The role of 5-HT, GABA and opioid peptides in presynaptic inhibition of tooth pulp input from the medial brainstem.
In decerebrate or chloralose-anaesthetized cats electrical stimulation in the spinal trigeminal nucleus evoked antidromic responses in the mandibular canine tooth pulp. Conditioning stimulation in nucleus raphe magnus (NRM) and in the adjacent contralateral medullary reticular formation, nucleus reticularis gigantocellularis (NRGC) and nucleus reticularis magnocellularis (NRMC), produced a decrease in the threshold for the antidromic responses in a proportion of the tooth pulp inputs. This was interpreted as being due to depolarization of the tooth pulp afferent terminals, reflecting presynaptic inhibition. The primary afferent depolarization (PAD) of tooth pulp afferent terminals by NRM stimulation could be selectively blocked by bicuculline applied intravenously or by iontophoresis in the terminal region. Intravenous naloxone, cinanserin and methysergide had no effect on the PAD evoked from NRM, NRGC or NRMC. Thus NRM appears to exert presynaptic inhibitory control of A delta tooth pulp input to the spinal trigeminal nucleus via GABA-containing neurones.
D000344:Afferent Pathways / Q000502:physiology; D000818:Animals; D001933:Brain Stem / Q000502:physiology*; D002415:Cats; D003782:Dental Pulp / Q000294:innervation*; D004558:Electric Stimulation; D004723:Endorphins / Q000502:physiology*; D005073:Evoked Potentials, Somatosensory; D009433:Neural Inhibition; D009619:Nociceptors / Q000502:physiology; D011903:Raphe Nuclei / Q000502:physiology*; D012154:Reticular Formation / Q000502:physiology*; D012684:Sensory Thresholds; D012701:Serotonin / Q000502:physiology*; D013569:Synapses / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
D004723:Endorphins; D012701:Serotonin; D005680:gamma-Aminobutyric Acid