scholarly journals Inhibition by 5-hydroxytryptamine and noradrenaline in substantia gelatinosa of guinea-pig spinal trigeminal nucleus.

1995 ◽  
Vol 485 (1) ◽  
pp. 113-120 ◽  
Author(s):  
T J Grudt ◽  
J T Williams ◽  
R A Travagli
Keyword(s):  
Guinea Pig ◽  
Substantia Gelatinosa ◽  
Spinal Trigeminal Nucleus ◽  
Trigeminal Nucleus

Muscarine receptor activation in the substantia gelatinosa of the spinal trigeminal nucleus of the guinea pig

1996 ◽  
Vol 76 (6) ◽  
pp. 3817-3822 ◽  
Author(s):  
R. A. Travagli
Keyword(s):  
Guinea Pig ◽  
Receptor Activation ◽  
Substantia Gelatinosa ◽  
Spinal Trigeminal Nucleus ◽  
Trigeminal Nucleus ◽  
Postsynaptic Potentials ◽  
Inhibitory Postsynaptic Potentials ◽  
M1 Receptors ◽  
Type Receptor ◽  
M1 Type

1. Intracellular recordings were made from slices of guinea pig spinal trigeminal nucleus pars caudalis (SG). 2. Muscarine [0.3–30 microM; half maximally effective concentration (EC50) = 2.9 microM] hyperpolarized 61% of SG neurons. The effect was mimicked by carbachol (0.3–30 microM; EC50 = 3.9 microM) and antagonized by pirenzepine (1 microM). Thirty-four percent of the neurons were depolarized by muscarine and carbachol (1–30 microM: EC50 = 5.7 microM), and the effect was antagonized by pirenzepine (100 nM). 3. In approximately 80% of recordings, muscarine (10–30 microM) evoked repetitive spontaneous inhibitory postsynaptic potentials (IPSPs) that were sensitive to bicuculline (10 microM). 4. Muscarine (1–30 microM; EC50 = 3 microM) decreased the amplitude of the majority of evoked excitatory postsynaptic potentials (EPSPs), and the effect was mimicked by carbachol and antagonized by pirenzepine (100 nM). 5. These results indicate that there are at least three mechanisms by which muscarine inhibits SG neurons: 1) hyperpolarization through activation of non-M1 receptors; 2) activation of gamma-amino-butyric acid-containing interneurons that mediate IPSPs in a subset of neurons; and 3) a decrease in evoked EPSP amplitude. Muscarine can also activate SG neurons via interaction with an M1-type receptor.

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