Interaction between thyrotropin-releasing hormone (TRH) and NMDA-receptor-mediated responses in hypoglossal motoneurones
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Interaction between thyrotropin-releasing hormone (TRH) and NMDA-receptor-mediated responses in hypoglossal motoneurones. / Rekling, J C.
In: Brain Research, Vol. 578, No. 1-2, 1992, p. 289-96.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Interaction between thyrotropin-releasing hormone (TRH) and NMDA-receptor-mediated responses in hypoglossal motoneurones
AU - Rekling, J C
N1 - Keywords: 2-Amino-5-phosphonovalerate; 6-Cyano-7-nitroquinoxaline-2,3-dione; Animals; Aspartic Acid; Brain Stem; Evoked Potentials; Glutamates; Glutamic Acid; Guinea Pigs; Hypoglossal Nerve; Membrane Potentials; Motor Neurons; N-Methylaspartate; Quinoxalines; Quisqualic Acid; Receptors, N-Methyl-D-Aspartate; Receptors, Neurotransmitter; Receptors, Thyrotropin-Releasing Hormone; Synapses; Tetrodotoxin; Thyrotropin-Releasing Hormone
PY - 1992
Y1 - 1992
N2 - The effect of thyrotropin-releasing hormone (TRH) on the responses to excitatory amino acids was investigated in hypoglossal motoneurones in an in vitro preparation of the brainstem from guinea pigs using current clamp and discontinuous single electrode voltage clamp (dSEVC). Bath application of 20-50 microM TRH markedly potentiated the response to iontophoretically applied NMDA, whereas no potentiation of the response to glutamate, aspartate or quisqualic acid was seen. Voltage clamp experiments showed that TRH did not increase the current flowing through NMDA channels, thus a direct modulatory role of TRH on NMDA channels was not a likely explanation of the potentiation. Voltage clamp studies of the current-voltage relationship showed that the potentiation of the response to NMDA and lack of potentiation of the response to quisqualic acid was a result of an interaction between the actions of TRH and the amino acids on the electroresponsive profile of the membrane. Endogenous NMDA receptor activation was produced by tetanic stimulation of the reticular formation dorsolaterally to the hypoglossal nucleus, evoking large APV sensitive EPSPs in the presence of CNQX, a non-NMDA blocker. The amplitude and duration of these potentials were increased at more positive membrane potentials in response to TRH. It is concluded that TRH can act as a neuromodulator-potentiating the response to NMDA receptor activation-simply by changing the electroresponsive properties of the membrane.
AB - The effect of thyrotropin-releasing hormone (TRH) on the responses to excitatory amino acids was investigated in hypoglossal motoneurones in an in vitro preparation of the brainstem from guinea pigs using current clamp and discontinuous single electrode voltage clamp (dSEVC). Bath application of 20-50 microM TRH markedly potentiated the response to iontophoretically applied NMDA, whereas no potentiation of the response to glutamate, aspartate or quisqualic acid was seen. Voltage clamp experiments showed that TRH did not increase the current flowing through NMDA channels, thus a direct modulatory role of TRH on NMDA channels was not a likely explanation of the potentiation. Voltage clamp studies of the current-voltage relationship showed that the potentiation of the response to NMDA and lack of potentiation of the response to quisqualic acid was a result of an interaction between the actions of TRH and the amino acids on the electroresponsive profile of the membrane. Endogenous NMDA receptor activation was produced by tetanic stimulation of the reticular formation dorsolaterally to the hypoglossal nucleus, evoking large APV sensitive EPSPs in the presence of CNQX, a non-NMDA blocker. The amplitude and duration of these potentials were increased at more positive membrane potentials in response to TRH. It is concluded that TRH can act as a neuromodulator-potentiating the response to NMDA receptor activation-simply by changing the electroresponsive properties of the membrane.
M3 - Journal article
C2 - 1354998
VL - 578
SP - 289
EP - 296
JO - Brain Research
JF - Brain Research
SN - 0006-8993
IS - 1-2
ER -
ID: 9256105