Journal of Neurophysiology

Alkan, Yelda; Morris, Alanna; Bisley, James W.

doi: 10.1152/jn.00022.2026pmid: 42053501

Maintaining stable perception amidst dynamic visual input driven by eye movements is a remarkable feat of the brain. One proposed mechanism underlying this phenomenon is receptive field remapping in the lateral intraparietal area (LIP), in which neurons predictively update their receptive fields to compensate for eye movements. Models of remapping have suggested that the underlying mechanism may involve either a wave of activity or a single jump in activity. To test these competing hypotheses, we investigated the timing of remapping as a function of saccade length. We predicted that if remapping occurs through a jump, the remapped response will align more closely with saccade onset, independent of saccade length. Alternatively, if remapping involves a wave moving over time, we predicted that the remapped response will occur later for longer saccades when aligned by saccade onset. We recorded the activity of single LIP neurons and multi-unit activity in animals performing a saccade task in which a probe appeared in the post-saccadic receptive field before a 7, 14 or 21 deg saccade. We found that responses to single neurons and to multi-units were all consistent with the wave hypothesis. Surprisingly, we also found that remapping responses starting before the saccade only occurred in conditions in which the probe was presented within the classical receptive field. These findings bring into question whether pre-saccadic remapped responses are a fundamental feature of LIP remapping and support the idea that the mechanism underlying remapping is driven by a wave of activity rather than a jump.

Lipton, Megan H.; Park, Seungbin; Dadarlat, Maria C.

doi: 10.1152/jn.00005.2026pmid: 42096295

Somatosensation constructs the body’s dynamic sense of state and allows for dexterous and precise movements. Encoding somatosensation via similar computational principles as motor commands would provide a simple and direct mechanism for sensorimotor integration. Here, we tested the hypothesis that neural encoding of somatosensory information from the limbs shares the known structure of motor commands, including: low dimensionality, encoding of specific kinematic variables during limb movements, orthogonal representations of bilateral limbs, and conserved representations across animals. To address this question, we used 2-photon imaging to record the activity of thousands of neurons in layers 2/3 of sensorimotor cortex of eight anesthetized mice during passive single-limb deflection. We additionally analyzed responses to passive single limb movements in eight awake mice, sourced from an open dataset. In both datasets, we computed the principal components of the neural population to overcome the heterogeneous responses of single neurons. In support of our hypothesis, we found that a small fraction of principal components explained a large fraction of response variance. These low-dimensional representations of limb movements were well conserved across animals, including the orthogonal representations of ipsilateral and contralateral limbs. Finally, neural populations encoded information about endpoints of limb movements in addition to dynamic changes in joint angles during movements. Together, these results demonstrate that population-level encoding of somatosensory information in mouse sensorimotor cortex is structured to facilitate sensorimotor integration across the brain.

Kalc, Miloš ; Holobar, Aleš; Kramberger, Matej; Murks, Nina; Škarabot, Jakob

doi: 10.1152/jn.00031.2026pmid: 42065627

This study investigated the spinal neural mechanisms underlying post-activation potentiation in ten healthy young males (21.9 ± 4.8 years). Participants performed a 10-second maximal isometric plantarflexion, after which we measured twitch torque and assessed spinal excitability using the soleus H-reflex, D1 presynaptic inhibition and heteronymous Ia facilitation (HF). High-density surface EMG was decomposed to track single motor unit responses. The conditioning contraction increased twitch torque by 12.2 Nm (p < 0.001) immediately and returning to baseline within nine minutes. This mechanical potentiation was accompanied by a 29% reduction in H-reflex amplitude (p < 0.001), which recovered within three minutes. Paradoxically, neurophysiological indices of presynaptic inhibition, D1 and HF were significantly increased (D1: p<0.017; HF: p<0.001), resulting in spinal facilitation. Single MU analysis revealed increased discharge probability, particularly in higher-threshold units indicating overall spinal facilitation. These results demonstrate that post-activation potentiation involves a complex dissociation: H-reflex pathway inhibition along with facilitation of presynaptic spinal mechanisms. This paradox can be explained by either post-activation depression (caused by depletion of neurotransmitter at the Ia–motoneuron synapse) or muscle thixotropy, a contraction history-dependent decrease in muscle spindle sensitivity, which reduces the efficacy of the Ia afferent volley independently of spinal inhibitory mechanisms. Our findings highlight a dissociation between spinal presynaptic facilitation and the decreased H-reflex, underscoring the need for future studies to explicitly test the roles of post-activation depression and muscle thixotropy after conditioning contractions.