Here we describe fully functional GABAergic communication within rodent peripheral sensory ganglia and show that it can modulate transmission of pain-related signals from the peripheral sensory nerves to the CNS.
First-pass extracted concept
local GABAergic signaling within sensory ganglia
Aliases
peripheral GABAergic signaling in sensory ganglia
Evidence Snippets
Supporting Sources
Linked Claims
In vivo focal infusion of GABA or a GABA reuptake inhibitor to sensory ganglia reduced acute peripherally induced nociception and alleviated neuropathic and inflammatory pain.
In vivo focal infusion of GABA or GABA reuptake inhibitor to sensory ganglia dramatically reduced acute peripherally induced nociception and alleviated neuropathic and inflammatory pain.
GABA depolarized most sensory neuron somata but still produced net inhibition of nociceptive transmission because of filtering at nociceptive fiber T-junctions.
Mechanistically, GABA depolarized the majority of sensory neuron somata, yet produced a net inhibitory effect on the nociceptive transmission due to the filtering effect at nociceptive fiber T-junctions.
Rodent peripheral sensory ganglia contain functional GABAergic communication that modulates transmission of pain-related signals from peripheral sensory nerves to the CNS.
Here we describe fully functional GABAergic communication within rodent peripheral sensory ganglia and show that it can modulate transmission of pain-related signals from the peripheral sensory nerves to the CNS.
Sensory neurons express major proteins necessary for GABA synthesis and release and release GABA in response to depolarization.
We found that sensory neurons express major proteins necessary for GABA synthesis and release and that sensory neurons released GABA in response to depolarization.
Focal application of GABA receptor antagonists to sensory ganglia triggered or exacerbated peripherally induced nociception.
In addition, focal application of GABA receptor antagonists to sensory ganglia triggered or exacerbated peripherally induced nociception.