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首页> 外文期刊>The European Journal of Neuroscience >Medial prefrontal cortex NMDA receptors and nitric oxide modulate the parasympathetic component of the baroreflex.
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Medial prefrontal cortex NMDA receptors and nitric oxide modulate the parasympathetic component of the baroreflex.

机译：内侧前额叶皮层NMDA受体和一氧化氮调节压力反射的副交感成分。

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The ventral portion of the medial prefrontal cortex (vMPFC) is involved in the modulation of the parasympathetic component of the baroreflex. In the present study, we verified the effect of blockade of vMPFC glutamatergic receptors and nitric oxide synthases (NOS) on the parasympathetic component of baroreflex in awake rats. Bilateral microinjection of the non-selective ionotropic glutamate antagonist kynurenic acid (KYN) into the vMPFC caused a shift of the threshold of reflex bradycardia toward higher pressures in response to increases in mean arterial pressure (MAP) caused by intravenous infusion of phenylephrine, thus indicating a tonic facilitatory influence action of vMPFC glutamate receptors on the parasympathetic component of the baroreflex. The effect of blockade of vMPFC-NMDA receptors by AP7 was similar to that observed after KYN, suggesting mediation via NMDA receptors. Pretreatment with the NOS inhibitor L-NAME or the specific neural NOS (nNOS) N(omega)-propyl-l-arginine microinjected in the vMPFC caused a shift of the reflex threshold toward higher pressures that was similar to that observed after blockade of NMDA receptors, thus indicating participation of the NO/NMDA-receptor pathway in the vMPFC modulation of the parasympathetic component of the baroreflex. In conclusion, our data indicate that glutamatergic neurotransmission in the vMPFC has a tonic facilitatory influence on the parasympathetic component of the baroreflex. Because local treatment with either the nNOS inhibitor N(omega)-propyl-l-arginine or the specific NMDA antagonist AP7 had similar effects on the baroreflex, it is also suggested that this modulation involves an NMDA-NO interaction within the vMPFC.
机译：内侧前额叶皮层的腹侧部分（vMPFC）参与压力感受性反射的副交感成分的调节。在本研究中，我们验证了vMPFC谷氨酸能受体和一氧化氮合酶（NOS）的阻断对清醒大鼠压力反射的副交感成分的影响。非选择性离子型谷氨酸拮抗剂强尿酸（KYN）的双侧显微注射响应于静脉输注去氧肾上腺素引起的平均动脉压（MAP）升高，导致反射性心动过缓阈值向更高的压力转移。 vMPFC谷氨酸受体对压力反射的副交感成分的促进作用。 AP7阻断vMPFC-NMDA受体的作用与KYN后观察到的相似，表明通过NMDA受体介导。用微注射到vMPFC中的NOS抑制剂L-NAME或特定的神经NOS（nNOS）N（ω）-丙基-1-精氨酸进行预处理会导致反射阈值向更高的压力偏移，这类似于在NMDA阻滞后观察到的受体，因此表明NO / NMDA受体途径参与了压力感受反射的副交感神经成分的vMPFC调节。总之，我们的数据表明vMPFC中的谷氨酸能神经传递对压力反射的副交感神经成分有滋补作用。因为使用nNOS抑制剂N（ω）-丙基-1-精氨酸或特定的NMDA拮抗剂AP7进行的局部治疗对压力反射具有相似的作用，所以还建议这种调节涉及vMPFC中的NMDA-NO相互作用。

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