Cerebellum plays a role in the regulation of cognitive processes. Cerebellar alterations could explain cognitive impairments in schizophrenia. We describe the case of a 50 years old patient with schizophrenia whom underwent cerebellar transcranial direct current stimulation (tDCS). In order to study the effect of cerebellar stimulation on cognitive functions, the patient underwent a neuropsychological assessment and an eyeblink conditioning (EBC) protocol. Although the effect of brain stimulation cannot be only assessed in a single-case study, our results suggest that cerebellar stimulation may have an effect on a broad range of cognitive functions typically impaired in patients with schizophrenia, including verbal episodic, short term, and working memory. In addition to neuropsychological tests, we evaluated the cerebellar function by performing EBC before and after tDCS. Our data suggest that tDCS can improve EBC. Further clinical trials are required for better understanding of how cerebellar stimulation can modulate cognitive processes in patients with schizophrenia and healthy controls.
The oculomotor delayed-response (ODR) task is a common experimental paradigm of working memory (WM) study, in which a monkey must fixate its gaze on the center of a screen and, following a brief cue that flashes on the screen, keep fixating for several more seconds before shifting its gaze to the location where the cue flashed. Consequently, in the delay period between the cue and the response the monkey must maintain a memory of cue location. Electrophysiological recordings from the prefrontal area of the cortex (PFC) revealed neurons that display selective persistent activity: their firing rate change induced by the cue persists through delay period, but only in response to a confined range of cue locations. This suggests that the representation of the cue is maintained in the network by a change in network activity profile. In this work, we study a network of rate-model neurons that is capable of preserving information about a past input, owing to structured connectivity and nonlinearities in the neuronal transfer function (TFs). Particularly, we focus on the acceleration of the TF close to firing threshold and the concavity around TF saturation. Any memory mechanism which exploits TF saturation means that some neurons must fire close to their saturation rates; with our model, however, we show that a certain relation between the excitatory and inhibitory neurons' TFs can cause an effective saturation in the network without forcing the neurons into the saturating parts of their TFs. In addition, this mechanism enables the erasure of memory at the end of the delay by a global excitatory signal. Finally, we demonstrate the mechanism in a model network of spiking neurons which describes with more detail the oscillatory dynamics in the state transition due to the interaction of membrane and synaptic time constants which is neglected in the rate model.
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