Energy saving with node sleep and power control mechanisms for wireless sensor networks

Energy efficiency sleep scheduling in wireless sensor networks is one of the most crucial technologies. In this paper, we propose a simple and feasible synchronous node sleeping and waking mechanisms for small scale wireless sensor networks. Sensor nodes are divided into forwarding nodes and listening nodes. Beacon frame containing sleep command from the coordinator can be forwarded to listening nodes via forwarding nodes. All the nodes in the network can enter sleep at about the same time. Through such network synchronization mechanisms, we can realize synchronous sleep and wake of the entire network. Furthermore, a new power control scheme based on routing protocol （PCBRP） in the medium access control （MAC） layer is proposed. It operates with the help of routing protocol and calculates optimal transmission power according to the distance between neighbor nodes. A mapping table including optimal transmission power and node address is established during the route building procedure. The transmission power can be obtained by searching the table with the address of next-hop neighbor in subsequent data transmissions. The proposed mechanisms are implemented in sensor nodes and are evaluated in a test-bed. The analysis and evaluation based on the experimental results confirm that the proposed energy-saving mechanisms are feasible and effective.

Whole-Brain Monosynaptic Inputs to Hypoglossal Motor Neurons in Mice

Hypoglossal motor neurons(HMNs) innervate tongue muscles and play key roles in a variety of physiological functions,including swallowing,mastication,suckling,vocalization,and respiration.Dysfunction of HMNs is associated with several diseases,such as obstructive sleep apnea(OSA) and sudden infant death syndrome.OS A is a serious breathing disorder associated with the activity of HMNs during different sleep-wake states.Identifying the neural mechanisms by which the statedependent activities of HMNs are controlled may be helpful in providing a theoretical basis for effective therapy for OSA.However,the presynaptic partners governing the activity of HMNs remain to be elucidated.In the present study,we used a cell-type-specific retrograde tracing system based on a modified rabies virus along with a Cre/loxP gene-expression strategy to map the whole-brain monosynaptic inputs to HMNs in mice.We identified 53 nuclei targeting HMNs from six brain regions:the amygdala,hypothalamus,midbrain,pons,medulla,and cerebellum.We discovered that GAB Aergic neurons in the central amygdaloid nucleus,as well as calretinin neurons in the parasubthalamic nucleus,sent monosynaptic projections to HMNs.In addition,HMNs received direct inputs from several regions associated with respiration,such as the preBotzinger complex,parabrachial nucleus,nucleus of the solitary tract,and hypothalamus.Some regions engaged in sleep-wake regulation(the parafacial zone,parabrachial nucleus,ventral medulla,sublaterodorsal tegmental nucleus,dorsal raphe nucleus,periaqueductal gray,and hypothalamus) also provided primary inputs to HMNs.These results contribute to further elucidating the neural circuits underlying disorders caused by the dysfunction of HMNs.