Electrospinning is a simple method for producing nanoscale or microscale fibers from a wide variety of materials. Intrinsically conductive polymers (ICPs), such as polyaniline (PANI), show higher conductivities with the use of secondary dopants like m-cresol. However, due to the low volatility of most secondary dopants, it has not been possible to electrospin secondary doped ICP fibers. In this work, the concept of secondary doping has been applied for the first time to electrospun fibers. Using a novel design for rotating drum electrospinning, fibers were efficiently and reliably produced from a mixture of low- and high-volatility solvents. The conductivity of electrospun PANI–poly­(ethylene oxide) (PEO) fibers prepared was 1.73 S/cm, two orders of magnitude higher than the average value reported in the literature. These conductive fibers were tested as electrodes for supercapacitors and were shown to have a specific capacitance as high as 3121 F/g at 0.1 A/g, the highest value reported, thus far, for PANI–PEO electrospun fibers.

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High-performance cellulose−halloysite hemostatic nanocomposite fibers (CHNFs) are fabricated using a onestep wet−wet electrospinning process and evaluated for human plasma coagulation by activated partial thromboplastin time. These novel biocompatible CHNFs exhibit 2.4 times faster plasma coagulation time compared with the industry gold standard QuikClot Combat Gauze (QCG). The CHNFs have superior antileaching property of clay with 3 times higher post-wetting clotting activity compared to QCG. The CHNFs also coagulate whole blood 1.3 times faster than the QCG and retain twice the clotting performance after washing. Halloysite clay is also more effective in plasma coagulation than commercial kaolin clay. The physical and thermal properties of the CHNFs were evaluated using scanning electron microscopy, energy-dispersive X-ray spectroscopy, X-ray diffraction, Brunauer−Emmett−Teller surface area analysis, and thermogravimetric analysis. CHNFs show a 7-fold greater clay loading than QCG and their small average diameter of 450 ± 260 nm affords a greater specific surface area (33.6 m 2 g −1 ) compared with the larger average diameter of 12.6 ± 0.9 μm for QCG with a specific surface area of 1.6 m 2 g −1 . The CHNFs were shown to be noncytotoxic and human primary fibroblasts proliferated on the composite material. The drastic reduction in coagulation time makes this novel nanocomposite a potential lifesaving material for victims of rapid blood loss such as military personnel and patients undergoing major surgical procedures or to aid in the treatment of unexpected bleeding episodes of patients suffering from hereditary blood clotting disorders. Since a person can die within minutes of heavy bleeding, every second counts for stopping traumatic hemorrhaging.

Synaptic plasticity is a critical process that regulates neuronal activity by allowing neurons to adjust their synaptic strength in response to changes in activity. Despite the high proximity of excitatory glutamatergic and inhibitory GABAergic postsynaptic zones and their functional integration within dendritic regions, concurrent plasticity has historically been underassessed. Growing evidence for pathological disruptions in the excitation and inhibition (E/I) balance in neurological and neurodevelopmental disorders indicates the need for an improved, more “holistic” understanding of synaptic interplay. There continues to be a long-standing focus on the persistent strengthening of excitation (excitatory long-term potentiation; eLTP) and its role in learning and memory, although the importance of inhibitory long-term potentiation (iLTP) and depression (iLTD) has become increasingly apparent. Emerging evidence further points to a dynamic dialogue between excitatory and inhibitory synapses, but much remains to be understood regarding the mechanisms and extent of this exchange. In this mini-review, we explore the role calcium signaling and synaptic crosstalk play in regulating postsynaptic plasticity and neuronal excitability. We examine current knowledge on GABAergic and glutamatergic synapse responses to perturbances in activity, with a focus on postsynaptic plasticity induced by short-term pharmacological treatments which act to either enhance or reduce neuronal excitability via ionotropic receptor regulation in neuronal culture. To delve deeper into potential mechanisms of synaptic crosstalk, we discuss the influence of synaptic activity on key regulatory proteins, including kinases, phosphatases, and synaptic structural/scaffolding proteins. Finally, we briefly suggest avenues for future research to better understand the crosstalk between glutamatergic and GABAergic synapses.