Biology subjects

Nandakumar, B.

Publications and source records attributed to Nandakumar, B..

6 recordsLinked to original sources

bioRxiv2026

Ultra-high-efficacy Wireless Neuromodulation Using a Conductive Ring Interface

An ab-initio physics study, supported with a COMSOL-based numerical simulation, presents a concept to enable wearable, highly targeted, and ultra-high-efficacy neuromodulation. A target site is defined by a relatively small gap of a miniaturized ring-shaped conductive interface implant. If the implant conductivity significantly exceeds the conductivity of the biological tissue, a highly localized electromotive force (emf) is induced in the ring upon application of an alternating current (AC) magnetic field. This emf generates an electric field in the gap, inducing local neural stimulation of the targeted site, e.g., translated to a nerve segment using circumferential cuffs. The wirelessly controlled autonomous stimulator implant acts as a low-resistance nearly-closed path to generate a highly localized electric field on the order of 50 V/m in the gap via application of a 1-kA/m AC magnetic field at a frequency of 10 kHz. The magnetic field is at least three orders of magnitude smaller than the magnetic field required to generate the same electric field strength via conventional transcranial magnetic stimulation. Therefore, this high-resolution, orientation-specific ring neuromodulation system could enable a highly localized, energy-efficient wearable device with significant preclinical and clinical potential.

bioengineering↗

bioRxiv2026

Spontaneous eye behavior is an objective marker of parkinsonian severity

Eye behavior disruption is reported in Parkinson's disease (PD), but its correlation with disease severity has not been well examined. Here, in a nonhuman primate model of PD, we show that spontaneous eye behavior is impaired in parkinsonism and correlates with clinical rating scores and subthalamic beta oscillatory activity. These findings suggest that spontaneous eye behavior could serve as an objective, non-invasive biomarker of parkinsonian severity.

neuroscience↗

bioRxiv2025

Sleep firing rate homeostasis is disrupted in mild parkinsonism

Sleep-associated downscaling of neuronal firing, i.e., firing rate homeostasis (FRH), is essential for restorative sleep. Sleep dysfunction is common in Parkinsons disease (PD), but FRH has not been investigated. Here, using a within-subject design in the nonhuman primate model of PD, we report that thalamocortical FRH is disrupted in parkinsonism. These findings can inform therapeutic approaches tailored towards normalizing FRH to reestablish restorative sleep in PD.

neuroscience↗

bioRxiv2023

Excessive cortical beta oscillations are associated with slow-wave sleep dysfunction in mild parkinsonism

Increasing evidence associates slow-wave sleep (SWS) dysfunction with neurodegeneration. Using a within-subject design in the nonhuman primate model of Parkinsons disease (PD), we found that reduced SWS quantity in mild parkinsonism was accompanied by elevated beta and reduced delta power during SWS in the motor cortex. Our findings support excessive beta oscillations as a mechanism for SWS dysfunction and will inform development of neuromodulation therapies for enhancing SWS in PD.

neuroscience↗

bioRxiv2020

Trunk sensory and motor cortex ispreferentially integrated with hindlimb sensoryinformation that supports trunk stabilization

Sensorimotor integration in the trunk system has been poorly studied despite its importance for examining functional recovery after neurological injury or disease. Here, we mapped the relationship between thoracic dorsal root ganglia and trunk sensory cortex (S1) to create a detailed map of the extent and internal organization of trunk primary sensory cortex, and trunk primary motor cortex (M1) and showed that both cortices are somatotopically complex structures that are larger than previously described. Surprisingly, projections from trunk S1 to trunk M1 were not anatomically organized. We found relatively weak sensorimotor integration between trunk M1 and S1 and between trunk M1 and forelimb S1 compared to extensive integration between trunk M1 and hindlimb S1 and M1. This strong trunk/hindlimb connection was identified for high intensity stimuli that activated proprioceptive pathways. To assess the implication of this integration, the responses in sensorimotor cortex were examined during a postural control task and supported sensorimotor integration between hindlimb sensory and lower trunk motor cortex. Together, these data suggest that trunk M1 is guided predominately by hindlimb proprioceptive information that reached the cortex directly via the thalamus. This unique sensorimotor integration suggests an essential role for the trunk system in postural control, and its consideration could be important for understanding studies regarding recovery of function after spinal cord injury. SignificanceThis work identifies extensive sensorimotor integration between trunk and hindlimb cortices, demonstrating that sensorimotor integration is an operational mode of the trunk cortex in intact animals. The functional role of this integration was demonstrated for postural control when the animal was subjected to lateral tilts. Furthermore, these results provide insight into cortical reorganization after spinal cord injury making clear that sensorimotor integration after SCI is an attempt to restore sensorimotor integration that existed in the intact system. These results could be used to tailor rehabilitative strategies to optimize sensorimotor integration for functional recovery.

neuroscience↗

bioRxiv2020

At-level allodynia after mid-thoracic contusion in the rat

The rat mid-thoracic contusion model has been used to study at-level tactile allodynia after spinal cord injury (SCI), one of the more common types of allodynia. An important advantage of this model is that not all animals develop allodynia and, therefore, it could be used to more clearly examine mechanisms that are strictly related to pain development separately from mechanisms related to the injury itself. However, how to separate those that develop allodynia from those that do not is unclear. The aims of the current study were to identify where allodynia and spasticity develop and use this information to identify metrics that separate animals that develop allodynia from those that do not in order study difference in their behavior. To accomplish these aims, a standardized grid was used to localize pain on the dorsal trunk and map it to thoracic dermatomes, providing for the development of a pain score that relied on supraspinal responses and separated subgroups of animals. Similar to human studies, the development of allodynia often occurred with the development of spasticity or hyperreflexia. Moreover, the time course and prevalence of pain phenotypes (at-, above-, or below level) produced by this model were similar to that observed in humans who have sustained an SCI. However, the amount of spared spinal matter in the injured cord did not explain the development of allodynia, as was previously reported. This approach can be used to study the mechanism underlying the development of allodynia separately from mechanisms related to the injury alone.

physiology↗