The variation of mutual inductance and load parameters will affect the transmission power and efficiency of the inductive power transfer (IPT) system. The identification of mutual inductance and load parameters is an essential part of establishing a stable and reliable IPT system. This paper presents a joint identification method of load and mutual inductance for LCC-S IPT system, which does not require the establishment of primary and secondary communication and related control. Firstly, the resistance-inductance characteristics of the equivalent load of the rectifier are analyzed by simulation, and then the rectifier and system load are equivalent to the circuit model of resistance and inductance in series. Secondly, the characteristics of the reflected impedance are analyzed, and the functional relationship between the transmitter impedance and the rectifier impedance is established by using the ratio of the real part to the imaginary part of the reflected impedance, which realizes the decoupling of the load and the mutual inductance. Thirdly, the functional relationship between the equivalent impedance of the rectifier and the load resistance of the system is obtained by data fitting. Then, the equations of the above two functional relationships are combined. By measuring the voltage of the parallel compensation capacitor at the transmitting side, the current of the transmitting coil and the phase difference between the two, the battery load can be solved first, and then the mutual inductance can be calculated, so that the high-precision identification of the load and mutual inductance can be realized. Finally, an experimental platform of LCC-S IPT system is built for experimental verification. The experimental results show that the maximum identification errors of mutual inductance and load are 5.20 % and 5.53 %, respectively, which proves that the proposed identification method can achieve high precision identification.

Excitation-inhibition imbalance of GABAergic interneurons is predisposed to develop chronic temporal lobe epilepsy (TLE). We have previously shown that virtually every neuronal nitric oxide synthase (nNOS)-positive cell is a GABAergic inhibitory interneuron in the denate gyrus. The present study was designed to quantify the number of nNOS-containing hilar interneurons using stereology in pilocapine- and kainic acid (KA)-exposed transgenic adult mice that expressed GFP under the nNOS promoter. In addition, we studied the properties of miniature excitatory postsynaptic current (mEPSC) and paired-pulse response ratio (PPR) of evoked EPSC in nNOS interneurons using whole cell recording techniques. Results showed that there were fewer nNOS-immunoreactive interneurons of chronically epileptic animals. Importantly, patch-clamp recordings revealed reduction in mEPSC frequency, indicating diminished global excitatory input. In contrast, PPR of evoked EPSC following the granule cell layer stimulation was increased in epileptic animals suggesting reduced neurotransmitter release from granule cell input. In summary, we propose that impaired excitatory drive onto hippocampal nNOS interneurons may be implicated in the development of refractory epilepsy.