Bidirectional brain-machine interfaces (BMIs) establish a two-way direct communication link 4 between the brain and the external world. A decoder translates recorded neural activity into motor 5 commands and an encoder delivers sensory information collected from the environment directly 6 to the brain creating a closed-loop system. These two modules are typically integrated in bulky 7 external devices. However, the clinical support of patients with severe motor and sensory deficits 8 requires compact, low-power, and fully implantable systems that can decode neural signals to 9 control external devices. As a first step toward this goal, we developed a modular bidirectional BMI 10 setup that uses a compact neuromorphic processor as a decoder. On this chip we implemented 11 a network of spiking neurons built using its ultra-low-power mixed-signal analog/digital circuits. 12 On-chip on-line spike-timing-dependent plasticity synapse circuits enabled the network to learn 13 to decode neural signals recorded from the brain into motor outputs controlling the movements 14 of an external device. The modularity of the BMI allowed us to tune the individual components 15 of the setup without modifying the whole system. In this paper we present the features of 16 this modular BMI, and describe how we configured the network of spiking neuron circuits to 17 implement the decoder and to coordinate it with the encoder in an experimental BMI paradigm 18 that connects bidirectionally the brain of an anesthetized rat with an external object. We show that 19 the chip learned the decoding task correctly, allowing the interfaced brain to control the object’s 20 trajectories robustly. Based on our demonstration, we propose that neuromorphic technology is 21 mature enough for the development of BMI modules that are sufficiently low-power and compact, 22 while being highly computationally powerful and adaptive.

Precise information flow during mnemonic and executive tasks requires the coactivation of adult prefrontal and hippocampal networks in oscillatory rhythms. This interplay emerges early in life, most likely as an anticipatory template of later cognitive performance. At neonatal age, hippocampal theta bursts drive the generation of prefrontal theta-gamma oscillations. In the absence of direct reciprocal interactions, the question arises of which feedback mechanisms control the early entrainment of prefrontal–hippocampal networks. Here, we demonstrate that prefrontal–hippocampal activity couples with discontinuous theta oscillations and neuronal firing in both lateral entorhinal cortex and ventral midline thalamic nuclei of neonatal rats. However, these two brain areas have different contributions to the neonatal long-range communication. The entorhinal cortex mainly modulates the hippocampal activity via direct axonal projections. In contrast, thalamic theta bursts are controlled by the prefrontal cortex via mutual projections and contribute to hippocampal activity. Thus, the neonatal prefrontal cortex modulates the level of hippocampal activation by directed interactions with the ventral midline thalamus. Similar to the adult task-related communication, theta-band activity ensures the feedback control of long-range coupling in the developing brain.SIGNIFICANCE STATEMENTMemories are encoded by finely tuned interactions within large-scale neuronal networks. This cognitive performance is not inherited, but progressively matures in relationship with the establishment of long-range coupling in the immature brain. The hippocampus initiates and unidirectionally drives the oscillatory entrainment of neonatal prefrontal cortex, yet feedback interactions that precisely control this early communication are still unresolved. Here, we identified distinct roles of entorhinal cortex and ventral midline thalamus for the functional development of prefrontal–hippocampal interactions. While entorhinal oscillations modulate the hippocampal activity by timing the neuronal firing via monosynaptic afferents, thalamic nuclei act as a relay station routing prefrontal activation back to hippocampus. Understanding the mechanisms of network maturation represents the prerequisite for assessing circuit dysfunction in neurodevelopmental disorders.

This paper presents Ring Optical Network (RingO), a wavelength-division-multiplexing (WDM), ring-based, optical packet network suitable for a high-capacity metro environment. We present three alternative architectural designs and elaborate on the effectiveness of optic with respect to electronic technologies, trying to identify an optimal mix. We present the design and prototyping of a simple but efficient access control protocol, based upon the equivalence of the proposed network architecture with input-buffering packet switches. We discuss the problem of node allocation to WDM channels, which can be viewed as a particular optical network design problem. We, finally, briefly illustrate the fault protection properties of the RingO architecture. The main contribution of this paper is the identification and experimental validation of an innovative optical network architecture, which is feasible and cost effective with technologies available today, and can be a valid alternative to more consolidated solutions in metro applications.

Cognitive deficits represent a major burden of neuropsychiatric disorders and result in part from abnormal communication within hippocampal–prefrontal circuits. While it has been hypothesized that this network dysfunction arises during development, long before the first clinical symptoms, experimental evidence is still missing. Here, we show that pre-juvenile mice mimicking genetic and environmental risk factors of disease (dual-hit GE mice) have poorer recognition memory that correlates with augmented coupling by synchrony and stronger directed interactions between prefrontal cortex and hippocampus. The network dysfunction emerges already during neonatal development, yet it initially consists in a diminished hippocampal theta drive and consequently, a weaker and disorganized entrainment of local prefrontal circuits in discontinuous oscillatory activity in dual-hit GE mice when compared with controls. Thus, impaired maturation of functional communication within hippocampal–prefrontal networks switching from hypo- to hyper-coupling may represent a mechanism underlying the pathophysiology of cognitive deficits in neuropsychiatric disorders.