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L'ocytocine, un neurotransmetteur qui soulage les douleurs
Spinal Cord Mechanisms in Acute and Chronic Pain States
Conséquences des perturbations périnatales sur les réponses douloureuses [= Consequences of perinatal disturbances on pain responses]
Neurohormonal effects of oxytocin and vasopressin receptor agonists on spinal pain processing in male rats.
Oxytocin Signaling in Pain: Cellular, Circuit, System, and Behavioral Levels.
Neurohormonal effects of oxytocin and vasopressin receptor agonists on spinal pain processing in male rats.
PKC activation sets an upper limit to the functional plasticity of GABAergic transmission induced by endogenous neurosteroids.
Etifoxine stimulates allopregnanolone synthesis in the spinal cord to produce analgesia in experimental mononeuropathy.
Radiotelemetric and symptomatic evaluation of pain in the rat after laparotomy: long-term benefits of perioperative ropivacaine care.
Conséquences sur les voies de la douleur d’une séparation précoce
Poincaré plot descriptors of heart rate variability as markers of persistent pain expression in freely moving rats.
Insights into the mechanisms and the emergence of sex-differences in pain.
Characterization of the fast GABAergic inhibitory action of etifoxine during spinal nociceptive processing in male rats.
Plasma glucocorticoids differentially modulate phasic and tonic GABA inhibition during early postnatal development in rat spinal lamina II.
Fast non-genomic effects of progesterone-derived neurosteroids on nociceptive thresholds and pain symptoms.
Analgesic strategies aimed at stimulating the endogenous production of allopregnanolone.
Corticosterone analgesia is mediated by the spinal production of neuroactive metabolites that enhance GABAergic inhibitory transmission on dorsal horn rat neurons.
Fast nongenomic effects of steroids on synaptic transmission and role of endogenous neurosteroids in spinal pain pathways.
Long-lasting spinal oxytocin analgesia is ensured by the stimulation of allopregnanolone synthesis which potentiates GABA(A) receptor-mediated synaptic inhibition.
Reduction and prevention of vincristine-induced neuropathic pain symptoms by the non-benzodiazepine anxiolytic etifoxine are mediated by 3alpha-reduced neurosteroids.

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