Experts have discovered an'impulsivity switch' in the brain that lets mammals suppress the urge to'jump the gun' and only act when the time is right. In lab experiments on mice, researchers found a brain area that's responsible for driving action and another that's responsible for suppressing that drive. Manipulating neurons, also known as nerve cells, in these areas can override our ability to control the urge to jump the gun and therefore trigger impulsive behaviour. Keeping the'impulsivity switch' on is how athletes stop themselves from running before the starting gun has fired, how dogs obey a command to resist a treat, or how lions in the wild can wait for the perfect moment to pounce on its prey. Keeping our'impulsivity switch' on is how athletes stop themselves from running before the starting gun has fired (file photo) 'We discovered a brain area responsible for driving action and another for suppressing that drive,' said study author Joe Paton, director of the Champalimaud Neuroscience Programme in Lisbon, Portugal.

Two Parkinson's patients receive deep brain stimulation (DBS) in their subthalamic nuclei. Despite accurate electrode placement, one patient is able to stand up and walk effortlessly around the room while the other breaks down into uncontrolled sobbing that only stops once the stimulator is turned off. This paradox exposes one of the major roadblocks in developing therapies for brain disorders: the elaborate and diffuse nature of neural circuits. Physically proximal neurons are often engaged in functionally different pathways; whereas modulation of one pathway might be therapeutic, modulation of those surrounding it may produce debilitating side effects. The problem with high-amplitude electrical stimulation, as applied during DBS, is that it affects not only the activity of neurons around the electrode, but also the activity of neurons whose long extensions happen to pass by the electrode.

One of the open issues in developing large-scale computational models of the brain is how the transfer of information between communicating cortical regions is controlled. Here, we present a model where the basal ganglia implement such a conditional information routing system. The basal ganglia are a set of subcortical nuclei that play a central role in cognition. Like a switchboard, the model basal ganglia direct the communication between cortical regions by alerting the destination regions to the presence of important signals coming from the source regions. This way, they can impose serial control on the massive parallel communication between cortical areas. The model also incorporates a possible mechanism by which subsequent transfers of information control the release of dopamine. This signal is used to produce novel stimulus-response associations by internalizing the representation being transferred in the striatum. We discuss how this neural circuit can be seen as a biological implementation of a production system. This comparison highlights the basal ganglia as bridge between computational models of small-size brain circuits and high-level characterizations of complex cognition, such as cognitive architectures.

There is a longstanding controversy on the site of the cerebellar motor learning. Different theories and experimental results suggest that either the cerebellar flocculus or the brainstem learns the task and stores the memory. With a dynamical system approach, we clarify the mechanism of transferring the memory generated in the flocculus to the brainstem and that of so-called savings phenomena. The brainstem learning must comply with a sort of Hebbian rule depending on Purkinje-cell activities. In contrast to earlier numerical models, our model is simple but it accommodates explanations and predictions of experimental situations as qualitative features of trajectories in the phase space of synaptic weights, without fine parameter tuning.

There is a longstanding controversy on the site of the cerebellar motor learning. Different theories and experimental results suggest that either the cerebellar flocculus or the brainstem learns the task and stores the memory. With a dynamical system approach, we clarify the mechanism of transferring the memory generated in the flocculus to the brainstem and that of so-called savings phenomena. The brainstem learning must comply with a sort of Hebbian rule depending on Purkinje-cell activities. In contrast to earlier numerical models, our model is simple but it accommodates explanations and predictions of experimental situations as qualitative features of trajectories in the phase space of synaptic weights, without fine parameter tuning.

There is a longstanding controversy on the site of the cerebellar motor learning. Different theories and experimental results suggest that either the cerebellar flocculus or the brainstem learns the task and stores the memory. With a dynamical system approach, we clarify the mechanism of transferring the memory generated in the flocculus to the brainstem and that of so-called savings phenomena. The brainstem learning must comply with a sort of Hebbian rule depending on Purkinje-cell activities. In contrast to earlier numerical models, our model is simple but it accommodates explanationsand predictions of experimental situations as qualitative features of trajectories in the phase space of synaptic weights, without fine parameter tuning.