Inhibitory control of nociceptive responses of trigeminal spinal nucleus cells by somatosensory corticofugal projection in rat.
The caudal division of the trigeminal spinal nucleus (Sp5C) is an important brainstem relay station of orofacial pain transmission. The aim of the present study was to examine the effect of cortical electrical stimulation on nociceptive responses in Sp5C neurons. Extracellular recordings were performed in the Sp5C nucleus by tungsten microelectrodes in urethane-anesthetized Sprague-Dawley rats. Nociceptive stimulation was produced by application of capsaicin cream on the whisker pad or by constriction of the infraorbital nerve. Capsaicin application evoked a long-lasting increase in the spontaneous firing rate from 1.4±0.2 to 3.4±0.6 spikes/s. Non-noxious tactile responses from stimuli delivered to the receptive field (RF) center decreased 5 min. after capsaicin application (from 2.3±0.1 to 1.6±0.1 spikes/stimulus) while responses from the whisker located at the RF periphery increased (from 1.3±0.2 to 2.0±0.1 spikes/stimulus under capsaicin). Electrical train stimulation of the primary (S1) or secondary (S2) somatosensory cortical areas reduced the increase in the firing rate evoked by capsaicin. Also, S1, but not S2, cortical stimulation reduced the increase in non-noxious tactile responses from the RF periphery. Inhibitory cortical effects were mediated by the activation of GABAergic and glycinergic neurons because they were blocked by bicuculline or strychnine. The S1 and S2 cortical stimulation also inhibited Sp5C neurons in animals with constriction of the infraorbital nerve. Consequently, the corticofugal projection from S1 and S2 cortical areas modulates nociceptive responses of Sp5C neurons and may control the transmission of nociceptive sensory stimulus.
Departamento de Anatomía, Histología y Neurociencia, Facultad de Medicina, Universidad Autónoma de Madrid, 28029 Madrid, Spain.
E
E
Malmierca
Y B
YB
Martin
A
A
Nuñez
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000344:Afferent Pathways / Q000502:physiology*; D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D001703:Biophysics; D002211:Capsaicin / Q000009:adverse effects; D003250:Constriction; D004195:Disease Models, Animal; D004558:Electric Stimulation / Q000009:adverse effects; D005260:Female; D058787:GABA-A Receptor Antagonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000494:pharmacology; D018684:Glycine Agents / Q000494:pharmacology; D006930:Hyperalgesia / Q000473:pathology / Q000503:physiopathology; D007478:Iontophoresis; D008297:Male; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D009437:Neuralgia / Q000209:etiology / Q000473:pathology; D009619:Nociceptors / Q000187:drug effects / Q000502:physiology*; D010146:Pain / Q000139:chemically induced / Q000473:pathology*; D010812:Physical Stimulation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013003:Somatosensory Cortex / Q000166:cytology / Q000502:physiology*; D013331:Strychnine / Q000494:pharmacology; D013997:Time Factors; D014279:Trigeminal Nucleus, Spinal / Q000166:cytology*
D058787:GABA-A Receptor Antagonists; D018684:Glycine Agents; D018698:Glutamic Acid; D013331:Strychnine; D002211:Capsaicin; D001640:Bicuculline