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PubMed1998

Neurotrophic factors in the tongue: expression patterns, biological activity, relation to innervation and studies of neurotrophin knockout mice.

How taste buds develop and how they become innervated has been a matter of debate for a long time. Brain-derived neurotropic factor (BDNF) and neurotrophin-3 (NT3) mRNA expression patterns suggested a possible involvement in lingual gustatory and somatosensory innervation. Studies of null-mutated mice showed that BDNF-/- mice had few abnormal taste buds and were unable to discriminate between primary tastes. NT3-/- mice had a severe loss of lingual somatosensory innervation. These novel findings may have clinical implications in rare human conditions such as familial dysautonomia and/or in more common cases of problems with loss of taste and sensation in the mouth such as those seen after injury to the nerves, either by accident or following oral/facial surgery. Knowledge about which proteins that are required to stimulate nerve fibers to grow into mucous membranes of the oral cavity during development suggests that these same proteins might become helpful in stimulating regeneration of injured nerves in patients, perhaps helping them to regain lost taste and sensory functions. Here, the presence of glial cell-derived neurotrophic factor (GDNF) families of neurotrophic factors and receptors in the tongue is also discussed. Further, a model for the development and innervation of taste buds in mammals is proposed.

Animals↗

PubMed2001

Current concepts of vestibular nucleus function: transformation of vestibular signals in the vestibular nuclei.

The vestibular nerve sends signals to the brain that code the movement and position of the head in space. These signals are used for a variety of functions, including the control of reflex and voluntary movements and the construction of a sense of self-motion. In order to carry out these functions, sensory vestibular signals need to be transformed in a variety of ways. Transformations are thought to occur at an early stage of sensory processing in the brain, and in many cases are apparent in the responses of neurons in the vestibular nuclei that receive direct inputs from the vestibular nerve. Several specific examples of sensory transformation in the vestibular nuclei are presented, and current hypotheses about the mechanisms that are used to produce the transformations are discussed.

Adaptation, Physiological↗

PubMed1995

The electrophysiological properties of rat primary afferent neurones with carbonic anhydrase activity.

1. Intracellular recordings of action potentials (APs) and after-hyperpolarizations (AHPs) were made from the L3, L4 and L5 dorsal root ganglia (DRGs) of 6- to 8-week-old anaesthetized female Wistar rats in vitro at 36.5 +/- 1 degree C. Neurones were classified by their conduction velocities (CVs) as A alpha/beta (> 12 m s-1), A delta (1.3-12 m s-1) or C fibre neurones (< 1.3 m s-1). 2. Following the recording, fluorescent dye was injected intracellularly. Sections of injected neurones were tested for carbonic anhydrase (CA) activity histochemically. Reaction product intensity and cell size were measured. Control experiments showed that intracellular dye, time in vitro, axotomy and electrical stimulation did not affect proportions of CA-positive neurones or their size distributions. 3. Approximately 28-30% of DRG neurones were CA positive. Their sizes were approximately normally distributed and covered the entire size range of DRG neurones with no correlation between size and CA intensity. A greater proportion of A alpha/beta cells (62%) than of A delta (32%) or C cells (38%) were CA positive, but CA intensity was not correlated with CV. 4. In A neurones mean AP duration was significantly shorter in CA-positive cells; for CA-positive and CA-negative cells, respectively, these values were 1.6 and 2.8 ms for A delta cells; 1.1 and 1.7 ms for A alpha/beta cells; and were 1.2 and 2.3 ms for all A cells. CA intensity was negatively correlated with AP duration at base in all these groups. 5. Again in A neurones, the mean AHP durations were significantly shorter in the CA-positive cells; the mean AHP durations to 80% recovery for positive and negative cells were 8.8 and 36 ms, respectively, for A alpha/beta cells and were 8.6 and 26 ms, respectively, for all A cells. CA intensity was negatively correlated with AHP duration in A alpha/beta cells and all A cells together. 6. A fibre cells with the longer AP and AHP durations were all CA negative, while cells with the shorter durations included both CA-positive and CA-negative cells. 7. CA-positive and CA-negative A fibre neurones therefore have different electrophysiological characteristics. It is suggested that CA-negative A fibre neurones may have slower somatic firing rates and different sensory functions from the CA-positive neurones.

Action Potentials↗

PubMed2002

Analysis of variance study of the rat cortical layer 4 barrel and layer 5b neurones.

Unique formation of rodent cortical barrels by layer 4 neurones attracts study of the sensory function of cortical input stage neurones (layer 4) compared with that of output stage neurones (layer 5). We have recorded extracellular responses from rat somatosensory cortical neurones to deflections of contralateral vibrissae. Thirty-two layer 4 barrel neurones and 29 layer 5b neurones were studied. Whisker stimulations were ramp-and-hold deflections with one of six different ramp velocities (100-2.5 mm s(-1)) and one of four different plateau amplitudes (2000-200 microm). Twenty-four (6 x 4) different stimulus forms were applied to the tip of a whisker trimmed to 10 mm in a predetermined order in stimulus cycles of 20-50 repetitions. Spike counts for a period of 2560 ms in 10 ms bins were summed to construct a matrix of 24 peristimulus histograms for each neurone. Twenty-four amplitude and 24 velocity values were computed from counts during the plateau and ramp phases, respectively. To determine the amplitude- and velocity dependence of a neurone, an amplitude F value (the ratio of variations among-/within-amplitude of the amplitude value) and a velocity F value (ratio of variations among-/within-velocity of the velocity value) were derived by analysis of variance. The amplitude F value of the layer 4 barrel neurones was greater than that of the layer 5b neurones (P < 0.0001). The velocity F value of the barrel neurones was smaller than that of the layer 5b neurones (P = 0.0226). The results suggests that barrel neurones and layer 5b neurones tend to detect amplitude and velocity components of whisker deflection, respectively.

Analysis of Variance↗

PubMed2003

Developmental changes in the expression of potassium currents of embryonic, neonatal and mature mouse inner hair cells.

Developmental changes in electrophysiological membrane properties of mouse cochlear inner hair cells (IHCs) were studied from just after terminal differentiation up to functional maturity. As early as embryonic day 14.5 (E14.5) newly differentiated IHCs express a very small outward K+ current that is largely insensitive to 4-aminopyridine (4-AP). One day later the inward rectifier, IK1, is first observed. These immature cells initially exhibit only slow graded voltage responses under current clamp. From E17.5 spontaneous action potentials occur. During the first week of postnatal development, the outward K+ current steadily increases in size and a progressively larger fraction of the current is sensitive to 4-AP. During the second postnatal week, the activation of the 4-AP-sensitive current, by now contributing about half of the outward K+ current, shifts in the hyperpolarizing direction. Together with an increase in size of IK1, this hyperpolarizes the cell, thus inhibiting the spontaneous spike activity, although spikes could still be evoked upon depolarizing current injection. Starting at about the onset of hearing (postnatal day 12, P12) immature IHCs make the final steps towards fully functional sensory receptors with fast graded voltage responses. This is achieved mainly by the expression of the large-conductance Ca2+-activated K+ current IK,f, but also of a current indistinguishable from the negatively activating IK,n previously described in mature outer hair cells (OHCs). The 4-AP-sensitive current continues to increase after the onset of hearing to form the major part of the mature delayed rectifier, IK,s. By P20 IHCs appear mature in terms of their complement of K+ conductances.

4-Aminopyridine↗

PubMed2006

Supporting sensory transduction: cochlear fluid homeostasis and the endocochlear potential.

The exquisite sensitivity of the cochlea, which mediates the transduction of sound waves into nerve impulses, depends on the endocochlear potential and requires a highly specialized environment that enables and sustains sensory function. Disturbance of cochlear homeostasis is the cause of many forms of hearing loss including the most frequently occurring syndromic and non-syndromic forms of hereditary hearing loss, Pendred syndrome and Cx26-related deafness. The occurrence of these and other monogenetic disorders illustrates that cochlear fluid homeostasis and the generation of the endocochlear potential are poorly secured by functional redundancy. This review summarizes the most prominent aspects of cochlear fluid homeostasis. It covers cochlear fluid composition, the generation of the endocochlear potential, K(+) secretion and cycling and its regulation, the role of gap junctions, mechanisms of acid-base homeostasis, and Ca(2+) transport.

Acid-Base Equilibrium↗

PubMed1983

Reflex inhibition procedures for animal audiometry: a technique for assessing ototoxicity.

A procedure for making rapid audiometric assessments of animal subjects, based on the ability of weak stimuli to modify the strength of reflexes elicited by subsequently presented strong stimuli, is described. Pure-tone detection thresholds for rats and guinea pigs determined by this procedure are quite comparable to those determined by operant techniques, and are similarly sensitive to ototoxic insult. The procedure is also applicable to the assessment of suprathreshold sensory function, and offers advantages over commonly used procedures for assessing ototoxicity.

Animals↗

PubMed1984

Speech recognition in a special case of low-frequency hearing loss.

Recognition of speech stimuli consisting of monosyllabic words, sentences, and nonsense syllables was tested in normal subjects and in a subject with a low-frequency sensorineural hearing loss characterized by an absence of functioning sensory units in the apical region of the cochlea, as determined in a previous experiment [C. W. Turner, E. M. Burns, and D. A. Nelson, J. Acoust. Soc. Am. 73, 966-975 (1983)]. Performance of all subjects was close to 100% correct for all stimuli presented unfiltered at a moderate intensity level. When stimuli were low-pass filtered, performance of the hearing-impaired subject fell below that of the normals, but was still considerably above chance. A further diminution in the impaired subject's recognition of nonsense syllables resulted from the addition of a high-pass masking noise, indicating that his performance in the filtered quiet condition was attributable in large part to the contribution of sensory units in basal and midcochlear regions. Normals' performance was also somewhat decreased by the masker, suggesting that they also may have been extracting some low-frequency speech cues from responses of sensory units located in the base of the cochlea.

Adult↗

PubMed1965

NEUROSECRETORY PROCESSES EXTENDING INTO THIRD VENTRICLE: SECRETORY OR SENSORY?

"Dendrites" projecting into the third ventricle from hypothalamic neurosecretory neurons of the Pacific tree frog, Hyla regilla, appear to be morphologically equipped to serve both secretory and sensory functions. These cell processes contain elementary neurosecretory granules, Golgi membranes, mitochondria, and endoplasmic reticulum, suggesting synthesis and possibly release of hormonal material. Each "dendrite" is provided with a single cilium which has an accessory centriole and a striated rootlet.

Animals↗

PubMed2000

Cholinergic synaptic inhibition of inner hair cells in the neonatal mammalian cochlea.

Efferent feedback onto sensory organs provides a means to modulate input to the central nervous system. In the developing mammalian cochlea, inner hair cells are transiently innervated by efferent fibers, even before sensory function begins. Here, we show that neonatal inner hair cells are inhibited by cholinergic synaptic input before the onset of hearing. The synaptic currents, as well as the inner hair cell's response to acetylcholine, are mediated by a nicotinic (alpha9-containing) receptor and result in the activation of small-conductance calcium-dependent potassium channels.

Acetylcholine↗

PubMed1988

Two trans-acting regulatory genes (vir and mod) control antigenic modulation in Bordetella pertussis.

Expression of virulence factors by Bordetella pertussis is altered by environmental signals (antigenic modulation) and is dependent on an activator encoded by a gene called vir. We have used TnphoA (Tn5 IS50L::phoA) gene fusions to define two sets of genes whose expression is either activated (vag loci) or repressed (vrg loci) by modulation signals. Both groups of genes appear to be regulated by the vir gene product in that, in the absence of modulators, null mutations in vir lead to the repression of vag gene fusions and derepression of vrg gene fusions. Mutants of B. pertussis were isolated that constitutively express virulence factors in the presence of the modulator MgSO4, nicotinic acid, or low incubation temperature. We designate the gene that carries such mutations mod (modulation) and have characterized one (mod-1) of these mod constitutive mutations. A method was developed for the insertional inactivation of the vir gene by using the integration of a suicide replicon. Inactivation of the vir gene in the mod-1 mutant, followed by transcomplementation with the cloned wild-type vir gene, gives the Mod-1 constitutive phenotype, showing that the mod-1 mutation defines a gene distinct from vir. The gene carrying the mod-1 mutation is linked to vir and was cloned on a recombinant cosmid (pLAF-C1) which transcomplements the vir-1::Tn5 mutation in B. pertussis 347. Introduction of pLAF-C1 into vir mutant and vir+ B. pertussis strains also gives the Mod-1 constitutive phenotype, indicating that mod-1 is a dominant allele. These data suggest that the mod gene product could have sensory functions for the environmental signals that affect the expression of vir-regulated genes of B. pertussis. The mod constitutive strains and plasmids described here also have applications in pertussis vaccine development.

Bordetella pertussis↗

PubMed1995

The Ras-related protein Cdc42Hs and bradykinin promote formation of peripheral actin microspikes and filopodia in Swiss 3T3 fibroblasts.

The Ras-related protein Cdc42 plays a role in yeast cell budding and polarity. Two related proteins, Rac1 and RhoA, promote formation in mammalian cells of membrane ruffles and stress fibers, respectively, which contain actin microfilaments. We now show that microinjection of the related human Cdc42Hs into Swiss 3T3 fibroblasts induced the formation of peripheral actin microspikes, determined by staining with phalloidin. A proportion of these microspikes was found to be components of filopodia, as analyzed by time-lapse phase-contrast microscopy. The formation of filopodia was also found to be promoted by Cdc42Hs microinjection. This was followed by activation of Rac1-mediated membrane ruffling. Treatment with bradykinin also promoted formation of microspikes and filopodia as well as subsequent effects similar to that seen upon Cdc42Hs microinjection. These effects of bradykinin were specifically inhibited by prior microinjection of dominant negative Cdc42HsT17N, suggesting that bradykinin acts by activating cellular Cdc42Hs. Since filopodia have been ascribed an important sensory function in fibroblasts and are required for guidance of neuronal growth cones, these results indicate that Cdc42Hs plays an important role in determining mammalian cell morphology.

Actin Cytoskeleton↗

PubMed2003

Neurons expressing the highest levels of gamma-synuclein are unaffected by targeted inactivation of the gene.

Homologous recombination in ES cells was employed to generate mice with targeted deletion of the first three exons of the gamma-synuclein gene. Complete inactivation of gene expression in null mutant mice was confirmed on the mRNA and protein levels. Null mutant mice are viable, are fertile, and do not display evident phenotypical abnormalities. The effects of gamma-synuclein deficiency on motor and peripheral sensory neurons were studied by various methods in vivo and in vitro. These two types of neurons were selected because they both express high levels of gamma-synuclein from the early stages of mouse embryonic development but later in the development they display different patterns of intracellular compartmentalization of the protein. We found no difference in the number of neurons between wild-type and null mutant animals in several brain stem motor nuclei, in lumbar dorsal root ganglia, and in the trigeminal ganglion. The survival of gamma-synuclein-deficient trigeminal neurons in various culture conditions was not different from that of wild-type neurons. There was no difference in the numbers of myelinated and nonmyelinated fibers in the saphenous nerves of these animals, and sensory reflex thresholds were also intact in gamma-synuclein null mutant mice. Nerve injury led to similar changes in sensory function in wild-type and mutant mice. Taken together, our data suggest that like alpha-synuclein, gamma-synuclein is dispensable for the development and function of the nervous system.

Animals↗

PubMed2002

Outcome at school age following antenatal detection of absent or reversed end diastolic flow velocity in the umbilical artery.

AIM: To determine whether fetal compromise, manifested by abnormalities of Doppler recordings of umbilical artery velocity waveforms in utero, is associated with neurodevelopmental or educational abnormalities at school age. METHODS: A cohort of neonates born following high risk pregnancies had been previously identified for a study of the perinatal sequelae of absent (AEDFV) and reversed (REDFV) end diastolic flow velocities. Seventy six children were assessed at 5-12 years of age by a developmental paediatrician who was blinded to perinatal course and Doppler assessments. Forty children born following pregnancies with forward end diastolic flow velocities (FEDFV), were compared with 27 with AEDFV and nine with REDFV. Tests of cognitive, neurological, and sensory function were performed, and reports of behavioural and educational progress were obtained from parents and teachers. RESULTS: There were no significant differences between FEDFV and AEDFV groups, but on tests of mental ability and neuromotor function the REDFV group had worse scores than either FEDFV or AEDFV. Comparing REDFV and FEDFV groups, the British Ability Scales general conceptual ability mean scores were 87.7 versus 101, and the Quick Neurological Screening Test mean scores were 32.8 versus 21.5. CONCLUSIONS: Absence of EDFV is well recognised as a marker of fetal compromise which is associated with acute perinatal sequelae. This study suggests it is not associated with adverse neurodevelopmental outcome. However, we found reversal of EDFV on antenatal assessment to be associated with a wide range of problems at school age, suggesting that REDFV represents intrauterine decompensation which may have adverse effects on the developing brain.

Blood Flow Velocity↗

PubMed1992

Disappearance of hepatic parenchymal nerves in human liver cirrhosis.

The normal human liver receives a substantial autonomic innervation that is thought to subserve motor, metabolic, and sensory functions. In this study an antibody to a neural axoplasmic protein (PGP 9.5) was used to visualise autonomic nerves in tissue from normal, precirrhotic, and cirrhotic livers. Nerve fibres were readily identified in the parenchyma and portal tracts of normal livers, and in those where the histological diagnosis was non-specific reactive hepatitis or acute liver injury. In precirrhotic and cirrhotic livers nerves in portal tracts and fibrous septae remained prominent, but the parenchymal innervation was reduced in precirrhotic livers and was absent from regenerating nodules in established cirrhosis. The causes and functional consequences of this parenchymal denervation in cirrhosis remain to be established.

Antibodies, Monoclonal↗

PubMed1997

Clinical features of idiopathic megarectum and idiopathic megacolon.

BACKGROUND: Dilatation of the rectum and/or colon, in the absence of demonstrable organic disease, is an uncommon and poorly characterised condition. AIMS: To characterise the clinical and diagnostic features, and response to treatment, of patients with idiopathic megarectum (IMR) and idiopathic megacolon (IMC). METHODS: A retrospective review was undertaken of all patients operated on for these conditions over a 23 year period. In addition all patients treated over a three year period were prospectively studied by means of a questionnaire, contrast studies of the upper and lower intestine, spine x rays to exclude spinal dysraphism, anorectal physiological studies, and assessment of clinical outcome. Patients with Hirschsprung's disease and other known causes of gut dilatation were excluded. RESULTS: (i) Retrospective study: Of 63 operated patients, 22 had IMR, 23 had IMR and IMC, and 18 had IMC only. Five patients with IMC had previous sigmoid volvulus, and three had associated non-gastrointestinal congenital abnormalities. Faecal incontinence was always associated with rectal impaction and 14 patients (82%) with IMR alone had had manual disimpaction. (ii) Prospective study: Twenty two patients had IMR, with a median rectal diameter of 10 cm (normal < 6.5 cm). Six patients had IMC and one patient had IMR and IMC. Patients with IMR were significantly (p = 0.0007) younger than patients with IMC. All patients with IMR became symptomatic in childhood, compared with half the patients with IMC who developed symptoms as adults. Patients with IMR all presented with soiling and impaction, compared with patients with IMC whose symptoms were variable and included constipation or increased bowel frequency, pain, and variable need for laxatives. No upper gut dilatation was seen in either group of patients. Spinal dysraphism was seen in two of 18 patients with IMR and two of four with IMC, suggesting extrinsic denervation as a possible cause in a minority. Twelve of 22 patients with IMR had a maximum anal resting pressure below normal, indicating sphincter damage or inhibition. Both IMR and IMC patients had altered rectal sensitivity to distension, suggesting that despite lack of dilatation the rectum in IMC has altered viscoelasticity, tone, or sensory function. Fifteen of 22 patients with IMR were successfully managed with laxatives or enemas, but seven required surgery. Two of seven patients with IMC required surgery, including one for sigmoid volvulus. CONCLUSIONS: Patients with IMR differ clinically, diagnostically, and in their outcome from patients with IMC. These conditions demand specific investigation, and intensive treatment, to achieve optimum care.

Adolescent↗

PubMed1980

Spinal cord stimulation in multiple sclerosis: clinical results.

Clinical results of spinal cord stimulation by means of epidural electrodes are reported in 19 patients with multiple sclerosis. On temporary stimulation with percutaneous electrodes, significant improvement in mobility occurred in 27.7% of 18 patients and the same number showed improved sensory function. Only one of 13 patients with severe upper limb ataxia improved. The major response, both in terms of the percentage of patients responding and the extent of the responses seen was in bladder function: 75% of 16 patients with bladder symptoms improved and seven of the 11 patients with severe bladder disturbance (Kurtzke grade 3 or more) improved. Four of these seven patients had before and after cystometry and 3 showed reduced detrusor hyperreflexia. Altogether, 10 patients had a worthwhile clinical response in one or more aspects of the disease and of these, nine have so far gone on to permanent stimulation. Medium-term results (up to two years) show that, with one exception, improvement in bladder function has been maintained as long as stimulation has been continued and at least 50% of improvement in mobility has been maintained. A favourable response depends not upon the fact of stimulation but upon the type of stimulation received. This, along with other evidence, indicates that the response is not caused either by a placebo effect or by the natural fluctuation of the disease.

Adult↗

PubMed2001

Ramsay Hunt syndrome.

The strict definition of the Ramsay Hunt syndrome is peripheral facial nerve palsy accompanied by an erythematous vesicular rash on the ear (zoster oticus) or in the mouth. J Ramsay Hunt, who described various clinical presentations of facial paralysis and rash, also recognised other frequent symptoms and signs such as tinnitus, hearing loss, nausea, vomiting, vertigo, and nystagmus. He explained these eighth nerve features by the close proximity of the geniculate ganglion to the vestibulocochlear nerve within the bony facial canal. Hunt's analysis of clinical variations of the syndrome now bearing his name led to his recognition of the general somatic sensory function of the facial nerve and his defining of the geniculate zone of the ear. It is now known that varicella zoster virus (VZV) causes Ramsay Hunt syndrome. Compared with Bell's palsy (facial paralysis without rash), patients with Ramsay Hunt syndrome often have more severe paralysis at onset and are less likely to recover completely. Studies suggest that treatment with prednisone and acyclovir may improve outcome, although a prospective randomised treatment trial remains to be undertaken. In the only prospective study of patients with Ramsay Hunt syndrome, 14% developed vesicles after the onset of facial weakness. Thus, Ramsay Hunt syndrome may initially be indistinguishable from Bell's palsy. Further, Bell's palsy is significantly associated with herpes simplex virus (HSV) infection. In the light of the known safety and effectiveness of antiviral drugs against VZV or HSV, consideration should be given to early treatment of all patients with Ramsay Hunt syndrome or Bell's palsy with a 7-10 day course of famciclovir (500 mg, three times daily) or acyclovir (800 mg, five times daily), as well as oral prednisone (60 mg daily for 3-5 days). Finally, some patients develop peripheral facial paralysis without ear or mouth rash, associated with either a fourfold rise in antibody to VZV or the presence of VZV DNA in auricular skin, blood mononuclear cells, middle ear fluid, or saliva. This indicates that a proportion of patients with "Bell's palsy" have Ramsay Hunt syndrome zoster sine herpete. Treatment of these patients with acyclovir and prednisone within 7 days of onset has been shown to improve the outcome of recovery from facial palsy.

Bell Palsy↗