Asaf Keller

The paper investigates sex differences in CGRP signaling within the BNST and finds that while peptide release is sex-independent, neuromodulation of excitability shows sex-dependent features.

The paper identifies CGRP receptors on OPCs and demonstrates close spatial contacts between CGRP and OPCs, suggesting direct signaling.

This study shows that gestational chlorpyrifos exposure increases neuronal activity and 5-HT1B receptor expression in rat somatosensory cortex, leading to persistent hyper-excitation.

The paper investigates nicotinic receptor responses in fast-spiking neurons of rat somatosensory cortex across development, finding presynaptic regulation but no postsynaptic responses despite receptor expression.

This study shows that gestational chlorpyrifos exposure causes lasting synaptic and structural changes in the rat somatosensory cortex, potentially explaining neurodevelopmental issues.

The paper investigates sex differences in glutamatergic signaling potentiation in CeLC neurons following CGRP release, finding greater potentiation in females than males.

The paper investigates changes in PBN neuron excitability in two mouse models of neuropathic pain and finds that increased excitability and enhanced GABAB-mediated inhibition contribute to chronic pain.

The paper investigates the role of serotonin in pain modulation, finding that sustained serotonin signaling in the spinal trigeminal nucleus is pronociceptive in chronic pain models.

This study tracks parabrachial nucleus neuronal activity in awake mice during pain and shows it correlates with arousal and can be conditioned to respond to innocuous stimuli.

This study examines transcriptomic changes in reward and sensory brain regions of juvenile mice exposed to perinatal fentanyl, revealing sex-specific gene expression patterns and enriched biological processes.

This study shows that norepinephrine transients in the parabrachial nucleus, induced by cNTScat input, amplify PB activity and sensory afferent responses in mice.

The paper identifies RVM neurons expressing the kappa-opioid receptor that inhibit pain and itch via a descending circuit in mice.

This study shows that environmental enrichment can reverse behavioral and synaptic deficits caused by perinatal fentanyl exposure in mice.

This study shows that perinatal fentanyl exposure causes long-term impairments in somatosensory function and behavior in mice, with changes in synaptic and morphological properties.

The paper identifies a direct trigeminal ganglion-to-parabrachial connection that processes dura inputs, suggesting a role in migraine pathogenesis.

The paper investigates how signaling pathways modulate synaptic transmission and neuronal excitability in the parabrachial nucleus, linking these changes to chronic pain mechanisms.

This study compares fentanyl withdrawal and associated pain in mice and rats, finding species-specific differences in withdrawal symptoms and pain expression.

The paper identifies a CeA-LPB pathway that regulates pain perception and shows its suppression in chronic pain.

This study shows that perinatal fentanyl exposure in mice leads to somatic withdrawal and lifelong neurobehavioral changes similar to human neonatal opioid withdrawal syndrome.

This study identifies 6-9 Hz cortical oscillations as a reliable biomarker for detecting chronic pain in rats by comparing individual pre-injury baselines to post-injury power changes.