Multisensory interactions of face and vocal information during perception and memory in ventrolateral prefrontal cortex.

The ventral frontal lobe is a critical node in the circuit that underlies communication, a multisensory process where sensory features of faces and vocalizations come together. The neural basis of face and vocal integration is a topic of great importance since the integration of multiple sensory signals is essential for the decisions that govern our social interactions. Investigations have shown that the macaque ventrolateral prefrontal cortex (VLPFC), a proposed homologue of the human inferior frontal gyrus, is involved in the processing, integration and remembering of audiovisual signals. Single neurons in VLPFC encode and integrate species-specific faces and corresponding vocalizations. During working memory, VLPFC neurons maintain face and vocal information online and exhibit selective activity for face and vocal stimuli. Population analyses indicate that identity, a critical feature of social stimuli, is encoded by VLPFC neurons and dictates the structure of dynamic population activity in the VLPFC during the perception of vocalizations and their corresponding facial expressions. These studies suggest that VLPFC may play a primary role in integrating face and vocal stimuli with contextual information, in order to support decision making during social communication. This article is part of the theme issue 'Decision and control processes in multisensory perception'.

Regression of Epileptogenesis by Inhibiting Tropomyosin Kinase B Signaling following a Seizure.

OBJECTIVE: Temporal lobe epilepsy (TLE) is a devastating disease in which seizures persist in 35% of patients despite optimal use of antiseizure drugs. Clinical and preclinical evidence implicates seizures themselves as one factor promoting epilepsy progression. What is the molecular consequence of a seizure that promotes progression? Evidence from preclinical studies led us to hypothesize that activation of tropomyosin kinase B (TrkB)-phospholipase-C-gamma-1 (PLCγ1) signaling induced by a seizure promotes epileptogenesis. METHODS: To examine the effects of inhibiting TrkB signaling on epileptogenesis following an isolated seizure, we implemented a modified kindling model in which we induced a seizure through amygdala stimulation and then used either a chemical-genetic strategy or pharmacologic methods to disrupt signaling for 2 days following the seizure. The severity of a subsequent seizure was assessed by behavioral and electrographic measures. RESULTS: Transient inhibition of TrkB-PLCγ1 signaling initiated after an isolated seizure limited progression of epileptogenesis, evidenced by the reduced severity and duration of subsequent seizures. Unexpectedly, transient inhibition of TrkB-PLCγ1 signaling initiated following a seizure also reverted a subset of animals to an earlier state of epileptogenesis. Remarkably, inhibition of TrkB-PLCγ1 signaling in the absence of a recent seizure did not reduce severity of subsequent seizures. INTERPRETATION: These results suggest a novel strategy for limiting progression or potentially ameliorating severity of TLE whereby transient inhibition of TrkB-PLCγ1 signaling is initiated following a seizure. ANN NEUROL 2019;86:939-950.