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PubMed2003

A decay of gap junctions associated with ganglion cell differentiation during retinal regeneration of the adult newt.

Changes in the gap junctional coupling and maturation of voltage-activated Na(+) currents during regeneration of newt retinas were examined by whole-cell patch-clamping in slice preparations. Progenitor cells in regenerating retinas did not exhibit Na(+) currents but showed prominent electrical and tracer couplings. Cells identified by LY-fills were typically slender. Na(+) currents were detected in premature ganglion cells with round somata in the 'intermediate-II' regenerating retina. No electrical and tracer couplings were observed between these cells. Mature ganglion cells did not exhibit electrical coupling, but showed tracer coupling. On average, the maximum Na(+) current amplitude recorded from premature ganglion cells was roughly 2.5-fold smaller than that of mature ganglion cells. In addition, the activation threshold of the Na(+) current was nearly 11 mV more positive than that of mature cells. We provide morphological and physiological evidence showing that loss of gap junctions between progenitor cells is associated with ganglion cell differentiation during retinal regeneration and that new gap junctions are recreated between mature ganglion cells. Also we provide evidence suggesting that the loss of gap junctions correlates with the appearance of voltage-activated Na(+) currents in ganglion cells.

Amphetamines↗
PubMed2006

Can the theory of "whitening" explain the center-surround properties of retinal ganglion cell receptive fields?

To account for the spatial and temporal response properties of the retina, a number of studies have proposed that these properties serve to "whiten" the visual input. In particular, it has been argued that the sensitivity of retinal ganglion cells is matched to the spatial frequency spectrum of natural scenes, resulting in a flattened or "whitened" response spectrum across a range of frequencies. However, we argue that there are two distinct hypotheses regarding the flattening of the spectrum. The decorrelation hypothesis proposes that the magnitude of each ganglion cell tuning curve rises with spatial frequency, resulting in a flattened response spectrum for natural scene stimuli. With appropriate sampling, this scheme allows neighboring neurons to be uncorrelated with each other. The response equalization hypothesis proposes that the overall response magnitude of neurons increases with spatial frequency. The proposed goal of this model is to allow neurons with different receptive field sizes to produce the same average response to natural scenes. The response equalization hypothesis proposes an explanation for the relative gain of different ganglion cells and we show that this proposal fits well with published data. We suggest that both hypotheses are important in understanding the tuning and sensitivity of ganglion cells. However, using a simulation, both models are shown to be insufficient to explain the center-surround receptive field organization of ganglion cells. We discuss other factors, including representational sparseness, which could be related to the goals of ganglion cell spatial processing. We suggest three constraints needed to describe the basic linear properties of P-type ganglion cells: decorrelation, response equalization, and a minimal wiring or minimal size constraint.

Animals↗
PubMed2000

Population coding in spike trains of simultaneously recorded retinal ganglion cells.

To achieve a better understanding of the parallel information processing that takes place in the nervous system, many researchers have recently begun to use multielectrode techniques to obtain high spatial- and temporal-resolution recordings of the firing patterns of neural ensembles. Apart from the complexities of acquiring and storing single unit responses from large numbers of neurons, the multielectrode technique has provided new challenges in the analysis of the responses from many simultaneously recorded neurons. This paper provides insights into the problem of coding/decoding of retinal images by ensembles of retinal ganglion cells. We have simultaneously recorded the responses of 15 ganglion cells to visual stimuli of various intensities and wavelengths and analyzed the data using discriminant analysis. Models of stimulus encoding were generated and discriminant analysis used to estimate the wavelength and intensity of the stimuli. We find that the ganglion cells we have recorded from are non-redundant encoders of these stimulus features. While single ganglion cells are poor classifiers of the stimulus parameters, examination of the responses of only a few ganglion cells greatly enhances our ability to specify the stimulus wavelength and intensity. Of the parameters studied, we find that the rate of firing of the ganglion cells provides the most information about these stimulus parameters, while the timing of the first action potential provides almost as much information. While we are not suggesting that the brain is using these variables, our results show how a population of sensory neurons can encode stimulus features and suggest that the brain could potentially deduce reliable information about stimulus features from response patterns of retinal ganglion cell populations.

Action Potentials↗
PubMed1997

Carotid bifurcation pressure modulation of spontaneous activity in external and internal carotid nerves can occur in the superior cervical ganglion.

Previous reports have suggested that a peripheral pressure-modulated reflex operates at the level of the superior cervical ganglion to alter evoked activity in the postganglionic nerves of the ganglion in both the cat and rabbit. In the present study we have examined if spontaneous activity of the external and internal carotid nerves of the rabbit superior cervical ganglion can be modulated during changes of the carotid bifurcation pressure (CBP), independent of central nervous system (CNS) integration. For external carotid nerve recordings increases in CBP resulted in a reduction in spontaneous activity while decreases in CBP were associated with an increase in spontaneous activity. For internal carotid nerve recordings similar effects were observed in the majority of recordings although a subset of recordings showed opposite effects or were not responsive to changes in pressure. To determine if vagus nerve afferents contribute to the observed pressure-modulated spontaneous activity effects, the influence of CBP on external carotid nerve recordings was examined before and after section of the vagus nerve rostral to the nodose ganglion. We found that even following section of the vagus nerve the external carotid nerve response to an increase in pressure remained intact. These results demonstrate that, after section of centrally-projecting afferent pathways from the carotid bifurcation to the CNS, changes in CBP can still modify spontaneous sympathetic activity of the rabbit superior cervical ganglion. The data reinforce previous findings related to evoked responses in the postganglionic nerves and also suggest that a pressure-modulated reflex, integrated at the level of the superior cervical ganglion, can influence ongoing sympathetic nervous outflow from the superior cervical ganglion in the rabbit.

Animals↗
PubMed1998

GABA- and glutamate-immunoreactive synapses on sympathetic preganglionic neurons projecting to the superior cervical ganglion.

Our previous work suggests that virtually all of the synapses on sympathetic preganglionic neurons projecting to the rat adrenal medulla are immunoreactive for either the inhibitory amino acid, gamma-aminobutyric acid (GABA) or the excitatory amino acid, L-glutamate. To investigate whether or not this is true for other groups of sympathetic preganglionic neurons, and to determine whether or not the proportion of inputs containing each type of amino acid neurotransmitter is the same for different groups of sympathetic preganglionic neurons, we retrogradely labelled rat and rabbit sympathetic preganglionic neurons projecting to the superior cervical ganglion and used post-embedding immunogold on ultrathin sections to localise GABA- and glutamate-immunoreactivity. The cell bodies and dendrites of both rat and rabbit sympathetic preganglionic neurons projecting to the superior cervical ganglion received synapses and direct contacts from nerve fibres immunoreactive for GABA and from nerve fibres immunoreactive for glutamate. In the rat, GABA was present in 48.9% of the inputs to sympathetic preganglionic neurons projecting to the superior cervical ganglion, and glutamate was present in 51.7% of inputs. Double immunogold labelling for glutamate and GABA on the same section, as well as labelling of consecutive serial sections for the two antigens, indicated that GABA and glutamate occur in separate populations of nerve fibres that provide input to rat sympathetic preganglionic neurons projecting to the superior cervical ganglion. We now have shown that GABA or glutamate is present in virtually all of the inputs to sympathetic preganglionic neurons projecting to the superior cervical ganglion and in essentially all of the inputs to sympathetic preganglionic neurons supplying the adrenal medulla. These findings are consistent with the hypothesis that all fast synaptic transmission in central autonomic pathways may be mediated by either excitatory or inhibitory amino acids. Furthermore, we showed a statistically significant difference in the proportion of glutamate-immunoreactive inputs between sympathetic preganglionic neurons projecting to the superior cervical ganglion and sympathoadrenal neurons (data from Llewellyn-Smith et al. [Llewellyn-Smith, I.J., Phend, K.D., Minson, J.B., Pilowsky, P.M., Chalmers, J.P., 1992. Glutamate immunoreactive synapses on retrogradely labelled sympathetic neurons in rat thoracic spinal cord. Brain Res. 581, 67-80]), with preganglionics supplying the adrenal medulla receiving more excitatory inputs than those supplying the superior cervical ganglion. This increased excitatory input to sympathoadrenal neurons may explain the predominant activation of these neurons following baroreceptor unloading.

Animals↗
PubMed1997

Transient somatostatin-immunoreactive ganglion cells in the developing rat retina.

The peptide somatostatin (SRIF) is likely to play important roles in neuronal differentiation and maturation. In the mammalian retina, it is reported to be expressed by populations of amacrine and/or displaced amacrine cells and, in some species, by some ganglion cells. Previous studies have shown that in the rat retina the maturation of somatostatinergic systems encompasses late prenatal and early postnatal periods, suggesting a role of SRIF in maturative events of the retina. SRIF-expressing ganglion cells have not been reported in the rat retina at any developmental age. In the present study, we re-evaluated the postnatal development of SRIF-containing neurons of the rat retina focusing on the analysis of SRIF-containing cells in the ganglion cell layer (GCL), to test the possibility that SRIF is expressed by some ganglion cells during development. To this aim we combined immunocytochemical staining of SRIF-positive neurons with retrograde tracing of ganglion cell bodies through Fluoro-Gold injections into the superior colliculus. Double-labelling experiments revealed the presence of SRIF-containing ganglion cells at postnatal day (PND) 10. They accounted for 14% of the total SRIF-containing cells in the GCL. Such double-labelled cells were not observed either before (PND 7) or after (PND 15 and PND 45) this period. This transient expression of SRIF in retinal ganglion cells suggests that SRIF may be a factor regulating the maturation of retinocollicular projections in a restricted period of postnatal development.

Aging↗
PubMed2001

Unbiased stereological quantification of neurons in the human spiral ganglion.

We applied an unbiased stereological technique, the optical fractionator, on five human archival temporal bone specimens to estimate the total number of spiral ganglion neurons. Available archival human temporal bone specimen has been serially sectioned at 20 microm and every tenth section was stained. All the stained sections passing through the spiral ganglion were used for the analysis. From each section sampled, the counting areas were systematically randomly sampled within the sectional area of the spiral ganglion. The neurons within the counting areas sampled were counted with the optical disector technique. The total number of the human spiral ganglion neurons was estimated by multiplying the number of neurons counted by the reciprocal of the aggregate sampling fraction. We found an average of 41700 neurons with a coefficient of variation of 0.14, which is a significant departure from the previously published data obtained with the assumption-based methods. The mean coefficient of error for the stereological estimates of the total number of human spiral ganglion neurons was 0.078. The present report presents unbiased stereological sampling and counting strategies for the future quantitative studies on the spiral ganglion neurons. The result of the present study provides the first unbiased baseline value of the human spiral ganglion neurons.

Adult↗
PubMed1997

Trigeminal ganglion neuronal activity and glial fibrillary acidic protein immunoreactivity after inferior alveolar nerve crush in the adult rat.

Nerve injury to the mandibular division of the trigeminal nerve has been shown to cause satellite cell reactions that extend beyond the mandibular division of the trigeminal ganglion into the maxillary and ophthalmic divisions. The goal of this study was to determine whether any physiological abnormalities correlated with this dispersal of satellite cell reaction. We investigated the electrophysiological and satellite cell glial fibrillary acidic protein immunoreactivity (GFAP-IR) changes that occur within the trigeminal ganglion 3, 10 and 59 days after a crush injury of the inferior alveolar nerve (IAN). At 3 days after IAN crush, there were no mechanically-evoked responses to ipsilateral stimulation of the skin and intraoral structures (e.g., mandibular incisor, lower lip and rostral mandibular gingiva) innervated by the IAN. However, the peripheral representations of the auriculotemporal, mylohyoid, lingual and maxillary nerve were intact and no abnormal responses to mechanical stimulation were detected to stimulation of tissue innervated by these nerves. By 10 days after the IAN crush, mandibular neurons responded to mechanical and electrical stimuli of the peripheral receptive field of the IAN, but with slower conduction velocities and higher electrical thresholds compared to control values. These abnormal electrophysiological response characteristics persisted 59 days following nerve injury. At 3, 10 and 59 days after IAN crush, 3-4% of the recorded mandibular neurons displayed spontaneous activity that was never observed in rats without nerve injury. Spontaneous activity was also never observed in neurons recorded in the maxillary or ophthalmic divisions of the trigeminal ganglion. Intense GFAP-IR in satellite cells was observed surrounding a mean of 131.7 neurons/section within the mandibular division of the trigeminal ganglion 3 days after nerve injury and around 50.3 neurons/section at 10 days. GFAP-IR was also present surrounding 16.5 and 10.3 neurons/section in the maxillary division of the trigeminal nerve at 3 and 10 days, respectively. At 59 days after IAN crush, GFAP-IR satellite cells were found around 22.9 neurons/section in the mandibular division of the trigeminal nerve, but were not found elsewhere in the trigeminal ganglion. The more extensive distribution of neurons encircled by satellite cell GFAP-IR compared to the trigeminal ganglion region containing abnormal electrophysiological responses demonstrates that abnormal neuronal signaling may not be characteristic of trigeminal ganglion neurons that are surrounded by GFAP injury reactions. However, the persistence of GFAP-IR 59 days after nerve injury suggests that satellite cell GFAP is involved in the long-term recovery of injured neurons.

Animals↗
PubMed2002

Injury to retinal ganglion cells induces expression of the small heat shock protein Hsp27 in the rat visual system.

Optic nerve transection results in apoptotic cell death of most adult rat retinal ganglion cells that begins at 4 days and leaves few surviving neurons at 14 days post-injury [Berkelaar et al. (1994) J. Neurosci. 14, 4368-4374]. The small heat shock protein Hsp27 has recently been shown to play a role in sensory neuron survival following peripheral nerve axotomy [Lewis et al. (1999) J. Neurosci. 19, 8945-8953]. To investigate the role of Hsp27 in injured CNS sensory neurons, we have studied the induction and cell-specific expression of Hsp27 in rat retinal ganglion cells 1-28 days after optic nerve transection. Immunohistochemical results indicate that Hsp27 is not present at detectable levels in the ganglion cell layer of control (uninjured) or sham-operated control rats. In contrast, Hsp27 is detected in retinal ganglion cells from 4 to 28 days following axotomy. Furthermore, the percentage of surviving retinal ganglion cells that are Hsp27-positive increased over the same time period. Hsp27 is also detected in glial fibrillary acidic protein-positive astrocytes in the optic layer of the superior colliculus from 4 to 28 days after optic nerve transection. These experiments demonstrate that transection of the optic nerve results in the expression of Hsp27 in three distinct regions of the rat visual system: sensory retinal ganglion cells in the eye, glial cells of the optic tract, and astrocytes in the optic layer of the superior colliculus. Hsp27 may be associated with enhanced survival of a subset of retinal ganglion cells, providing evidence of a protective role for Hsp27 in CNS neuronal injury.

Animals↗
PubMed2002

Retinal ganglion cell death after acute retinal ischemia is an ongoing process whose severity and duration depends on the duration of the insult.

In adult Sprague-Dawley rats we have investigated retinal ganglion cell survival after transient intervals of retinal ischemia of 30, 45, 60, 90 or 120 min duration, induced by ligature of the ophthalmic vessels. Animals were killed 5, 7, 14, 21, 30, 60, 90 or 180 days later and densities of surviving retinal ganglion cells were estimated in retinal whole mounts by counting cells labelled with diAsp. This dye was applied, 3 days prior to death, to the ocular stump of the intraorbitally transected optic nerve. We found that retinal ganglion cell loss after retinal ischemia proceeds for different lengths of time. All the ischemic intervals induced loss of retinal ganglion cells whose severity and duration was related to the length of the ischemic interval. Following 30 or 45 min of ischemia, cell loss lasted 14 days and caused the death of 46 or 50%, respectively, of the population of retinal ganglion cells. Sixty, 90 or 120 min of retinal ischemia were followed by a period of cell loss that lasted up to 90 days and caused the death of 75%, 87% or 99%, respectively, of the population of retinal ganglion cells. We conclude that retinal ganglion cell loss after retinal ischemia is an ongoing process that may last up to 3 months after the injury and that its severity and duration are determined by the ischemic interval.

Acute Disease↗
PubMed2002

Reduced redox state allows prolonged survival of axotomized neonatal retinal ganglion cells.

Axonal injury to CNS neurons results in apoptotic cell death. The processes by which axotomy signals apoptosis are diverse, and may include deprivation of target-derived factors, induction of injury factors, bursts of reactive oxygen species (ROS), and other mechanisms. Our previous studies demonstrated that death of a dissociated retinal ganglion cell, an identified CNS neuron, is ROS-dependent. To better define the mechanisms by which ROS induce retinal ganglion cell death after axotomy, we studied their effects in dissociated neonatal rat retinal cultures. Postnatal day 2-4 Long-Evans rat retinal ganglion cells were retrogradely labeled with the fluorescent tracer 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine (DiI). Postnatal day 7-9 retinas were dissociated and cultured in the presence of specific ROS generating systems, scavengers, or redox modulators. Retinal ganglion cells were identified by DiI positivity and viability determined by metabolism of calcein-acetoxymethyl ester. We found that ROS scavengers protected against retinal ganglion cell death after acute dissociation, and the effects of ROS appeared to be due to shifts in the redox potential, as retinal ganglion cell survival was critically dependent on redox state, with greatest survival under mildly reducing conditions. Culture of retinal ganglion cell with the non-thiol-containing reducing agent tris(carboxyethyl)phosphine resulted in long-term survival equivalent to or better than with neurotrophic factors. Our data suggest that axotomy-associated neuronal death induced by acute dissociation may be partly dependent on ROS production, acting to shift the redox state and oxidize one or more key thiols. Understanding the mechanisms by which ROS signal neuronal death could result in strategies for increasing their long-term survival after axonal injury.

Animals↗
PubMed2004

Effects of adenoviral-mediated gene transfer of interleukin-10, interleukin-4, and transforming growth factor-beta on the survival of axotomized retinal ganglion cells.

Nitric oxide, synthesized by reactive microglia and astrocytes has been implicated in promoting neuronal degeneration observed in many diseases and insults of the central nervous system. We have recently shown that inducible nitric oxide synthase is expressed by retinal glial cells following optic nerve transection and that inhibition of nitric oxide synthesis enhances the survival of injured retinal ganglion cells. Anti-inflammatory cytokines including interleukin-10 (IL-10), interleukin-4 (IL-4), and transforming growth factor-beta (TGF-beta) have been shown to prevent inducible nitric oxide synthase expression, and inhibit nitric oxide synthesis by microglia and astrocytes in culture. In the present study, we examined the effects of adenoviral mediated gene transfer of anti-inflammatory cytokines on the survival of axotomized retinal ganglion cells. Intraocular administration of adenoviral vectors encoding interleukin-10 (Ad.IL-10) and interleukin-4 (Ad.IL-4) enhanced the survival of axotomized retinal ganglion cells at 14 days after axotomy. Adenoviral vectors encoding TGF-beta (Ad.TGF-beta) had no effect on retinal ganglion cell survival. Separate animals were pretreated by injection of Ad.IL-10 or Ad.IL-4 into the superior colliculus (s.c.), the major target of ganglion cells, 7 days prior to axotomy. S.c. administration of Ad.IL-10 or Ad.IL-4 significantly increased ganglion cell survival compared with intraocular injection. IL-10 and IL-4 gene transfer also reduced the density of infiltrating ED1 positive monocytes in the nerve fiber layer at 14 days postaxotomy. Ad.TGF-beta increased the density of ED1 positive monocytes infiltrating the nerve fiber layer after axotomy. Vectors encoding IL-10 or IL-4 also decreased nitrotyrosine immunoreactivity in the inner retina at 7 days postaxotomy, suggesting that these cytokines protect retinal ganglion cells from peroxynitrite formation that results from nitric oxide synthesis by activated glial cells. The present study has implications for the treatment of CNS injury and diseases that involve reactive microglia and astrocytes. Our results suggest that interleukin-10 and interleukin-4 may help prevent neurodegeneration caused by the activation of glial cells after CNS injury.

Adenoviridae↗
PubMed1997

Transient expression of alpha-1B adrenoceptor messenger ribonucleic acids in the rat superior cervical ganglion during postnatal development.

We have examined the developmental profile of the alpha-1 and alpha-2 adrenergic receptor messenger ribonucleic acids expression in the rat superior cervical ganglion. The expression of the six messenger ribonucleic acids was studied using reverse transcription-polymerase chain reaction. At four weeks, the dominant messenger ribonucleic acids transcripts in this sympathetic ganglion were alpha-1C, alpha-2A, alpha-2B and alpha-2C. The expression of alpha-1 genes in the superior cervical ganglion appears to be regulated during postnatal development in that two alpha-1 (alpha-1B, alpha-1C) genes were expressed at birth, three, seven and 14 days postnatal but no amplified product for alpha-1B was detected at 28 days and in the aged animals, while the alpha-1C transcript continued to be expressed. No amplified product for alpha-1D was detected in superior cervical ganglion at any of the ages studied. While all three alpha-2 genes were expressed in the superior cervical ganglion at four weeks the dominant alpha-2 messenger ribonucleic acids transcript expressed in the superior cervical ganglion was alpha-2A. This pattern of alpha-2 adrenoceptor gene expression was maintained from birth, throughout development and into old age. These results suggest that the expression of alpha-1 adrenergic receptors in the superior cervical ganglion is regulated developmentally while the expression of alpha-2 genes remains unchanged.

Aging↗
PubMed1997

Dystrophin and its isoforms in a sympathetic ganglion of normal and dystrophic mdx mice: immunolocalization by electron microscopy and biochemical characterization.

In normal mouse superior cervical ganglion, dystrophin immunoreactivity is present in ganglionic neurons, satellite cells and Schwann cells. It is associated with several cytoplasmic organelles and specialized plasma membrane domains, including two types of structurally and functionally different intercellular junctions: synapses, where it is located at postsynaptic densities, and adherens junctions. Dystrophin immunostaining can be ascribed to the 427,000 mol. wt full-length dystrophin, as well as to the several dystrophin isoforms present in superior cervical ganglion, as revealed by western immunoblots. In mdx mouse superior cervical ganglion, which lacks the 427,000 mol. wt dystrophin, the unchanged pattern of dystrophin immunolabelling observed at several subcellular structures indicates the presence of dystrophin isoforms at these sites. Moreover, the absence of labelled adherens junctions indicates the presence of full-length dystrophin at this type of junction in the normal mouse superior cervical ganglion. The lower number of immunopositive postsynaptic densities in mdx mouse superior cervical ganglion than in normal mouse ganglion suggests the presence, in the latter, of postsynaptic densities with differently organized dystrophin cytoskeleton: some containing dystrophin isoforms alone or together with 427,000 mol. wt dystrophin, and others containing 427,000 mol. wt dystrophin alone.

Animals↗
PubMed1998

Activation and inactivation properties of voltage-gated calcium currents in developing cat retinal ganglion cells.

The correlated activity of developing retinal ganglion cells is essential for the reorganization and refinement of retinogeniculate projections. Previous studies have uncovered marked changes in the spiking properties of retinal ganglion cells during this period of reorganization; however, a full understanding of the changes in the underlying ionic conductances has yet to be obtained. To this end, the whole-cell configuration of the patch-clamp technique was used to record currents conducted by voltage-gated calcium channels in 83 dissociated cat retinal ganglion cells obtained from animals aged between embryonic day 34 and postnatal day 105. Calcium currents, magnified by using barium as the major charge carrier, were isolated by substituting choline for Na+ in the bathing solution and Cs+ for K+ in the electrode solution. Three voltage-gated Ca2+ conductances were identified based on their voltage dependence and kinetics of activation and inactivation: a transient low-voltage-activated conductance, a transient high-voltage-activated conductance and a sustained high-voltage-activated conductance. During the developmental period examined there were significant increases in the densities of all three conductances, as well as significant changes in some of their activation and inactivation properties. These findings, together with those reported previously for the voltage-gated Na+ and K+ conductances, are related to the generation of excitability in developing retinal ganglion cells during a period critical to the normal development of the visual system. Furthermore, while the sustained high-voltage-activated conductance was present in all of the retinal ganglion cells observed, only about 72% expressed the transient high-voltage-activated current. During the developmental period examined, there was also an increase in the proportion of cells expressing the transient low-voltage-activated conductance. This, along with our previous finding that retinal ganglion cells heterogeneously express different types of voltage-gated K+ channels, strongly suggests that the spiking patterns observed in different classes of retinal ganglion cell may be due, in part, to their intrinsic membrane properties.

Animals↗
PubMed2000

Synapses on human spiral ganglion cells: a transmission electron microscopy and immunohistochemical study.

A transmission electron microscopy (TEM) study and synaptophysin immunoreactivity analysis of neurons in the human spiral ganglion was performed with particular emphasis on the demonstration of synapses. The study was based on surgical biopsy material obtained during transcochlear meningioma surgery. Vesiculated nerve endings of unmyelinated nerve fibers occurred frequently on the small ganglion cells at all levels. The nerve terminals exhibited abundant clear synaptic vesicles but also dense-core vesicles. Multisynaptic contact sites were also seen with fibers of the intraganglionic spiral bundle (IGSB). Complex associations of synapses could be demonstrated, including several synaptic terminals in conjunction with contact sites or an adherent type of junctions on large ganglion cells. These contact sites exhibited membrane densities which were symmetric or asymmetric, changed their polarity recurrently over their extension from one cell to the other and back and lacked clear synaptic vesicles. This suggests the existence of connections between efferents, belonging to the olivocochlear bundle, and both small and large ganglion cells. Thus, both the inner and outer hair cell system may be under the influence of efferent innervation in the human spiral ganglion. The morphology and course of synaptophysin-positive nerve fibers indicated that synaptic contacts within the spiral ganglion, as observed under the electron microscope, may be abundant. These results indicate that complex neural processing may occur at the level of the spiral ganglion in man.

Humans↗
PubMed2000

Pattern of degeneration of the spiral ganglion cell and its processes in the C57BL/6J mouse.

Although degeneration of spiral ganglion cells has been described as a histopathologic correlate of hearing loss both in animals and humans, the pattern and sequence of this degeneration remain controversial. Degeneration of hair cells and of spiral ganglion cells and their dendritic processes was evaluated in the C57BL/6J mouse, in which there is a genetically determined progressive sensorineural loss starting in the high frequencies that is similar to the pattern commonly seen in the human. Auditory function was evaluated by brainstem evoked responses, and degeneration of hair cells, ganglion cells and their dendrites was evaluated histologically at 3, 8, 12 and 18 months of age. Progressive loss of auditory sensitivity was correlated with the loss of outer and inner hair cells and spiral ganglion cells and their dendritic processes. In addition, dendritic counts were consistently lower at a distal location in the osseous spiral lamina (i.e. near the organ of Corti) than at a proximal location (i.e. near the spiral ganglion), and the difference between the number of distal dendrites and the number of proximal dendrites tended to be greater with advancing age. These observations suggest an age-related progressive retrograde degeneration of spiral ganglion cells. Thus, in degenerating cochleas, some remaining spiral ganglion cells may have no distal dendritic processes near the organ of Corti. This may have implications for successful stimulation of the cochlear neuron in cochlear implantation.

Age Factors↗
PubMed2001

Presence of neuronal nitric oxide synthase in autonomic and sensory ganglion neurons innervating the lacrimal glands of the cat: an immunofluorescent and retrograde tracer double-labeling study.

It is generally considered that parasympathetic postganglionic nerve fibers innervating the lacrimal gland (LG) arise from the pterygopalatine ganglion (PPG), while sympathetic and sensory innervations arise from the superior cervical ganglion (SCG) and trigeminal ganglion (TG), respectively. Recently, we reported for the first time that the parasympathetic innervation of the cat LG was also provided by the otic ganglion (OG) and ciliary ganglion (CG), and that the sensory innervation was also provided by the superior vagal ganglion (SVG) and superior glossopharyngeal ganglion (SGG). To determine if nitric oxide (NO) is a neurotransmitter of the autonomic and sensory neurons innervating the LG, we injected the cholera toxin B subunit (CTB) as a retrograde tracer into the cat LG, and used double-labeling fluorescent immunohistochemistry for CTB and nitric oxide synthase (NOS). We found that NOS-/CTB-immunofluorescent double-labeled perikarya were localized in the PPG, OG, TG, SVG and SGG, but not in the CG and SCG. The highest numbers of NOS-/CTB-immunofluorescent double-labeled neurons were found in the PPG and TG. In addition, we examined the presence of nitrergic nerve fibers in the LG using NADPH-d histochemistry and found that a large amount of NADPH-d-stained nerve fibers were distributed around the glandular acini and in the walls of glandular ducts and blood vessels. This study provides the first direct evidence showing that NO may act as a neurotransmitter or modulator involved in the parasympathetic and sensory regulation of lacrimal secretion and blood circulation, but may not be implicated in the sympathetic control of LG activities, and that nitrergic nerve fibers in the LG arise mainly from parasympathetic postganglionic neurons in the PPG and sensory neurons in the TG. The present results suggest that NO plays an important role in the regulation of LG activities.

Animals↗