Activation of synaptic receptors initiates long-lasting changes in neuronal excitability. Neurons also exhibit plasticity in their intrinsic excitability (intrinsic plasticity). Neurons become unusually sensitive and develop spontaneously pathological activity and abnormal excitability. Phenylephrine may cause side effects such as headache, reflex bradycardia, excitability, restlessness and cardiac arrhythmias. Increased intracellular cGMP has been shown to contribute to excessive neuron excitability and locomotor activity. Cathodal (V-) stimulation decreases the neuronal excitability of the area being stimulated. Veratridine increases nerve excitability and intracellular Ca concentrations. Metabotropic responses occur in dopamine neurons through the regulation of the excitability of cells. GABA controls the excitability of neurons by binding to the GABA receptor. Symptoms of tutin poisoning include vomiting, delirium, giddiness, increased excitability, stupor, coma, and violent convulsions. Veratridine acts a neurotoxin by increasing nerve excitability. Besides hypertension, common side-effects include sleeplessness, anxiety, dizziness, excitability, and nervousness. Pathological visual illusions usually occur throughout the visual field, suggesting global excitability or sensitivity alterations. In order for excitability and conduction to occur, voltage-gated sodium channels must be activated. This structure provides a filter for the excitability of neurons.