RESUMEN
Wireless passive neural recording systems integrate sensory electrophysiological interfaces with a backscattering-based telemetry system. Despite the circuit simplicity and miniaturization with this topology, the high electrode-tissue impedance creates a major barrier to achieving high signal sensitivity and low telemetry power. In this paper, buffered impedance is utilized to address this limitation. The resulting passive telemetry-based wireless neural recording is implemented with thin flexible packages. Thus, the paper reports neural recording implants and integrator systems with three improved features: (1) passive high impedance matching with a simple buffer circuit, (2) a bypass capacitor to route the high frequency and improve mixer performance, and (3) system packaging with an integrated, flexible, biocompatible patch to capture the neural signal. The patch consists of a U-slot dual-band patch antenna that receives the transmitted power from the interrogator and backscatters the modulated carrier power at a different frequency. When the incoming power was 5-10 dBm, the neurosensor could communicate with the interrogator at a maximum distance of 5 cm. A biosignal as low as 80 µV peak was detected at the receiver.
RESUMEN
Accumulating evidence links the gut microbiome to neuronal functions in the brain. Given the increasing prevalence of brain disorders, there is a critical need to understand how gut microbes impact neuronal functions so that targeted therapeutic interventions can be developed. In this commentary, we discuss what makes the nematode Caenorhabditis elegans a valuable model for dissecting the molecular basis of gut microbiome-brain interactions. With a fully mapped neuronal circuitry, C. elegans is an effective model for studying signaling of the nervous system in a context that bears translational relevance to human disease. We highlight C. elegans as a potent but underexploited tool to interrogate the influence of the bacterial variable on the complex equation of the nervous system. We envision that routine use of gnotobiotic C. elegans to examine the gut-brain axis will be an enabling technology for the development of novel therapeutic interventions for brain diseases.
RESUMEN
Recent interferences of hemodynamic functions via modified brain neuronal mechanisms have proven to be major causes of dementia and sleeping disorders. In this work, cerebral expression differences of the neuroactive vesicular chromogranin A (CgA) and distinct α GABA(A)R subunits were detected in the facultative hibernating hamster. In particular, damaged neuronal fields of hypotensive torpor (TORP) state were correlated to elevated CgA and GABA(A)R α1, α4 mRNA levels in the paraventricular hypothalamic nucleus (PVN), central amygdalar nucleus (CeA) plus solitary tractus nucleus (NTS). Conversely, few neurodegeneration signals of hypertensive arousal (AROU) state, accounted for mostly lower CgA levels in the same areas. This state also provided increased α2-containing sites in amygdala, hippocampal and NTS neurons together with elevated α4-containing receptors in the periventricular hypothalamic nucleus (Pe). Interestingly in our hibernating model, CgA appeared to preferentially feature inhibitory neurosignals as indicated by preliminary perfusion of amygdalar sites with its highly specific antihypertensive derived peptide (catestatin) promoting GABA-dependent sIPSCs. Overall, evident neuronal damages plus altered expression capacities of CgA and α1-, α2-, α4-GABA(A)Rs in CeA, Pe, PVN as well as NTS during both hibernating states corroborate for the first time key molecular switching events guaranteeing useful cardiovascular rescuing abilities of neurodegenerative disorders.