its integrative properties to process also the stimulushedonicvalue.
Abstract: Primary sensory cortices are remarkably organized in spatial maps according to specific sensory features of the stimuli. These cortical maps can undergo plastic rearrangements after changes in afferent ("bottom-up") sensory inputs such as peripheral lesions or passive sensory experience. However, much less is known about the influence of "top-down" factors on cortical plasticity. Here, we studied the effect of a visceral malaise on taste representations in the gustatory cortex (GC). Using in vivo optical imaging, we showed that inducing conditioned taste aversion (CTA) to a sweet and pleasant stimulus induced plastic rearrangement of its cortical representation, becoming more similar to a bitter and unpleasant taste representation. Using a behavior task, we showed that changes in hedonic perception are directly related to the maps plasticity in the GC. Indeed imaging the animals after CTA extinction indicated that sweet and bitter representations were dissimilar. In conclusion, we showed that an internal state of malaise induces plastic reshaping in the GC associated to behavioral shift of the stimulus hedonic value. We propose that the GC not only encodes taste modality, intensity, and memory but extends its integrative properties to process also the stimulus hedonic value.
101 citations
TL;DR: A subcortical neural circuit is identified from the superior colliculus to the zona incerta that triggers predatory hunting in mice and is specifically engaged in translating sensory cues into neural signals to provoke predatory hunting.
Abstract: Predatory hunting plays a fundamental role in animal survival. Little is known about the neural circuits that convert sensory cues into neural signals to drive this behavior. Here we identified an excitatory subcortical neural circuit from the superior colliculus to the zona incerta that triggers predatory hunting. The superior colliculus neurons that form this pathway integrate motion-related visual and vibrissal somatosensory cues of prey. During hunting, these neurons send out neural signals that are temporally correlated with predatory attacks, but not with feeding after prey capture. Synaptic inactivation of this pathway selectively blocks hunting for prey without impairing other sensory-triggered behaviors. These data reveal a subcortical neural circuit that is specifically engaged in translating sensory cues into neural signals to provoke predatory hunting.
101 citations