| It is well known that vestibular apparatus is the important reception and regulation system controls posture and movement. The medial vestibular nucleus (MVN), one of the most important nuclei in the vestibular nucleus complex in the brainstem, is the main nucleus for transmission of information from peripheral vestibular input to the central pathways. Although many studies have focused on vestibulo-ocular reflex and vestibulo-spinal reflex, little have known about vestibulo-autonomic reflex. MVN is the important relay station of vestibulo-autonomic reflex. Stimulation of the vestibular apparatus can influence the activity of internal organs such as blood pressure, heart rate and breath. On the contraly blood pressure can influence the function of vestibular apparatus. Numerous previous studies suggest that amino acids are the main neurotransmitters in vestibulo-ocular reflex. Our previous study observede that hemorrhag-induced acute hypotension influence the activity of the neurons in the MVN by the afferent impulses from the peripheral vestibular organ of anaesthetic rats and that some amino acids are involved in this process. However, the detailed role of amino acids in the MVN following acute hypotension of conscious rats was not investigated and the detailed mechanism of receptor is still not clear.Therefore, in order to investigate some neurochemistry mechanism of vestibular nuclei excitation following acute hypotension, we used microdialysis technique and high performance liquid chromatography (HPLC) to measure the changes of amino acids in this central area of conscious rats. And in order to study the relationship between types of glutamate receptor and intracellular signal transduction system in the function of VN affected by acute hypotension, we obserbed cFos like protein expression by using immunohistochemistry and pharmacology.Results as follows:1. The vestibular symptoms were observed from 6 h to 168 h after infusing arsanilic acid into the tympanic cavity. Some of these symptoms gradually disappeared over time, but others continued. Frequency of spontaneous nystagmus gradually enhanced from its appearance, the high incidence of spontaneous nystagmus appeared at 24 h after UL, then reduced and disappeared at 120 h. The head deviation gradually augmented, the peak time appeared at 120 h, and did not restore until 168 h. The body rolling appeared from 6 h, and the peak time appeared at 96 h after UL, then reduced and disappeared at 168 h.2. In the control group, the level of Asp, Glu, Ala release increased, but Gln, Gly, Tau and GABA release decreased in the MVN following SNP-induced acute hypotension in conscious rats (P< 0.05, n=12).3. The level of Asp, Glu, Ala release increased, but Gln, Gly, Tau and GABA release decreased in the contralateral MVN to the lesion side following SNP-induced acute hypotension 14 days after UL in conscious rats (P< 0.05, n=12). But acute hypotension induced by SNP did not change the levels of Asp, Glu, Ala, Gln, Gly, Tau and GABA release in the ipsilateral MVN to the lesion side after UL 14 days in conscious rats (P>0.05, n=12).4. In the control group, the intravenous administration of saline at the same volume and rate as the infused SNP did not induce significant expression of cFL immunoreactive neuron in the MVN of intact labyrinthine conscious rats. Acute hypotension was induced by intravenous infusion of SNP. Compared to the control group, there was significant expression of cFL immunoreactive neurons bilaterally in the MVN after acute hypotension 30 min,60 min and 120 min of intact labyrinthine conscious rats. Expression of cFL immunoreactive neurons peaked at 60 min after SNP injection. There was significant difference between control group and SNP-injection group (P< 0.001, n=6).5. Unilateral chemical labyrinthectomy was performed 14 days before the start of the experiment to eliminate afferent signals from the peripheral vestibular receptors in the inner ear. Acute hypotension was induced by intravenous infusion of SNP. Few numbers of cFL immunoreactive neuron were expressed in the ipsilateral MVN to the lesion side following SNP-induced acute hypotension 14 days after UL. There were significant expression of cFL immunoreactive neurons in contralateral MVN to the lesion side following SNP-induced acute hypotension 30 min,60 min and 120 min of UL conscious rats. Expression of cFL immunoreactive neurons peaked at 60 min in contralateral MVN to the lesion side following SNP-induced acute hypotension of UL conscious rats. There was significant difference between bilateral MVN following SNP-induced acute hypotension of UL conscious rats (P< 0.001, n=6).6. After intracerebro ventricular microinjection NMD A 60 min, a NMD A receptor agonist of glutamate, there were significant expression of cFL immunoreactive neurons bilaterally in the MVN of intact labyrinthine conscious rats. But in the control group few numbers of cFL immunoreactive neuron was expressed in the MVN after intracerebroventricular microinjection of artificial cerebrospinal fluid(ACSF) of intact labyrinthine conscious rats. There was significant difference between control group and NMDA group of intact labyrinthine conscious rats(P< 0.001, n=6).7. After intracerebroventricular microinjection 60 min of AMPA, an AMPA receptor agonist of glutamate, there were significant expression of cFL immunoreactive neurons bilaterally in the MVN of intact labyrinthine conscious rats. But in the control group few numbers of cFL immunoreactive neuron was expressed in the MVN after intracerebroventricular microinjection of ACSF of intact labyrinthine conscious rats. There was significant difference between control group and AMPA group of intact labyrinthine conscious rats (P< 0.001, n=6).8. In the control group, after intracerebroventricular microinjection of ACSF, there were significant expression of cFL immunoreactive neurons bilaterally in the MVN following SNP-induced acute hypotension 60 min of intact labyrinthine conscious rats. But after intracerebroventricular microinjection of MK-801, a NMDA receptor antagonist of glutamate, few numbers of cFL immunoreactive neuron was expressed in the MVN after SNP-induced acute hypotension 60 min of intact labyrinthine conscious rats. There was significant difference between control group and MK-801 group of intact labyrinthine conscious rats (P< 0.001, n=6).9. In the control group, after intracerebroventricular microinjection of ACSF, there were significant expression of cFL immunoreactive neurons bilaterally in the MVN following SNP-induced acute hypotension 60 min of intact labyrinthine conscious rats. But after intracerebroventricular microinjection of CNQX, an AMPA receptor antagonist of glutamate, few numbers of cFL immunoreactive neuron was expressed in the MVN following SNP-induced acute hypotension 60 min of intact labyrinthine conscious rats. There was significant difference between control group and CNQX group of intact labyrinthine conscious rats (P< 0.001, n=6).10. Unilateral chemical labyrinthectomy was performed 14 days before the start of the experiment to eliminate afferent signals from the peripheral vestibular receptors in the inner ear. Acute hypotension was induced by intravenous infusion of SNP. In the control group, after intracerebroventricular microinjection of ACSF, there were significant expression of cFL immunoreactive neurons in contralateral MVN to the lesion side following SNP-induced acute hypotension 60 min of UL conscious rats; but few numbers of cFL immunoreactive neuron was expressed in ipsilateral MVN to the lesion side following SNP-induced acute hypotension 60 min of UL conscious rats. There was significant asymmetric expression between bilateral MVN of UL conscious rats (P< 0.001, n=6).11. Unilateral chemical labyrinthectomy was performed 14 days before the start of the experiment to eliminate afferent signals from the peripheral vestibular receptors in the inner ear. Acute hypotension was induced by intravenous infusion of SNP. After intracerebroventricular microinjection of MK-801, a NMDA receptor antagonist of glutamate, few numbers of cFL immunoreactive neuron was expressed in the bilateral MVN following SNP-induced acute hypotension 60 min of UL conscious rats. There was no significant difference between bilateral MVN of UL conscious rats in the experimental group. But there was significant difference between control group(ACSF+SNP) and MK-801 group(MK-801+SNP) in contralateral MVN to the lesion side of UL conscious rats (P< 0.001, n=6).12. Unilateral chemical labyrinthectomy was performed 14 days before the start of the experiment to eliminate afferent signals from the peripheral vestibular receptors in the inner ear. Acute hypotension was induced by intravenous infusion of SNP. After intracerebro ventricular microinjection of CNQX, an AMP A receptor antagonist of glutamate, few numbers of cFL immunoreactive neurons was expressed in the bilateral MVN following SNP-induced acute hypotension 60 min of UL conscious rats. There was no significant difference between bilateral MVN of UL conscious rats. But, there was significant difference between control group(ACSF+SNP) and CNQX group(CNQX+SNP) in contralateral MVN to the lesion side of UL conscious rats (P < 0.001, n=6).The results of this study suggested:1. The SNP-induced acute hypotension may influence the activity of the neurons in the MVN by the afferent impulses from the peripheral vestibular organ, and that some amino acids such as Asp, Glu, Ala, Gln, Gly, Tau and GABA may be involved in this process.2.The afferent signals from the peripheral vestibular receptors are essential for cFos protein expression in the vestibular nuclei following acute hypotension.3. The excitatory afferent signals from the peripheral vestibular receptors, resulting from acute hypotension, release glutamate into postsynaptic neurons in the vestibular nuclei and the excitatory signals are transmitted through the NMDA receptors and AMPA receptors of glutamate in the vestibular system. |
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