Ionotropic NMDA receptor evokes an excitatory response in superior salivatory nucleus neurons in anaesthetized rats.
Extracellular recordings were taken from preganglionic superior salivatory nucleus (SSN) neurons projecting to submandibular and intra-lingual ganglia, in order to study the action of SSN neurons resulting from ionophoretic application of ionotropic NMDA receptor agonist in urethane-chloralose anaesthetized rats. Single SSN neurons were identified by their antidromic spike responses following stimulation of the chorda-lingual nerve (CLN), chorda tympani branches (CTBs) and the lingual nerve (LN). About one-third (33%, 10/30) of the identified SSN neurons were induced to fire by ionophoretic application of the NMDA receptor agonists used, dl-homocysteic acid (DLH) and N-methyl-D-aspartic acid (NMDA). More than half exhibited firing at high frequencies, often exceeding 40 Hz. About one-fifth (20%; 6/30) of the identified SSN neurons exhibited orthodromic spike responses to the combination of NMDA receptor agonist application and sensory nerve (CLN or LN) stimulus. These excitatory responses evoked by application of NMDA receptor agonist were attenuated (n = 4) by ionophoretic application of DL-2-amino-5-phosphonovaleric acid (AP5; NMDA receptor antagonist). About half (47%) of the neurons did not respond to any combination of NMDA receptor agonist and sensory nerve stimuli. No differences were observed between SSN neurons with B fibre axons and those with C fibre axons in response to ionophoresis of the NMDA receptor agonists. The NMDA-sensitive neurons, which exhibited high frequency firing, were predominantly found in the rostral part of the SSN. In summary, activation of ionotropic NMDA receptors exerts an excitatory effect on about half of the SSN neurons. These data support the view that NMDA receptors are involved in information processing and transmission on SSN neurons.
Oskutyte
Diana
D
Department of Physiology, The Nippon Dental University, School of Dentistry at Niigata, 1-8 Hamaura-cho Niigata 951-8580, Japan.
Ishizuka
Ken'Ichi
K
Satoh
Yoshihide
Y
Murakami
Toshiki
T
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000777:Anesthetics / Q000494:pharmacology; D000818:Animals; D002814:Chorda Tympani Nerve / Q000502:physiology; D004558:Electric Stimulation; D005071:Evoked Potentials / Q000502:physiology; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D009431:Neural Conduction / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000166:cytology / Q000187:drug effects* / Q000502:physiology; D010275:Parasympathetic Nervous System / Q000166:cytology / Q000187:drug effects* / Q000502:physiology; D011149:Pons / Q000166:cytology / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000819:agonists* / Q000378:metabolism; D012469:Salivary Glands / Q000294:innervation* / Q000502:physiology; D013361:Sublingual Gland / Q000294:innervation / Q000502:physiology; D013363:Submandibular Gland / Q000294:innervation / Q000502:physiology; D017833:Visceral Afferents / Q000502:physiology
D000777:Anesthetics; D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D016194:Receptors, N-Methyl-D-Aspartate