Wireless communication using electro-magnetic (EM) fields acts as the backbone for information exchange among wearable devices around the human body. However, for Implanted devices, EM fields incur high amount of absorption in the tissue, while alternative modes of transmission including ultrasound, optical and magneto-electric methods result in large amount of transduction losses due to conversion of one form of energy to another, thereby increasing the overall end-to-end energy loss. To solve the challenge of wireless powering and communication in a brain implant with low end-end channel loss, we present Bi-Phasic Quasistatic Brain Communication (BP-QBC), achieving < 60dB worst-case end-to-end channel loss at a channel length of ~55mm, by using Electro-quasistatic (EQS) Signaling that avoids transduction losses due to no field-modality conversion. BP-QBC utilizes dipole coupling based signal transmission within the brain tissue using differential excitation in the transmitter (TX) and differential signal pick-up at the receiver (RX), while offering ~41X lower power w.r.t. traditional Galvanic Human Body Communication (G-HBC) at a carrier frequency of 1MHz, by blocking any DC current paths through the brain tissue. Since the electrical signal transfer through the human tissue is electro-quasistatic up to several 10’s of MHz range, BP-QBC allows a scalable (bps-10Mbps) duty-cycled uplink (UL) from the implant to an external wearable. The power consumption in the BP-QBC TX is only 0.52 μW at 1Mbps (with 1% duty cycling), which is within the range of harvested power in the downlink (DL) from a wearable hub to an implant through the EQS brain channel, with externally applied electric currents < 1/5th of ICNIRP safety limits. Furthermore, BP-QBC eliminates the need for sub-cranial interrogators/repeaters, as it offers better signal strength due to no field transduction. Such low end-to-end channel loss with high data rates enabled by a completely new modality of brain communication and powering has deep societal and scientific impact in the fields of neurobiological research, brain-machine interfaces, electroceuticals and connected healthcare.
Basal dendrites of layer 5 cortical pyramidal neurons exhibit Na+ and NMDAR spikes, and are uniquely poised to influence somatic output. Nevertheless, due to technical limitations, how multibranch basal dendritic integration shapes action-potential output remains poorly mapped. Here, we combine 3D two-photon holographic transmitter-uncaging, whole-cell dynamic-clamp, and biophysical modeling, to reveal how synchronously activated synapses (distributed and clustered) across multiple basal dendritic branches impacts action-potential generation, under quiescent and in vivo like conditions. While dendritic Na+ spikes promote milli-second precision, distributed inputs and NMDAR spikes modulate firing rates via axo-somatic persistent sodium channel amplification. Action-potential precision, noise-enhanced responsiveness, and improved temporal resolution, were observed under high conductance states, revealing multiplexed dendritic control of somatic output amidst noisy membrane-voltage fluctuations and backpropagating spikes. Our results unveil a critical multibranch integration framework in which a delicate interplay between distributed synapses, clustered synapses, and axo-somatic subthreshold conductances, dictates somatic spike precision and gain.
Wireless communication and powering in a brain implant for freely moving subjects has been a research area of paramount importance in the recent past due to the multitude of medical, neuroscientific and societal applications that it can unveil. Unfortunately, traditional electromagnetic (EM) fields are significantly absorbed in the brain tissue, making it imperative to explore alternative modalities of signal transfer. Recently investigated ultrasonic, optical and magneto-electric modes of communication/powering suffer from large transduction losses when converting electrical energy to other forms of energies (and vice versa) during field transduction, leading to high end-to-end system loss (> 80 dB). To solve the challenge of powering and communication in a brain implant with low end-end channel loss, we present Bi-Phasic Quasistatic Brain Communication (BP-QBC), which achieves < 60 dB worst-case end-to-end channel loss at a channel length of ~55 mm, by using Electro-quasistatic Signaling that avoids transduction losses due to no field-modality conversion. BP-QBC utilizes dipole coupling based signal transmission within the brain tissue using differential excitation in the transmitter (TX) and differential signal pick-up at the receiver (RX), and uses electroquasistatic (EQS) signaling for low-leakage and low-power. Understanding that the EQS signal transfer through the brain channel occurs through AC electric fields, while the primary source of power consumption is due to galvanic DC currents arising from the finite conductivity of brain tissues, we propose to block the DC current paths through the tissue using a DC-blocking capacitor without significantly affecting the bi-phasic AC communication at EQS frequencies. The power consumption in the BP-QBC TX is only 0.52 μW at 1 Mbps (with 1% duty cycling), which is within the range of harvested power from an external wearable to the brain implant through the EQS brain channel, and is ~41× lower than traditional Galvanic Human Body Communication at 1 MHz. Furthermore, unlike optical and ultrasonic techniques, BP-QBC does not require sub-cranial interrogators/repeaters as the EQS signals can penetrate through the skull and has enough strength due to the low loss channel. Such low end-to-end channel loss with high data rates enabled by a completely new modality of brain communication and powering has deep societal and scientific impact in the fields of neurobiological research, brain-machine interfaces, electroceuticals and connected healthcare.
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