Role of the medullary lateral tegmental field in reflex-mediated sympathoexcitation in cats.
We tested the hypothesis that blockade of N-methyl-D-aspartate (NMDA) and non-NMDA receptors on medullary lateral tegmental field (LTF) neurons would reduce the sympathoexcitatory responses elicited by electrical stimulation of vagal, trigeminal, and sciatic afferents, posterior hypothalamus, and midbrain periaqueductal gray as well as by activation of arterial chemoreceptors with intravenous NaCN. Bilateral microinjection of a non-NMDA receptor antagonist into LTF of urethane-anesthetized cats significantly decreased vagal afferent-evoked excitatory responses in inferior cardiac and vertebral nerves to 29 +/- 8 and 24 +/- 6% of control (n = 7), respectively. Likewise, blockade of non-NMDA receptors significantly reduced chemoreceptor reflex-induced increases in inferior cardiac (from 210 +/- 22 to 129 +/- 13% of control; n = 4) and vertebral nerves (from 253 +/- 41 to 154 +/- 20% of control; n = 7) and mean arterial pressure (from 39 +/- 7 to 21 +/- 5 mmHg; n = 8). Microinjection of muscimol, but not an NMDA receptor antagonist, caused similar attenuation of these excitatory responses. Sympathoexcitatory responses to the other stimuli were not attenuated by microinjection of a non-NMDA receptor antagonist or muscimol into LTF. In fact, excitatory responses elicited by stimulation of trigeminal, and in some cases sciatic, afferents were enhanced. These data reveal two new roles for the LTF in control of sympathetic nerve activity in cats. One, LTF neurons are involved in mediating sympathoexcitation elicited by activation of vagal afferents and arterial chemoreceptors, primarily via activation of non-NMDA receptors. Two, non-NMDA receptor-mediated activation of other LTF neurons tonically suppresses transmission in trigeminal-sympathetic and sciatic-sympathetic reflex pathways.
Orer
Hakan S
HS
Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan 48824, USA.
Gebber
Gerard L
GL
Phillips
Shaun W
SW
Barman
Susan M
SM
D015763:2-Amino-5-phosphonovalerate / Q000008:administration & dosage / Q000494:pharmacology; D000818:Animals; D001158:Arteries / Q000187:drug effects / Q000502:physiology; D002415:Cats; D002628:Chemoreceptor Cells / Q000502:physiology; D003714:Denervation; D004558:Electric Stimulation; D018691:Excitatory Amino Acid Antagonists / Q000008:administration & dosage / Q000494:pharmacology; D018755:GABA Agonists / Q000494:pharmacology; D008526:Medulla Oblongata / Q000502:physiology*; D008845:Microinjections; D009118:Muscimol / Q000494:pharmacology; D010487:Periaqueductal Gray / Q000502:physiology; D011311:Pressoreceptors / Q000502:physiology; D011810:Quinoxalines / Q000008:administration & dosage / Q000494:pharmacology; D018079:Receptors, GABA / Q000187:drug effects; D017470:Receptors, Glutamate / Q000187:drug effects / Q000502:physiology; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors; D012018:Reflex / Q000502:physiology*; D012584:Sciatic Nerve / Q000502:physiology; D012966:Sodium Cyanide / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000502:physiology*; D014276:Trigeminal Nerve / Q000502:physiology
D018691:Excitatory Amino Acid Antagonists; D018755:GABA Agonists; D011810:Quinoxalines; D018079:Receptors, GABA; D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate; C062865:2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline; D009118:Muscimol; D015763:2-Amino-5-phosphonovalerate; D012966:Sodium Cyanide