Brain‐inspired neuromorphic computing is intended to provide effective emulation of the functionality of the human brain via the integration of electronic components. Recent studies of synaptic plasticity, which represents one of the most significant neurochemical bases of learning and memory, have enhanced the general comprehension of how the brain functions and have thereby eased the development of artificial neuromorphic devices. An understanding of the synaptic plasticity induced by various types of stimuli is essential for neuromorphic system construction. The realization of multiple stimuli‐enabled synapses will be important for future neuromorphic computing applications. In this Review, state‐of‐the‐art synaptic devices with particular emphasis on their synaptic behaviors under excitation by a variety of external stimuli are summarized, including electric fields, light, magnetic fields, pressure, and temperature. The switching mechanisms of these synaptic devices are discussed in detail, including ion migration, electron/hole transfer, phase transition, redox‐based resistive switching, and other mechanisms. This Review aims to provide a comprehensive understanding of the operating mechanisms of artificial synapses and thus provides the principles required for design of multifunctional neuromorphic systems with parallel processing capabilities.

Epidemiological studies indicate that physical activity and exercise may reduce the risk of developing Parkinson's disease (PD), and clinical observations suggest that physical exercise can reduce the motor symptoms in PD patients. In experimental animals, a profound observation is that exercise of appropriate timing, duration, and intensity can reduce toxin-induced lesion of the nigrostriatal dopamine (DA) system in animal PD models, although negative results have also been reported, potentially due to inappropriate timing and intensity of the exercise regimen. Exercise may also minimize DA denervation-induced medium spiny neuron (MSN) dendritic atrophy and other abnormalities such as enlarged corticostriatal synapse and abnormal MSN excitability and spiking activity. Taken together, epidemiological studies, clinical observations, and animal research indicate that appropriately dosed physical activity and exercise may not only reduce the risk of developing PD in vulnerable populations but also benefit PD patients by potentially protecting the residual DA neurons or directly restoring the dysfunctional cortico-basal ganglia motor control circuit, and these benefits may be mediated by exercise-triggered production of endogenous neuroprotective molecules such as neurotrophic factors. Thus, exercise is a universally available, side effect-free medicine that should be prescribed to vulnerable populations as a preventive measure and to PD patients as a component of treatment. Future research needs to establish standardized exercise protocols that can reliably induce DA neuron protection, enabling the delineation of the underlying cellular and molecular mechanisms that in turn can maximize exercise-induced neuroprotection and neurorestoration in animal PD models and eventually in PD patients.