BackgroundSensory gating, often described as the ability to filter out irrelevant information that is repeated in close temporal proximity, is essential for the selection, processing, and storage of more salient information. This study aimed to test the effect of sensory gating under anesthesia in the prefrontal cortex (PFC) of monkeys following injection of bromocriptine, haloperidol, and phencyclidine (PCP).Material/MethodsWe used an auditory evoked potential that can be elicited by sound to examine sensory gating during treatment with haloperidol, bromocriptine, and PCP in the PFC in the cynomolgus monkey. Scalp electrodes were located in the bilateral PFC and bilateral temporal, bilateral parietal, and occipital lobes. Administration of bromocriptine (0.313 mg/kg, 0.625 mg/kg, and 1.25 mg/kg), haloperidol (0.001 mg/kg, 0.01 mg/kg, and 0.05 mg/kg), and the N-methyl-D-aspartic acid receptor antagonist PCP (0.3 mg/kg) influenced sensory gating.ResultsWe demonstrated the following: (1) Administration of mid-dose bromocriptine disrupted sensory gating (N100) in the right temporal lobe, while neither low-dose nor high-dose bromocriptine impaired gating. (2) Low-dose haloperidol impaired gating in the right prefrontal cortex. Mid-dose haloperidol disrupted sensory gating in left occipital lobe. High-dose haloperidol had no obvious effect on sensory gating. (3) Gating was impaired by PCP in the left parietal lobe.ConclusionsOur studies showed that information processing was regulated by the dopaminergic system, which might play an important role in the PFC. The dopaminergic system influenced sensory gating in a dose- and region-dependent pattern, which might modulate the different stages that receive further processing due to novel information.

Background: The immunotherapy that is more effective for seizures caused by viral encephalitis and autoimmune encephalitis and the long-term use of anti-epileptic drugs is not clear. We aimed to compare the immunotherapy and prognosis of seizures caused by viral encephalitis and autoimmune encephalitis.Methods: Clinical data of 121 patients with seizures caused by viral encephalitis and autoimmune encephalitis diagnosed and treated in the two largest tertiary general hospitals in the Yunnan Province were retrospectively collected to compare the immunotherapy used. Dynamic follow-up was performed to observe seizures and the use of antiepileptic drugs.Results: The seizure-free rates at 6 months and 12 months after the onset of viral encephalitis were 77.8% and 80.8%, respectively. In total, 79.1% of autoimmune encephalitis cases were seizure-free at 6 months after onset, and the seizure-free rate at 12 months was 91.9%. A total of 75.0% of viral encephalitis and 67.7% of autoimmune encephalitis patients discontinued antiepileptic drugs and were seizure-free at 12 months after onset. Patients with viral encephalitis treated with glucocorticoids alone had a lower risk of seizures after the acute phase than those treated with glucocorticoids combined with immunoglobulin (P < 0.05). The risk of seizures in patients with autoimmune encephalitis treated with glucocorticoids combined with immunoglobulin was lower than that in patients treated with glucocorticoids and immunoglobulin alone (P < 0.05).Conclusions: Immunotherapy may improve the seizure prognosis of patients with acute encephalitis. The prognosis of seizures due to viral encephalitis may be determined as early as 6 months after onset, while the seizure outcome of autoimmune encephalitis is further improved 12 months after onset.