A fundamental challenge for bioelectronics is to deliver power to miniature devices inside the body. Wires are common failure points and limit device placement. Wireless power by electromagnetic or ultrasound waves must overcome absorption by the body and impedance mismatches between air, bone, and tissue. Magnetic fields, on the other hand, suffer little absorption by the body or differences in impedance at interfaces between air, bone, and tissue. These advantages have led to magnetically-powered stimulators based on induction or magnetothermal effects. However, fundamental limitations in these power transfer technologies have prevented miniature magneticallypowered stimulators from applications in many therapies and disease models because they do not operate in clinical "high-frequency" ranges above 20 Hz. Here we show that magnetoelectric materials -applied for the first time in bioelectronics devices -enable miniature magnetically-powered neural stimulators that operate at clinically relevant high-frequencies. As an example, we show that ME neural stimulators can effectively treat the symptoms of a Parkinson's disease model in a freely behaving rodent. We also show that ME-powered devices can be miniaturized to sizes smaller than a grain of rice while maintaining effective stimulation voltages. These results suggest that ME materials are an excellent candidate for wireless power delivery that will enable miniature neural stimulators in both clinical and research applications. Wireless neural stimulators have the potential to provide less invasive, longer lasting interfaces to brain regions and peripheral nerves compared to batterypowered devices or wired stimulators. Indeed, wires are a common failure point for bioelectronic devices. Percutaneous wires present a pathway for infection 1 and implanted wires can also limit the ability of the stimulators to move with the tissue, leading to a foreign body response or loss of contact with the target tissue 2,3 . Additionally, chronic stress and strain on wires, particularly for devices in the periphery, can lead to failure in the wire itself or its connection to the stimulator 4 . In small animals like rats and mice, wires used to power neural stimulators can interfere with natural behavior, particularly when studying social interaction between multiple animals 5 .

Epigenetic mechanisms such as DNA methylation are essential regulators of the function and information storage capacity of neurons. DNA methylation is highly dynamic in the developing and adult brain, and is actively regulated by neuronal activity and behavioural experiences. However, it is presently unclear how methylation status at individual genes is targeted for modification. Here, we report that extra-coding RNAs (ecRNAs) interact with DNA methyltransferases and regulate neuronal DNA methylation. Expression of ecRNA species is associated with gene promoter hypomethylation, is altered by neuronal activity, and is overrepresented at genes involved in neuronal function. Knockdown of the Fos ecRNA locus results in gene hypermethylation and mRNA silencing, and hippocampal expression of Fos ecRNA is required for long-term fear memory formation in rats. These results suggest that ecRNAs are fundamental regulators of DNA methylation patterns in neuronal systems, and reveal a promising avenue for therapeutic targeting in neuropsychiatric disease states.

Survival depends on a balance between seeking rewards and avoiding potential threats, but the neural circuits that regulate this motivational conflict remain largely unknown. Using an approach-food vs. avoid-predator threat conflict test in rats, we identified a subpopulation of neurons in the anterior portion of the paraventricular thalamic nucleus (aPVT) which express corticotrophin-releasing factor (CRF) and are preferentially recruited during conflict. Inactivation of aPVTCRF neurons during conflict biases animal’s response toward food, whereas activation of these cells recapitulates the food-seeking suppression observed during conflict. aPVTCRF neurons project densely to the nucleus accumbens (NAc), and activity in this pathway reduces food seeking and increases avoidance. In addition, we identified the ventromedial hypothalamus (VMH) as a critical input to aPVTCRF neurons, and demonstrated that VMH-aPVT neurons mediate defensive behaviors exclusively during conflict. Together, our findings describe a hypothalamic-thalamostriatal circuit that suppresses reward-seeking behavior under the competing demands of avoiding threats.

The effect of intermittent noise upon attention span was investigated in two experiments. In Exp. 1, 4 levels of noise intensity were used (no noise, 75 db, 85 db, and 100 db). The task was a serial anticipation task in which the relevant stimuli were 4-letter words located in the center of a projected slide. 3-letter words were peripherally located; the peripheral words were not mentioned to Ss. Ss in the 85-db and the 100-db conditions learned fewer of the peripheral words as indicated by a free-recall test than Ss in the no-noise and the 75-db conditions, indicating a narrowing of attention due to the higher noise levels. In Exp. 2, Ss operating under noise (85 db) performed significantly better on the Stroop Color-Word Test than did Ss operating under no noise, again indicating a focusing of attention due to noise-induced arousal. The results are consistent with the proposal of several authors that increasing emotional arousal causes a narrowing of attention.

A fundamental challenge for bioelectronics is to deliver power to miniature devices inside the body. Wires are common failure points and limit device placement. On the other hand, wireless power by electromagnetic or ultrasound waves must overcome absorption by the body and impedance mismatches between air, bone, and tissue. In contrast, magnetic fields suffer little absorption by the body or differences in impedance at interfaces between air, bone, and tissue. These advantages have led to magneticallypowered stimulators based on induction or magnetothermal effects. However, fundamental limitations in these power transfer technologies have prevented miniature magnetically-powered stimulators from applications in many therapies and disease models because they do not operate in clinical "highfrequency" ranges above 50 Hz. Here we show that magnetoelectric materials -applied in bioelectronic devices -enable miniature magnetically-powered neural stimulators that can operate up to clinically-relevant high-frequencies.As an example, we show that ME neural stimulators can effectively treat the symptoms of a hemi-Parkinson's disease model in freely behaving rodents. We further demonstrate that ME-powered devices can be miniaturized to mmsized devices, fully implanted, and wirelessly powered in freely behaving rodents. These results suggest that ME materials are an excellent candidate for wireless power delivery that will enable miniature bioelectronics for both clinical and research applications.