CA1 PYRAMIDAL CELL DIVERSITY IS ROOTED IN THE TIME OF NEUROGENESIS

Published in eLife on Nov 1, 2021

We used a combination of genetic fate mapping, neuroanatomy, slice physiology, connectivity tracing, and c-Fos staining in mice to show that the date of birth of excitatory pyramidal neurons of the hippocampus is a critical determinant of their morphological and functional characteristics in adulthood.

HIPPOCAMPAL HUB NEURONS MAINTAIN DISTINCT CONNECTIVITY THROUGHOUT THEIR LIFETIME

Published in Nature Communications on Sep 11, 2020

We used a combination of genetic fate mapping, electrophysiology, neurochemical analysis, optogenetic connectivity mapping and calcium imaging to show that the date of birth of inhibitory neurons of the hippocampus dictates their future functions. Early-born inhibitory neurons operate as "hubs" during development, but also maintain distinct morpho-physiological and connectivity profiles in adulthood.

GROUP II METABOTROPIC GLUTAMATE RECEPTORS MEDIATE PRESYNAPTIC INHIBITION OF EXCITATORY TRANSMISSION IN PYRAMIDAL NEURONS OF THE HUMAN CEREBRAL CORTEX

Published in Frontiers in Cellular Neuroscience on Jan 8, 2019

We performed slice patch clamp recordings from live human brain tissue resected during tumour or epilepsy neurosurgeries to study the neuropharmacology of human cortical synapses. We found that group II metabotropic glutamate receptors, potential novel drug targets for neurological and psychiatric disorders, depress excitatory transmission onto human pyramidal neurons, mostly via presynaptic mechanisms.

SYNAPTIC PLASTICITY, ENGRAMS, AND NETWORK OSCILLATIONS IN AMYGDALA CIRCUITS FOR STORAGE AND RETRIEVAL OF EMOTIONAL MEMORIES

Published in Neuron on May 17, 2017

In this review, we described the neural mechanisms underlying learning and memory in the amygdala. We attempt to bridge mechanistically three neural underpinnings of learning that have remained largely distinct thus far: synaptic plasticity, memory engrams and oscillations.

CONTROL OF AMYGDALA CIRCUITS BY 5-HT NEURONS VIA 5-HT AND GLUTAMATE CO-TRANSMISSION

Published in The Journal of Neuroscience on Feb 15, 2017

One of the first studies to use optogenetics to study the endogeneous release of serotonin. We combined optogenetic, electrophysiological, and pharmacological approaches to study the effects of activation of serotonin axons in the amygdala, We found that serotonin neurons co-release serotonin and glutamate onto amygdala neurons in a cell-type-specific and frequency-dependent manner.

SLEEP AND SEROTONIN MODULATE PARACAPSULAR NITRIC OXIDE SYNTHASE EXPRESSING NEURONS OF THE AMYGDALA

Published in eNeuro on Oct 5, 2016

We discovered a new inhibitory neuron type in the amygdala characterised by high levels of nitric oxide synthase (NOS). These neurons show unique functional properties: they are activated during sleep following sleep deprivation and inhibited by serotonin (mostly released during wakefulness). Given the strong links between mood, sleep deprivation, and serotonin, the recruitment of these neurons following high sleep pressure may represent an important mechanism in emotion regulation.

SEROTONIN, AMYGDALA AND FEAR: ASSEMBLING THE PUZZLE

Published in Frontiers in Neural Circuits on Apr 5, 2016

In this review, we propose a multidisciplinary framework to decipher the role of serotonin the processing of aversive events via the amygdala. We review evidence suggesting that serotonin has facilitating effects on learning and plasticity, and that examining the action of serotonin going from single neurons to networks to behaviour is necessary to build a comprehensive theory of this neuromodulator in fear processing.

INCREASED SEROTONIN TRANSPORTER EXPRESSION REDUCES FEAR AND RECRUITMENT OF PARVALBUMIN INTERNEURONS OF THE AMYGDALA

Published in Neuropsychopharmacology on Jun 8, 2015

We showed that higher levels of serotonin transporter lead to lower levels of conditioned fear and weaker activation of parvalbumin-expressing interneurons of the amygdala by fear and serotonin. These findings provide a cellular mechanism that is likely to contribute to differences in emotional behaviors linked with genetic variations of the serotonin transporter.