Vestibular compensation is an important model for developing the prevention and intervention strategies of vestibular disorders, and investigating the plasticity of the adult central nervous system induced by peripheral injury. Medial vestibular nucleus (MVN) in brainstem is critical center for vestibular compensation. Its neuronal excitability and sensitivity have been implicated in normal function of vestibular system. Previous studies mainly focused on the changes in neuronal excitability of the MVN in lesional side of the rat model of vestibular compensation following the unilateral labyrinthectomy (UL). However, the plasticity of sensitivity of bilateral MVN neurons dynamically responding to input stimuli is still largely unknown. In the present study, by using qPCR, whole-cell patch clamp recording in acute brain slices and behavioral techniques, we observed that 6 h after UL, rats showed a significant deficit in spontaneous locomotion, and a decrease in excitability of type B neurons in the ipsilesional rather than contralesional MVN. By contrast, type B neurons in the contralesional rather than ipsilesional MVN exhibited an increase in response sensitivity to the ramp and step input current stimuli. One week after UL, both the neuronal excitability of the ipsilesional MVN and the neuronal sensitivity of the contralesional MVN recovered to the baseline, accompanied by a compensation of spontaneous locomotion. In addition, the data showed that the small conductance Ca²⁺-activated K⁺ (SK) channel involved in the regulation of type B MVN neuronal sensitivity, showed a selective decrease in expression in the contralesional MVN 6 h after UL, and returned to normal level 1 week later. Pharmacological blockage of SK channel in contralateral MVN to inhibit the UL-induced functional plasticity of SK channel significantly delayed the compensation of vestibular motor dysfunction. These results suggest that the changes in plasticity of the ipsilesional MVN neuronal excitability, together with changes in the contralesional MVN neuronal sensitivity, may both contribute to the development of vestibular symptoms as well as vestibular compensation, and SK channel may be an essential ionic mechanism responsible for the dynamic changes of MVN neuronal sensitivity during vestibular compensation.
Animals ; Locomotion ; Neurons/physiology* ; Patch-Clamp Techniques ; Rats ; Vestibular Nuclei/metabolism* ; Vestibule, Labyrinth

OBJECTIVES: Excitability o medial vestibular nucleus (MVN) in the brainstem can be affected by changes in the arterial blood pressure. Several animal studies have demonstrated that acute hypotension results in the alteration of multiunit activities and expression of cFos protein in the MVN. In the field of extracellular electrophysiological recording, tetrode technology and spike sorting algorithms can easily identify single unit activity from multiunit activities in the brain. However, detailed properties of electrophysiological changes in single unit of the MVN during acute hypotension have been unknown. METHODS: Therefore, we applied tetrode techniques and electrophysiological characterization methods to know the effect of acute hypotension on single unit activities of the MVN of rats. RESULTS: Two or 3 types of unit could be classified according to the morphology of spikes and firing properties of neurons. Acute hypotension elicited 4 types of changes in spontaneous firing of single unit in the MVN. Most of these neurons showed excitatory responses for about within 1 minute after the induction of acute hypotension and then returned to the baseline activity 10 minutes after the injection of sodium nitroprusside. There was also gradual increase in spontaneous firing in some units. In contrast small proportion of units showed rapid reduction of firing rate just after acute hypotension. CONCLUSIONS: Therefore, application of tetrode technology and spike sorting algorithms is another method for the monitoring of electrical activity of vestibular nuclear during acute hypotension.
Animals ; Arterial Pressure ; Brain ; Brain Stem ; Fires ; Hypotension ; Methods ; Neurons ; Nitroprusside ; Rats ; Vestibular Nuclei

What is memory? How does the brain process the sensory information and modify an organism's behavior? Many neuroscientists have focused on the activity- and experience-dependent modifications of synaptic functions in order to solve these fundamental questions in neuroscience. Recently, the plasticity of intrinsic excitability (called intrinsic plasticity) has emerged as an important element for information processing and storage in the brain. As the cerebellar Purkinje cells are the sole output neurons in the cerebellar cortex and the information is conveyed from a neuron to its relay neurons by forms of action potential firing, the modulation of the intrinsic firing activity may play a critical role in the cerebellar learning. Many voltage-gated and/or Ca²⁺-activated ion channels are involved in shaping the spiking output as well as integrating synaptic inputs to finely tune the cerebellar output. Recent studies suggested that the modulation of the intrinsic excitability and its plasticity in the cerebellar Purkinje cells might function as an integrator for information processing and memory formation. Moreover, the intrinsic plasticity might also determine the strength of connectivity to the sub-cortical areas such as deep cerebellar nuclei and vestibular nuclei to trigger the consolidation of the cerebellar-dependent memory by transferring the information.
Action Potentials ; Automatic Data Processing ; Brain ; Cerebellar Cortex ; Cerebellar Nuclei ; Cerebellum ; Fires ; Ion Channels ; Learning* ; Memory ; Neuronal Plasticity ; Neurons ; Neurosciences ; Plastics* ; Purkinje Cells* ; Vestibular Nuclei

Hypotension is one of the potential causes of dizziness. In this review, we summarize the studies published in recent years about the electrophysiological and pharmacological mechanisms of hypotension-induced dizziness and the role of the vestibular system in the control of blood pressure in response to hypotension. It is postulated that ischemic excitation of the peripheral vestibular hair cells as a result of a reduction in blood flow to the inner ear following hypotension leads to excitation of the central vestibular nuclei, which in turn may produce dizziness after hypotension. In addition, excitation of the vestibular nuclei following hypotension elicits the vestibulosympathetic reflex, and the reflex then regulates blood pressure by a dual-control (neurogenic and humoral control) mechanism. In fact, recent studies have shown that peripheral vestibular receptors play a role in the control of blood pressure through neural reflex pathways. This review illustrates the dual-control mechanism of peripheral vestibular receptors in the regulation of blood pressure following hypotension.
Blood Pressure* ; Dizziness ; Ear, Inner ; Epinephrine ; Glutamic Acid ; Hair Cells, Vestibular ; Hypotension* ; Reflex ; Vestibular Nuclei

Orthostatic hypotension (OH) is associated with symptoms including headache, dizziness, and syncope. The incidence of OH increases with age. Attenuation of the vestibulosympathetic reflex (VSR) is also associated with an increased incidence of OH. In order to understand the pathophysiology of OH, we investigated the physiological characteristics of the VSR in the disorder. We applied sodium nitroprusside (SNP) to conscious rats with sinoaortic denervation in order to induce hypotension. Expression of pERK in the intermediolateral cell column (IMC) of the T4~7 thoracic spinal regions, blood epinephrine levels, and blood pressure were evaluated following the administration of glutamate and/or SNP. SNP-induced hypotension led to increased pERK expression in the medial vestibular nucleus (MVN), rostral ventrolateral medullary nucleus (RVLM) and the IMC, as well as increased blood epinephrine levels. We co-administered either a glutamate receptor agonist or a glutamate receptor antagonist to the MVN or the RVLM. The administration of the glutamate receptor agonists, AMPA or NMDA, to the MVN or RVLM led to elevated blood pressure, increased pERK expression in the IMC, and increased blood epinephrine levels. Administration of the glutamate receptor antagonists, CNQX or MK801, to the MVN or RVLM attenuated the increased pERK expression and blood epinephrine levels caused by SNP-induced hypotension. These results suggest that two components of the pathway which maintains blood pressure are involved in the VSR induced by SNP. These are the neurogenic control of blood pressure via the RVLM and the humoral control of blood pressure via epinephrine release from the adrenal medulla.
6-Cyano-7-nitroquinoxaline-2,3-dione ; Adrenal Medulla ; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid ; Animals ; Blood Pressure ; Denervation ; Dizocilpine Maleate ; Dizziness ; Epinephrine ; Excitatory Amino Acid Antagonists ; Glutamic Acid ; Headache ; Hypotension* ; Hypotension, Orthostatic ; Incidence ; N-Methylaspartate ; Nitroprusside ; Rats* ; Receptors, Glutamate ; Reflex* ; Spinal Cord Lateral Horn ; Syncope ; Vestibular Nuclei

Periodic alternating nystagmus (PAN) is characterized by a periodical reversal in the direction of the nystagmus. Acquired PAN is caused by lesions of the inferior cerebellar vermis, causing disinhibition of the velocity storage mechanism, which is mediated by the vestibular nuclei. An eighty-year-old woman with abscess in midline cerebellum experienced dizziness and imbalance. We observed short period PAN with 7-8 seconds.
Abscess ; Cerebellum ; Dizziness ; Female ; Humans ; Nystagmus, Pathologic ; Vestibular Nuclei

OBJECTIVE: Growing hypotheses indicate the galvanic vestibular stimulation (GVS) as an alternative method to manage the symptoms of parkinson's disease (PD). GVS is easy and safe for use, and non-invasive. However, it is elusive how the neural information caused by GVS is transmitted in the central nervous system and relieves PD symptoms. To answer this question, we investigated the transmission of neural information by GVS in the central vestibular system, focused on vestibular nucleus (VN). METHODS: Twenty guinea pigs were used for this study for the extracellular neuronal recordings in the VN. The neuronal responses to rotation and GVS were analyzed by curve-fitting, and the numerical responding features, amplitudes and baselines, were computed. The effects of stimuli were examined by comparing these features. RESULTS: Twenty six vestibular neurons (15 regular and 11 irregular neurons) were recorded. Comparing the difference of baselines, we found the neural information was linearly transmitted with a reduced sensitivity (0.75). The linearity in the neural transmission was stronger in the neuronal groups with regular (correlation coefficient [Cor. Coef.]=0.91) and low sensitive units (Cor. Coef.=0.93), compared with those with irregular (Cor. Coef.=0.86) and high-sensitive neurons (Cor. Coef.=0.77). CONCLUSION: The neural information by GVS was linearly transmitted no matter what the neuronal characteristics were.
Animals ; Central Nervous System ; Guinea Pigs ; Methods ; Neurons ; Parkinson Disease ; Synaptic Transmission ; Vestibular Nuclei

OBJECTIVE: The cerebral cortex can modulate vestibular functions through direct control of neuronal activities in the vestibular nuclei. The purpose of this study was to investigate the effect of unilateral cortical lesion or cortical stimulation on static vestibular symptoms and vestibular nuclear activities at the acute stage of vestibular compensation following unilateral labyrinthectomy (UL) in rats. METHODS: The photothrombic ischemic injury using rose bengal was induced in the primary motor cortex or primary sensory cortex, and electrical stimulation was applied to the primary motor cortex, primary sensory cortex, or sencondary sensory cortex, respectively, in unilateral labyrinthectomized rats. Static vestibular symptoms including ocular movement and postural deficits, and expression of c-Fos protein in the medial vestibular nucleus (MVN) were measured. RESULTS: Lesion of the motor cortex produced a marked postural deficit with paralytic weakness in the hindlimb contralateral to UL. Number of spontaneous nystagmus in animals receiving cortical lesion was significantly increased 2, 6, and 12 hours after UL compared with animals being UL only. Lesion of the primary motor cortex or stimulation of the S2 sensory cortex decreased expression of c-Fos protein in MVN following UL compared with UL only group. Electrical stimulation of S2 sensory areas caused significant reduction of static vestibular symptoms and decreased expression of c-Fos protein in MVN 24 hours following UL. CONCLUSION: The present results suggest that cerebral cortex involves in recovery of static vestibular symptoms during vestibular compensation following UL.
Animals ; Cerebral Cortex ; Compensation and Redress ; Electric Stimulation ; Hindlimb ; Motor Cortex ; Neurons ; Rats ; Rose Bengal ; Vestibular Nuclei

OBJECTIVE: The vestibular system contributes control of blood pressure during postural changes through the vestibulosympathetic reflex. In the vestibulosympathetic reflex, afferent signals from the peripheral vestibular receptors are transmitted to the vestibular nuclei, rostral ventrolateral medullary nuclei, and then to the intermediolateral cell column of the thoracolumbar spinal cord. Physiological characteristics of the vestibulosympathetic reflex in terms of neurogenic and humoral control of blood pressure were investigated in this study. METHODS: Conscious rats with sinoaortic denervation were used for removal of baroreceptors in reflex control of blood pressure, and hypotension was induced by intravenous infusion of sodium nitroprusside (SNP). Expression of c-Fos protein was measured in the medial vestibular nuclei (MVN), rostral vestrolateral medullary nuclei(RVLM), and intermediolateral cell column (IMC) in T4-7, and levels of blood epinephrine were measured following SNP-induced hypotension. RESULTS: SNP-induced hypotension significantly increased expression of c-Fos protein in the MVN, RVLM, and IMC, also significantly increased level of blood epinephrine compared to normotensive control animals. CONCLUSION: These results suggest that the vestibulosympathetic reflex regulates blood pressure through neurogenic control including MVN, RVLM, and IMC, also through humoral control including epinephrine secretion by the adrenal medulla following SNP-induced hypotension. The physiological characteristics of the reflex may contribute to basic treatment of impairment of blood pressure control during postural changes.
Adrenal Medulla ; Animals ; Blood Pressure ; Denervation ; Epinephrine ; Hypotension ; Infusions, Intravenous ; Nitroprusside ; Pressoreceptors ; Rats ; Reflex ; Spinal Cord ; Vestibular Nuclei

Significant evidence supports the role of the vestibular system in the regulation of blood pressure during postural movements. In the present study, the role of the vestibulo-spino-adrenal (VSA) axis in the modulation of blood pressure via the vestibulosympathetic reflex was clarified by immunohistochemical and enzyme immunoassay methods in conscious rats with sinoaortic denervation. Expression of c-Fos protein in the intermediolateral cell column of the middle thoracic spinal regions and blood epinephrine levels were investigated, following microinjection of glutamate receptor agonists or antagonists into the medial vestibular nucleus (MVN) and/or sodium nitroprusside (SNP)-induced hypotension. Both microinjection of glutamate receptor agonists (NMDA and AMPA) into the MVN or rostral ventrolateral medullary nucleus (RVLM) and SNP-induced hypotension led to increased number of c-Fos positive neurons in the intermediolateral cell column of the middle thoracic spinal regions and increased blood epinephrine levels. Pretreatment with microinjection of glutamate receptor antagonists (MK-801 and CNQX) into the MVN or RVLM prevented the increased number of c-Fos positive neurons resulting from SNP-induced hypotension, and reversed the increased blood epinephrine levels. These results indicate that the VSA axis may be a key component of the pathway used by the vestibulosympathetic reflex to maintain blood pressure during postural movements.
Animals ; Axis, Cervical Vertebra* ; Blood Pressure* ; Denervation ; Epinephrine ; Excitatory Amino Acid Antagonists ; Glutamic Acid ; Hypotension ; Immunoenzyme Techniques ; Microinjections ; Neurons ; Nitroprusside ; Rats* ; Receptors, Glutamate ; Reflex* ; Vestibular Nuclei ; Natural Resources