Fully Implantable Low-Power High Frequency Range Optoelectronic Devices for Dual-Channel Modulation in the Brain.

Wireless optoelectronic devices can deliver light to targeted regions in the brain and modulate discrete circuits in an animal that is awake. Here, we propose a miniaturized fully implantable low-power optoelectronic device that allows for advanced operational modes and the stimulation/inhibition of deep brain circuits in a freely-behaving animal. The combination of low power control logic circuits, including a reed switch and dual-coil wireless power transfer platform, provides powerful capabilities for the dissection of discrete brain circuits in wide spatial coverage for mouse activity. The actuating mechanism enabled by a reed switch results in a simplified, low-power wireless operation and systematic experimental studies that are required for a range of logical operating conditions. In this study, we suggest two different actuating mechanisms by (1) a magnet or (2) a radio-frequency signal that consumes only under 300 µA for switching or channel selection, which is a several ten-folds reduction in power consumption when compared with any other existing systems such as embedded microcontrollers, near field communication, and Bluetooth. With the efficient dual-coil transmission antenna, the proposed platform leads to more advantageous power budgets that offer improved volumetric and angular coverage in a cage while minimizing the secondary effects associated with a corresponding increase in transmitted power.

Posterior amygdala regulates sexual and aggressive behaviors in male mice.

Sexual and aggressive behaviors are fundamental to animal survival and reproduction. The medial preoptic nucleus (MPN) and ventrolateral part of the ventromedial hypothalamus (VMHvl) are essential regions for male sexual and aggressive behaviors, respectively. While key inhibitory inputs to the VMHvl and MPN have been identified, the extrahypothalamic excitatory inputs essential for social behaviors remain elusive. Here we identify estrogen receptor alpha (Esr1)-expressing cells in the posterior amygdala (PA) as a main source of excitatory inputs to the hypothalamus and key mediators for mating and fighting in male mice. We find two largely distinct PA subpopulations that differ in connectivity, gene expression, in vivo responses and social behavior relevance. MPN-projecting PAEsr1+ cells are activated during mating and are necessary and sufficient for male sexual behaviors, while VMHvl-projecting PAEsr1+ cells are excited during intermale aggression and promote attacks. These findings place the PA as a key node in both male aggression and reproduction circuits.

Cocaine exposure in utero alters synaptic plasticity in the medial prefrontal cortex of postnatal rats.

Cocaine exposure during pregnancy causes abnormality in fetal brain development, leading to cognitive dysfunction of the offspring, but the underlying cellular mechanism remains mostly unclear. In this study, we examined synaptic functions in the medial prefrontal cortex (mPFC) of postnatal rats that were exposed to cocaine in utero, using whole-cell recording from mPFC layer V pyramidal neurons in acute brain slices. Cocaine exposure in utero resulted in a facilitated activity-induced long-term potentiation (LTP) of excitatory synapses on these pyramidal neurons and an elevated neuronal excitability in postnatal rat pups after postnatal day 15 (P15). This facilitated LTP could be primarily attributed to the reduction of GABAergic inhibition. Biochemical assays of isolated mPFC tissue from postnatal rats further showed that cocaine exposure in utero caused a marked reduction in the surface expression of GABA(A) receptor subunits alpha1, beta2, and beta3, but had no effect on glutamate receptor subunit GluR1. Both facilitated LTP and reduced surface expression of GABA(A) receptors persisted in rats up to at least P42. Finally, the behavioral consequence of cocaine exposure in utero was reflected by the reduction in the sensitivity of locomotor activity in postnatal rats to cocaine and the dopamine receptor agonist apomorphine. Since the mPFC is an important part of the reward circuit in the rat brain and plays important roles in cognitive functions, these findings offer new insights into the cellular mechanism underlying the adverse effects of cocaine exposure in utero on brain development and cognitive functions.