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Biomedical subjects

P F Smith

Publications and source records attributed to P F Smith.

At least 19 recordsLinked to original sources
PubMed2001

Menstrual cycle effects on postural stability but not optokinetic function.

We investigated the effects of the menstrual cycle on visual-vestibular interaction by measuring optokinetic function and postural stability at different phases of the cycle. Menstrual cycle phase had no significant effect on gaze-holding, optokinetic nystagmus slow phase velocity, amplitude or frequency, circularvection latency or optokinetic afternystagmus frequency, amplitude or duration. While menstrual cycle phase had no significant effect on anterior-posterior sway, it did significantly affect lateral sway (P<0.001), with sway on day 5 significantly greater than on days 12 and 21 (P<0.05 and 0.01, respectively), and sway on day 25 significantly greater than that on day 21 (P<0.05).

Adolescent↗
PubMed2001

Optokinetic reflex dysfunction in multiple sclerosis.

The aim of this study was to further investigate optokinetic reflex function in multiple sclerosis. Gaze-holding in darkness, optokinetic nystagmus, optokinetic afternystagmus and latency to circularvection were measured using electro-oculography and a rotating optokinetic drum. Gaze-holding was not significantly different between the multiple sclerosis and control groups; however, four of 23 multiple sclerosis patients exhibited eccentric gaze-evoked nystagmus. There were no significant differences in either optokinetic nystagmus frequency or latency to circularvection. However, optokinetic nystagmus slow phase velocity during rise time and amplitude during beat time were significantly reduced in the multiple sclerosis group (p < 0.05 and p < 0.0001, respectively). The time constant of optokinetic afternystagmus was also significantly reduced in the multiple sclerosis group (p < 0.005). These results indicate that optokinetic nystagmus and optokinetic afternystagmus are significantly impaired multiple sclerosis.

Adult↗
PubMed2001

Differences in NOS protein expression and activity in the rat vestibular nucleus following unilateral labyrinthectomy.

We used Western blotting to analyse the expression of different isoforms of nitric oxide synthase (NOS) in the rat vestibular nucleus complex (VNC) at various times following unilateral vestibular deafferentation (UVD), together with a radioenzymatic assay to compare NOS activity at the same time points. nNOS expression did not change significantly in the ipsilateral or contralateral VNC at any time following UVD. However, eNOS expression decreased significantly (P<0.05) in the contralateral VNC at 6 h post-UVD, recovering to normal levels by 50 h. iNOS was not expressed at any time following UVD. NOS activity demonstrated a significant increase in the contralateral VNC at 6 h post-UVD (P<0.05), recovering toward normal levels by 50 h.

Animals↗
PubMed2001

Quantitative changes in gene expression of glutamate receptor subunits/subtypes in the vestibular nucleus, inferior olive and flocculus before and following unilateral labyrinthectomy in the rat: real-time quantitative PCR method.

Spontaneous recovery from the oculomotor and postural symptoms of unilateral labyrinthectomy (UL) is known as vestibular compensation, which is a useful model for investigation of the mechanisms of lesion-induced CNS plasticity. In the present study, to elucidate the molecular biological basis of vestibular compensation, we investigated changes in the mRNA expression of glutamate receptor subunit/subtypes in the rat central vestibular system, including the vestibular nucleus complex (VNC), inferior olive (IO), and cerebellar flocculus following UL, using a real-time quantitative polymerase chain reaction (PCR) method. In normal control animals, regional differences in the expression of several glutamate receptor subunit/subtypes, e.g., NR1 and NR2A subunits of the N-methyl-D-aspartic acid (NMDA) receptor, GluR2 and KA2 subtypes of non-NMDA receptors, and mGluR1 and mGluR7 metabotropic glutamate receptors, were consistent with previous results from studies using in situ hybridization histochemistry, suggesting that the real-time quantitative PCR method was a reliable procedure for evaluation of changes in mRNA expression. In the vestibular nucleus complex, NR2A, GluR2 and mGluR7 mRNA were ipsilaterally downregulated by 6 h following UL (P<0.05, P<0.05 and P<0.01, respectively). In the inferior olive, no changes in gene expression were observed. In the ipsilateral flocculus, KA2 mRNA expression was increased by 50 h post-UL (P<0.05). However, in the contralateral flocculus, mGluR1 mRNA was downregulated by 6 h post-UL (P<0.005). Both the increase in KA2 mRNA expression in the ipsilateral flocculus and the decrease in mGluR1 mRNA expression in the contralateral flocculus may have had the effect of reducing Purkinje cell inhibition of ipsilateral VNC neurons, thereby contributing to the rebalancing of spontaneous resting activity between the ipsilateral and contralateral VNCs. It is suggested that such changes in the activities of the floccular-VNC pathways may be important to the vestibular compensation process.

Animals↗
PubMed2001

Pharmacokinetics and pharmacodynamics of aztreonam and tobramycin in hospitalized patients.

BACKGROUND: Pharmacokinetic/pharmacodynamic (PK/PD) optimization of antibiotic therapy has been shown to improve outcomes in several antibiotic classes. Despite the frequent use of beta-lactams, clinical data in humans remain limited. OBJECTIVE: This study evaluated the relationship between serum pharmacokinetics, pharmacodynamics, pathogen susceptibility, and clinical outcomes in patients receiving aztreonam or tobramycin monotherapy. METHODS: The case-report forms of hospitalized patients who received either aztreonam or tobramycin for a bacterial infection in 3 clinical trials conducted between 1982 and 1984 were reviewed for the present study. A pathogen was identified for all included patients, and susceptibility testing was performed to determine the minimum inhibitory concentration (MIC) for each agent. Pharmacokinetic parameters for each antibiotic were determined using population modeling, and variables potentially related to outcomes were evaluated using tree-based modeling, logistic regression, and nonlinear regression methods. RESULTS: Data from 91 patients were analyzed, 68 treated with aztreonam monotherapy and 23 treated with tobramycin monotherapy. Of the types of infections treated, 39 were intra-abdominal, 42 involved the lower respiratory tract, and 10 involved the skin and skin structures. The pharmacodynamic ratio of the 24-hour area under the curve (AUC24) to the MIC was associated with clinical outcome for both antibiotics: aztreonam and to-bramycin patients with ratios meeting or exceeding the respective 24-hour inverse serum inhibitory titer breakpoints of 184 and 110 were significantly more likely to achieve a successful outcome than were those with ratios not meeting these values (P < 0.01). The probabilities of clinical success in patients at or above and below the AUC24/MIC breakpoints were a respective 85% and 53% for aztreonam and 80% and 47% for tobramycin (both, P < 0.01). When all patients were considered, the likelihood of achieving cure was 5.1 times greater in patients exceeding the target ratios (P < 0.01). CONCLUSION: PK/PD optimization of both aztreonam and tobramycin is associated with improved patient outcomes.

Adult↗
PubMed2001

Damage to the vestibular inner ear causes long-term changes in neuronal nitric oxide synthase expression in the rat hippocampus.

The vestibular inner ear detects head acceleration and initiates compensatory eye movement and postural reflexes that help keep the visual image of the world stable on the retina, and maintain balance, during unexpected head movement. The most primitive vestibular systems are estimated to have evolved more than 500 million years ago and in mammalian and submammalian species the vestibular reflexes are mediated by basic brainstem pathways (see Wilson and Melvill Jones, 1979 for review). Although the contributions of the vestibular system to higher cognitive function have generally received less attention than its reflexive roles, vestibular sensory information is transmitted to higher centres in the brain and humans with vestibular damage are known to experience debilitating perceptual illusions (see Curthoys and Halmagyi, 1995; Berthoz, 1996 for reviews). Increasing behavioural and neurophysiological evidence suggests that the hippocampus uses information from the vestibular inner ear in order to build up maps of space that can be used in the development of spatial memory during learning tasks (McNaughton et al., 1991; Chapuis et al., 1992; Wiener and Berthoz, 1993; O'Mara et al., 1994; Wiener et al., 1995; Gavrilov et al., 1995; Stackman and Taube, 1996; Vitte et al., 1996; Taube et al., 1996; Save et al., 1998; Peruch et al., 1999; Cuthbert et al., 2000; Russell et al., 2000). However, to date, there has been no indication of the long-term neurochemical effects of the loss of vestibular input on hippocampal function. Since nitric oxide has been implicated in the mechanisms of hippocampal synaptic plasticity associated with the development of short-term memory (e.g. Schuman and Madison, 1991; Schuman et al., 1994; Arancio et al., 1996; Wu et al., 1997; Lu et al., 1999), we examined whether changes occur in the activity and expression of the enzymes responsible for nitric oxide production (nitric oxide synthases) in subregions of the rat hippocampus at different times following unilateral peripheral vestibular lesions, using western blotting and radioenzymatic assays. We found a decreased expression of neuronal nitric oxide synthase in the ipsilateral dentate gyrus at 2 weeks following the vestibular damage and not before, that may be related to the long-term effects of the loss of vestibular input on hippocampal function. These results support the hypothesis that head movement and position information derived from the vestibular inner ear may be important for the normal function of the hippocampus.

Afferent Pathways↗
PubMed2001

The contribution of nitric oxide to vestibular compensation: are there species differences?

Nitric oxide (NO) has been implicated in the processes by which animals recover from peripheral vestibular damage ("vestibular compensation"). However, there is little systematic data available on the effects of NO inhibition on the vestibular compensation process. In the present study we administered the nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) using a subcutaneous osmotic minipump and examined its effects on the compensation of spontaneous nystagmus (SN), yaw head tilt (YHT) and roll head tilt (RHT) in guinea pigs. Following unilateral labyrinthectomy (UL), treatment with 5, 10, 50 or 100 mM L-NAME had no effect on the expression of any of these symptoms or their rate of compensation. By contrast, pre-UL treatment with 100 mM L-NAME resulted in a decrease in SN frequency at 10 h post-UL and an increase in its rate of compensation. Lower concentrations had no effect on SN. Pre-UL treatment with L-NAME had no significant effect on YHT or RHT at any particular time point. Analysis of NOS activity demonstrated that the highest concentration of L-NAME inhibited NOS activity in the contralateral vestibular nucleus complex, bilateral cerebellum and bilateral cortices. These results suggest that L-NAME may have different effects on vestibular compensation in guinea pigs compared to other species, such as the rat and frog.

Animals↗
PubMed2001

West Nile virus: a case study in how NY State Health Information infrastructure facilitates preparation and response to disease outbreaks.

New York's (NY) Health Information Network (HIN) provided timely access to West Nile Virus (WNV) data during the initial outbreak in the late Summer 1999. In December 1999, NY developed a plan to deal with WNV in 2000 that required an integrated surveillance system for humans, birds, mammals, and mosquitoes. The HIN infrastructure allowed NY to deploy this system statewide in three months. Local health departments throughout NY used the system to report, track, and retrieve surveillance data as WNV spread throughout NY in 2000. The HIN infrastructure includes partnerships, training/support, technical capacity and architecture similar to NEDSS as proposed by the US CDC.

Animals↗
PubMed2001

Intussusception, rotavirus diarrhea, and rotavirus vaccine use among children in New York state.

OBJECTIVE: To describe epidemiologic features of intussusception and rotavirus diarrhea in New York, to examine the baseline incidence and trends over time, and to ascertain whether an excess of cases occurred in the 9 months of vaccination with the newly licensed rotavirus vaccine. METHODS: Hospital discharge data from 1989 through 1998 were reviewed for children (<1 year old) whose primary or secondary diagnosis was coded as intussusception or rotavirus diarrhea. Characteristics of patients admitted for intussusception and rotavirus diarrhea were compared, and trends over time were examined. For a subset of patients, medical records and vaccine histories for intussusception hospitalizations from October 1998 through June 1999 were analyzed. The number of intussusception cases attributable to rotavirus vaccine was calculated based on the penetration of the vaccine (21%) and a range of excess risks of intussusception among vaccinated children as estimated by the National Immunization Program (NIP). RESULTS: From 1989 through 1998, 1450 intussusception-associated hospitalizations were reported in children <1 year old (average annual incidence 5.4/10 000). Among these children, 47% were treated medically and 53% had surgery, with 9% needing surgical resection. The incidence of intussusception declined over time from 6.1 per 10 000 in 1989 to 3.9 per 10 000 in 1998. Intussusception hospitalizations occurred throughout the year, whereas rotavirus-associated hospitalizations peaked from February to April. Of 20 patients with intussusception whose hospitalization charts were reviewed, 5 had received rotavirus vaccine. All 5 were hospitalized after their first dose of vaccine, were admitted before 7 months of age, were white, and had private insurance. A total of 81 cases of intussusception occurred during the 9-month period of rotavirus vaccination, compared with 78 during the same period in the prevaccination year. The number of excess intussusception cases observed (n = 3) was lower than expected using the NIP estimate of excess risk (1.8) among rotavirus vaccinated children (n = 12) but not significantly different from the risks identified in the NIP cohort studies (1 in 12 000). CONCLUSION: Our data suggest that in New York the rate of intussusception has declined, and approximately 1 child in 2600 develops intussusception before 1 year of age. The different seasonality between intussusception and rotavirus-related hospitalizations suggests that if any causal association exists, it must be small. Unlike other studies, analysis of New York hospitalized discharge data failed to show an appreciable increase in the incidence of intussusception after introduction of the rotavirus vaccine.

Diarrhea↗
PubMed2001

Clinical pharmacokinetics of non-nucleoside reverse transcriptase inhibitors.

Non-nucleoside reverse transcriptase inhibitors (NNRTIs) are a diverse group of compounds that induce allosteric changes in the human immunodeficiency virus type 1 (HIV-1) reverse transcriptase, thus rendering the enzyme incapable of converting viral RNA to DNA. Unlike nucleoside analogue inhibitors of reverse transcriptase, NNRTIs do not require sequential phosphorylation to elicit antiretroviral activity. There are currently 3 approved NNRTIs: nevirapine, delavirdine and efavirenz. Although possessing a common mechanism of action, these agents can be differentiated by both molecular and pharmacokinetic characteristics. Each of the NNRTIs is metabolised to some degree by the cytochrome P450 (CYP) system of enzymes, making them prone to clinically significant drug interactions. In addition, they elicit variable effects on other medications, acting as either inducers or inhibitors of drugs metabolised by CYP. These drug interactions are an important consideration in the clinical use of these agents as a part of combination antiretroviral therapy. Additional factors such as the influence of food and pH on oral absorption, and protein binding, must also be considered.

Alkynes↗
PubMed2000

The effects of protein kinase C and calmodulin kinase II inhibitors on vestibular compensation in the guinea pig.

Previous studies have demonstrated that vestibular compensation, the process of behavioural recovery which occurs following unilateral deafferentation of the vestibular labyrinth (UVD), is correlated with changes in in vitro phosphorylation of various protein substrates in the brainstem vestibular nucleus complex (VNC). The aim of the present study was to investigate the possible causal relationship between protein kinase activity and the induction of the vestibular compensation process, by delivering inhibitors of protein kinase C (PKC) or Ca(2+)/calmodulin-dependent kinase II (CaMKII) into the ipsilateral VNC at the time of the UVD and determining their effects on three static symptoms of UVD, spontaneous nystagmus (SN), yaw head tilt (YHT) and roll head tilt (RHT) in guinea pigs. Infusion of the PKC inhibitor, 3-[1-(3-dimethylaminopropyl)-1H-indol-3-yl]-4-(1H-indol-3-yl)-1H-pyrr ole-2,5-dione, HCl (bisindolylmaleimide I, HCl/GF 109203X, HCl) ('Bis I'), at a concentration of 5 or 50 microM, significantly increased SN frequency at the earliest time points (6 and 8 h post-UVD) compared to vehicle controls and the less selective analogue, 2,3-bis(1H-indol-3-yl)-N-methylmaleimide (bisindolylmaleimide V) ('Bis V'). However, the compensation of YHT and RHT was unaffected by the PKC inhibitor. By contrast, the cell-permeable CaMKII inhibitor, myristoylated autocamtide-2 related inhibitory peptide (N-Myr-Lys-Lys-Ala-Leu-Arg-Arg-Gln-Glu-Ala-Val-Asp-Ala-Leu-OH) ('myr-AIP') or the cell-impermeable analogue, autocamtide-2 related inhibitory peptide (N-Lys-Lys-Ala-Leu-Arg-Arg-Cln-Glu-Ala-Val-Asp-Ala-Leu-OH) ('AIP'), failed to alter the compensation of SN, YHT or RHT at any dose compared to vehicle controls. These results implicate PKC-, but not CaMKII-, signal transduction pathways in the initiation of SN compensation in guinea pig.

Animals↗
PubMed2000

The effects of L-NAME on vestibular compensation and NOS activity in the vestibular nucleus, cerebellum and cortex of the guinea pig.

Nitric oxide (NO) has been implicated in the processes by which animals recover from peripheral vestibular damage ('vestibular compensation'). However, few data exist on the dose-response effects of systemic administration of the nitric oxide synthase (NOS) inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), on the vestibular compensation process. The aim of this study was to investigate the effects on compensation of 5, 10, 50 or 100 mM L-NAME administered by s.c osmotic minipump for 50 h following unilateral vestibular deafferentation (UVD) in guinea pig, either commencing the drug treatment at 4 h pre-UVD or at the time of the UVD (i.e., post-UVD). Post-UVD treatment with L-NAME, at any of the four concentrations used, had no effect on the compensation of spontaneous nystagmus (SN), yaw head tilt (YHT) or roll head tilt (RHT). By contrast, pre-UVD treatment with 100 mM L-NAME resulted in a significant decrease in SN frequency (P<0.05) and a change in the rate of its compensation (P<0.0005). Pre-UVD L-NAME resulted in a significant increase in the overall magnitude of YHT (P<0.005); however, post-hoc comparisons revealed no significant differences between any specific L-NAME and vehicle groups. Pre-UVD L-NAME had no effect on RHT at any concentration. Analysis of NOS activity in the pre-UVD L-NAME treatment groups at 50 h post-UVD showed that only 100 mM L-NAME resulted in a significant decrease in NOS activity in the contralateral medial vestibular nucleus (MVN)/prepositus hypoglossi (PH) (P<0.05) and that NOS activity in the ipsilateral MVN/PH was not significantly affected. However, NOS activity was significantly inhibited in the bilateral cerebellum and cortices for several concentrations of L-NAME. These results suggest that pre-UVD systemic administration of L-NAME can significantly increase the rate of SN compensation in guinea pig and that this effect is correlated with inhibition of NOS activity in several regions of the CNS.

Animals↗
PubMed2000

The effects of intra-vestibular nucleus administration of brain-derived neurotrophic factor (BDNF) on recovery from peripheral vestibular damage in guinea pig.

Brain-derived neurotrophic factor (BDNF), at doses of 0.04, 0.4 or 4.0 microg/day, was delivered by cannula and s.c osmotic minipump into the ipsilateral vestibular nucleus complex from 0 to 50 h following unilateral labyrinthectomy (UL) in guinea pigs. Compared to the vehicle control group, the frequency of spontaneous nystagmus was significantly reduced (p < 0.02) and the rate of yaw head tilt compensation increased (p < 0.02). However, roll head tilt was not signifcantly affected. There were also no significant effects of BDNF administration into the IVth ventricle (4.0 microg/day) on any UL symptom. These results further support the hypothesis that neurotrophins such as BDNF may enhance the vestibular compensation process.

Animals↗
PubMed2000

Vestibular nucleus N-methyl-D-aspartate receptors contribute to spontaneous nystagmus generation following unilateral labyrinthectomy in guinea pigs.

We investigated the effects of a non-competitive N-methyl-D-aspartate (NMDA) receptor/channel antagonist ((+)MK-801)) or an L-type Ca(2+) channel antagonist (nifedipine), delivered into the ipsilateral vestibular nucleus complex (VNC) before a unilateral labyrinthectomy (UL), on spontaneous nystagmus (SN) generation. Guinea pigs received either (+)MK-801 (5 or 12.5 microg); the less active enantiomer, (-)MK-801 (5 or 12.5 microg); nifedipine (5 or 10 microg); or vehicle, via cannula in the ipsilateral VNC. (+)MK-801, but not nifedipine, significantly decreased mean SN frequencies at 6 h post-UL, compared to controls (P<0.02) and reduced the rate of SN compensation (P<0.05). These results suggest that the SN expression is partly induced by NMDA receptor activation in the ipsilateral VNC at the time of the UL.

Animals↗
PubMed2000

Comparison of visual--vestibular interaction in insulin-dependent and non-insulin-dependent diabetes mellitus.

We compared various measures of visual-vestibular interaction in subjects with insulin-dependent diabetes mellitus (IDDM) or non-insulin-dependent diabetes mellitus (NIDDM), as well as non-diabetic controls. Subjects with IDDM exhibited significantly greater postural sway than controls on those conditions in the Clinical Test of Sensory Interaction and Balance (CTSIB) which require greater reliance on the vestibular system (p < 0.005). The IDDM group also exhibited significantly worse gaze-holding in darkness and a significantly higher mean slow phase eye velocity (SPV) of optokinetic nystagmus (OKN; p<0.05 for both comparisons). However, there were no significant differences in latency to circularvection (CV). The NIDDM group showed a significant increase in postural sway across all 12 conditions compared with the controls, as well as a significant decrease in gaze-holding in darkness (p < 0.05 and p < 0.0005, respectively). However, they showed no significant difference in OKN SPV and a significant decrease in latency to CV for anticlockwise trials only (p < 0.05). These results suggest that IDDM and NIDDM are both associated with specific but different changes in visual-vestibular interaction.

Adult↗
PubMed2000

Effects of intra-vestibular nucleus injection of the group I metabotropic glutamate receptor antagonist AIDA on vestibular compensation in guinea pigs.

Removal of the peripheral vestibular receptor cells in one inner ear (unilateral vestibular deafferentation, UVD) results in a syndrome of ocular motor and postural disorders, many of which disappear over time in a process of behavioural recovery known as vestibular compensation. Excitatory amino acid receptors, in particular the N-methyl-D-aspartate (NMDA) receptor, have been implicated in vestibular compensation; however, the metabotropic glutamate receptors (mGluRs) have not been studied in this context. The aim of this study was to determine whether group I mGluRs in the brainstem vestibular nucleus complex (VNC) ipsilateral to the UVD are involved in vestibular compensation of the static symptoms of UVD in guinea pig. The selective group I mGluR antagonist (RS)-1-aminoindan-1,5,dicarboxylic acid (AIDA) was continuously infused into the ipsilateral VNC for 30-min pre-UVD and 30-min post-UVD by cannula, at a rate of 1 microl/h, using one of four doses: 0.1 fg, 0.1 pg, 0.1 ng or 0.1 microg (n=5 animals in each case). In control conditions, a 0.1-fg (n=4) or 0.1-microg (n=5) NaOH vehicle was infused into the ipsilateral VNC using the same protocol. In order to control for the possibility that AIDA disrupted spontaneous neuronal activity in the VNC in normal animals, 0.1 microg AIDA (n=4) or 0.1 microg NaOH (n=2) was infused into the VNC in labyrinthine-intact animals. In both groups, static symptoms of UVD (i.e. spontaneous nystagmus, SN, yaw head tilt, YHT and roll head tilt, RHT) were measured at 8, 10, 12, 15, 20, 25, 30, 35, 45 and 50 h post-UVD. In addition, the righting reflex latency (RRL) was measured in labyrinthine-intact animals in order to assess whether AIDA impaired motor coordination in labyrinthine-intact animals. In UVD animals, the highest dose of AIDA significantly reduced SN frequency and changed its rate of compensation (P<0.001 and P<0.0001, respectively). This dose of AIDA also caused a significant reduction in YHT (P<0.005) as well as a significant change in its rate of compensation (P<0.0001). However, RHT was not significantly affected. In the labyrinthine-intact animals, AIDA infusion did not induce a UVD syndrome, nor did it significantly affect RRL. These results suggest that group I mGluRs in the ipsilateral VNC may be involved in the expression of ocular motor and some postural symptoms following UVD. Furthermore, group I mGluRs may not contribute to the resting activity of vestibular nucleus neurons.

Adaptation, Physiological↗
PubMed2000

Molecular mechanisms of recovery from vestibular damage in mammals: recent advances.

The aim of this review is to summarise and critically evaluate studies of vestibular compensation published over the last 2 years, with emphasis on those concerned with the molecular mechanisms of this process of lesion-induced plasticity. Recent studies of vestibular compensation have confirmed and extended the previous findings that: (i) compensation of the static ocular motor and postural symptoms occurs relatively rapidly and completely compared to the dynamic symptoms, many of which either do not compensate substantially or else compensate variably due to sensory substitution and the development of sensori-motor strategies which suppress or minimize symptoms; (ii) static compensation is associated with, and may be at least partially caused by a substantial recovery of resting activity in the ipsilateral vestibular nucleus complex (VNC), which starts to develop very quickly following the unilateral vestibular deafferentation (UVD) but does not correlate perfectly with the development of some aspects of static compensation (e.g., postural compensation); and (iii) many complex biochemical changes are occurring in the VNC, cerebellum and even areas of the central nervous system like the hippocampus, following UVD. However, despite many recent studies which suggest the importance of excitatory amino acid receptors such as the N-methyl-D-aspartate receptor, expression of immediate early gene proteins, glucocorticoids, neurotrophins and nitric oxide in the vestibular compensation process, how these various factors are linked and which of them may have a causal relationship with the physiological changes underlying compensation, remains to be determined.

Animals↗