Nerve injury elicits a complex pattern of phenotypic changes in DRG neurons, including alterations in the expression of neurotransmitters, neuromodulators, receptors, ion channels, and structural proteins. While some of these changes are related to repair or regeneration, others may contribute to neuropathic pain.
Spinal GABA and modulation of neuropathic pain. Interneurons containing γ-aminobutyric acid (GABA) or glycine inhibit the spinal transmission of noxious sensory signals, and numerous studies indicate that spinal GABAergic inhibition is reduced after experimental nerve injury [48].
Interneurons containing γ-aminobutyric acid (GABA) or glycine inhibit the spinal transmission of noxious sensory signals, and numerous studies indicate that spinal GABAergic inhibition is reduced after experimental nerve injury [48].
Spinal endogenous inhibitory systems serve as opposing compensatory influences, and are gaining recognition for their powerful capacity to restrain allodynia and hyperalgesia.
When you get pinched, neurotransmitters are released that tell your neurons to signal pain. This signal travels to your brain and is what makes you feel pain.
When you get pinched, neurotransmitters are released that tell your neurons to signal pain. This signal travels to your brain and is what makes you feel pain.