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PubMed1999

Plasticity in the phenotypic expression of catecholamines and vasoactive intestinal peptide in adult rat superior cervical and stellate ganglia after long-term hypoxia in vivo.

Sympathetic ganglia in the adult rat contain various populations of nerve cells which demonstrate plasticity with respect to their transmitter phenotype. The plasticity of the neuronal cell bodies and of the small intensely fluorescent cells in the superior cervical and stellate ganglia in response to hypoxia in vivo (10% O2 for seven days) was assessed by studying the expression of catecholamines and vasoactive intestinal peptide. The levels of norepinephrine, dopamine, 3,4-dihydroxyphenylacetic acid and vasoactive intestinal peptide immunoreactivity were determined. In addition, the density of the immunohistochemical staining of cells for tyrosine hydroxylase and vasoactive intestinal peptide was evaluated. In the intact superior cervical ganglion, hypoxia increased the dopamine level as well as the density of small intensely fluorescent cells immunolabelled for tyrosine hydroxylase and vasoactive intestinal peptide. In the axotomized ganglion, hypoxia elicited a twofold rise in the level of the vasoactive intestinal peptide as well as enhancing the density of neuronal cell bodies immunostained for this peptide. Thus, the effect of hypoxia on the expression of vasoactive intestinal peptide expression in neurons was dependent on neural interactions. In the intact stellate ganglion, hypoxia alone induced a 1.5-fold increase in the density of neuronal cell bodies immunostained for vasoactive intestinal peptide. Thus, ganglia-specific factors appeared to play a role in determining changes in neuronal phenotype in response to hypoxia. The present study provides evidence for the involvement of dopamine and vasoactive intestinal peptide in ganglionic responses to long-term hypoxia as well as for differential responses by the two ganglionic cell populations, i.e. neuronal cell bodies and small intensely fluorescent cells. Changes in the expression of the vasoactive intestinal peptide during long-term hypoxia may be of energetic, trophic and/or synaptic significance. Hypoxia may be considered to be a vasoactive intestinal peptide-inducing factor in sympathetic ganglia.

Animals↗
PubMed2000

Development of the nigrostriatal dopamine neuron and the pathways in the basal ganglia.

The nigrostriatal (NS) dopamine (DA) neuron and the basal ganglia show marked functional age variation in the first three decades. Neurohistochemical studies revealed marked age variation of activities of tyrosine hydroxylase at the terminal of the NS-DA neuron, which show exponential decremental variation from early childhood and subside in the fourth decade. DA-D2 receptors, examined by PET scan, are in high levels in the third decade which decrease dramatically to the bottom or 'adult' levels in the fourth decade. The examination of voluntary saccade suggested the striatal indirect pathways are functionally immature in the childhood and attain adult levels in around the middle of the second decade, while the striatal direct pathways have already been functionally matured in childhood. Clinical evidence suggests that among efferents of the basal ganglia those descending to the brainstem and the midbrain mature earlier while those ascending to the thalamus later. These developmental variation of the NS-DA neurons and the basal ganglia could modulate the ages at onset and clinical courses of the diseases with abnormalities in the NS-DA neuron or the basal ganglia which occur in these age periods.

Adolescent↗
PubMed1999

What are the computations of the cerebellum, the basal ganglia and the cerebral cortex?

The classical notion that the cerebellum and the basal ganglia are dedicated to motor control is under dispute given increasing evidence of their involvement in non-motor functions. Is it then impossible to characterize the functions of the cerebellum, the basal ganglia and the cerebral cortex in a simplistic manner? This paper presents a novel view that their computational roles can be characterized not by asking what are the "goals" of their computation, such as motor or sensory, but by asking what are the "methods" of their computation, specifically, their learning algorithms. There is currently enough anatomical, physiological, and theoretical evidence to support the hypotheses that the cerebellum is a specialized organism for supervised learning, the basal ganglia are for reinforcement learning, and the cerebral cortex is for unsupervised learning.This paper investigates how the learning modules specialized for these three kinds of learning can be assembled into goal-oriented behaving systems. In general, supervised learning modules in the cerebellum can be utilized as "internal models" of the environment. Reinforcement learning modules in the basal ganglia enable action selection by an "evaluation" of environmental states. Unsupervised learning modules in the cerebral cortex can provide statistically efficient representation of the states of the environment and the behaving system. Two basic action selection architectures are shown, namely, reactive action selection and predictive action selection. They can be implemented within the anatomical constraint of the network linking these structures. Furthermore, the use of the cerebellar supervised learning modules for state estimation, behavioral simulation, and encapsulation of learned skill is considered. Finally, the usefulness of such theoretical frameworks in interpreting brain imaging data is demonstrated in the paradigm of procedural learning.

Journal Article↗
PubMed1998

Differential time course of neuronal and glial apoptosis in neonatal rat dorsal root ganglia after sciatic nerve axotomy.

Sensory neurons in neonatal rat lumbar dorsal root ganglia die after sciatic nerve axotomy, and previous studies have estimated the total cell loss to be 40-95%. We have used the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labelling (TUNEL) technique, combined with immunohistochemistry, to investigate the contribution of apoptosis to the cell loss that occurs after unilaterally transecting the sciatic nerve of new-born rats. TUNEL-positive cells were detected 1 day post-lesion, and their number peaked 3 days after the injury. Combining TUNEL labelling with immunohistochemistry, for neuron-specific neurofilament 150 kDa, or glial-specific S-100beta, enabled us to identify dying neurons and dying glia. One day after axotomy, most of the TUNEL-positive cells (58%) were neurons, whereas 3 days post-injury, only a small number of dying cells (6%) were neuronal. This lower incidence was due to a decrease in neuronal death and an increase in glial death. The glia in the dorsal root ganglia therefore die subsequent to the neurons. The apoptotic nature of the cell death was confirmed by electron microscopy, with fine structural features of apoptotic cell death, e.g. chromatin compaction and membrane blebbing, being observed in both glia and neurons. Our results confirm that extensive apoptosis occurs in the neonatal lumbar dorsal root ganglia after sciatic nerve section, and show that neurons and glial cells die with different time-courses. The results suggest a neuron-glia trophic interdependence in the dorsal root ganglia.

Animals↗
PubMed2002

Expression of adenosine triphosphate P2X3 receptors in rat molar pulp and trigeminal ganglia.

OBJECTIVE: The objective of this study was to investigate the expression of adenosine triphosphate P2X3 receptor subunits in rat molar pulp and trigeminal ganglia and their relationship to substance P. STUDY DESIGN: Rat molar pulp and trigeminal ganglia were fixed and sectioned. Double immunostaining with anti-P2X3 and anti-substance P were used to localize P2X3 and substance P expression simultaneously with different stains. RESULTS: P2X3 immunoreactivity (IR) fibers were present in root and coronal pulp. P2X3-IR fibers formed subodontoblastic plexus and advanced into the predentin and dentin. P2X3-IR neurons were localized in small and medium-sized cells in trigeminal ganglia. Colocalization of P2X3 and substance P was not found in either molar pulp or trigeminal ganglia. CONCLUSION: The results of this study indicated that adenosine triphosphate in pulp tissues may stimulate a subpopulation of non-substance P trigeminal afferent fibers through activation of P2X3 receptors.

Adenosine Triphosphate↗
PubMed1988

Expression of varicella-zoster virus and herpes simplex virus in normal human trigeminal ganglia.

Lysates of radiolabeled explants from four human trigeminal ganglia were immunoprecipitated with antibodies to varicella-zoster virus (VZV) and to herpes simplex virus. Both herpes simplex virus- and VZV-specific proteins were detected in lysates of all four ganglia. Absence of reactivity in ganglion explants with monoclonal antibodies suggested that herpes simplex virus and VZV were not reactivated during the culture period. In situ hybridization studies demonstrated the presence of RNA transcripts from the VZV immediate early gene 63. This approach to the detection of herpes simplex virus and VZV expression in human ganglia should facilitate analysis of viral RNA and proteins in human sensory ganglia.

Adult↗
PubMed2003

The herpes simplex virus type 1 ICP0 promoter is activated by viral reactivation stimuli in trigeminal ganglia neurons of transgenic mice.

Herpes simplex virus type 1 (HSV-1) causes a latent infection in sensory ganglia neurons in humans and in the mouse model. The ability of the virus to latently infect neurons and reactivate is central to the ability of HSV-1 to remain in the human population and spread to new hosts. It is possible that neuronal transcriptional proteins control latency and reactivation by modulating activation of the HSV-1 immediate-early (IE) gene ICP0. We have previously shown that factors in trigeminal ganglia neurons can differentially activate the IE ICP0 promoter and the IE ICP4 promoter in developing trigeminal ganglia neurons of transgenic mice. Ultraviolet (UV) irradiation and hyperthermic stress have been shown to result in HSV-1 reactivation from sensory neurons in the mouse model. Reporter transgenic mice were exposed to UV irradiation or hyperthermia to test whether stimuli that are known to reactivate HSV-1 could activate viral IE promoters in the absence of viral proteins. Measurement of beta-galactosidase activity in trigeminal ganglia from these transgenic mice indicated that the ICP0 promoter activity was significantly increased by both UV irradiation and hyperthermia. The IE genes ICP4 and ICP27 and the late gene gC reporter transgenes failed to be activated in parallel experiments. These results suggest that the ICP0 promoter is a target for activation by host transcription factors in sensory neurons that have undergone damage. It further suggests the possibility that activation of ICP0 gene expression by neuronal transcription factors may be important in reactivation of HSV-1 in neurons.

Animals↗
PubMed1996

Inducible nitric oxide synthase increases in regenerating rat ganglia.

Nitric oxide synthase (NOS) exists in several isoforms. In this study we used immunocytochemistry to investigate one isoform, inducible NOS (iNOS), in the nodose ganglia (NG) and in the superior cervical ganglia (SCG) of the rat. iNOS was present in many neurones of the NG, while no iNOS-positive cells could be observed in the SCG. At 24 and 48 h following a crush lesion to the vagus nerve, expression of iNOS-immunoreactivity had increased in the NG. iNOS-immunoreactivity increased in both the NG and SCG of ganglia cultured for 24 and 48 h. The results show that an increase in iNOS-immunoreactivity accompanies regenerative processes in two peripheral ganglia, suggesting that nitric oxide, the product of iNOS activity, could be involved in nerve regeneration.

Animals↗
PubMed1994

Detection of herpes simplex virus type 1-encoded RNA by polymerase chain reaction: different pattern of viral RNA detection in latently infected murine trigeminal ganglia following in vitro or in vivo reactivation.

Herpes simplex virus type 1 (HSV-1) establishes latent infection in the sensory ganglia. To investigate the process of reactivation from latency, we used the RNA polymerase chain reaction (RNA-PCR) to detect the expression of several HSV genes. BALB/c mice were inoculated in the anterior ocular chamber with HSV-1 strain KOS and the trigeminal ganglia were examined at least 8 weeks after inoculation. Latency-associated transcripts (LATs) were found in the latently infected ganglia and remained detectable 120 h after explantation. Besides LATs, we detected transcripts for infected cell protein 0 (ICP0) (Vmw110) 24 h after explantation, but RNAs encoding ICP4 (Vmw175), ICP27, thymidine kinase and VP16 (ICP25; Vmw65) remained undetectable for 120 h after explantation. Following in vivo reactivation of HSV-1 by administration of cyclophosphamide and dexamethasone, all viral transcripts including ICP0 RNA became detectable. The RNA-PCR enabled us to detect ICP0 RNA much earlier than has been previously reported in studies using the Northern blot technique and has laid a foundation for further study of viral and cellular transcripts during reactivation. Our results suggest that the process of reactivation of HSV-1 from trigeminal ganglia may be divided into at least two steps: (i) initiation of ICP0 gene transcription and (ii) detectable transcription of the other genes. The second step may be regulated in part by the host immune system, since cyclophosphamide and dexamethasone administration enabled the detection of several viral transcripts.

Animals↗
PubMed1997

Equine herpesvirus 4 DNA in trigeminal ganglia of naturally infected horses detected by direct in situ PCR.

Neuronal and lymphoid tissues of 15 randomly selected horses were analysed post mortem by liquid nested-PCR to study the tropism of equine herpesvirus 4 (EHV-4). In four animals the trigeminal ganglia and in one case the lung were positive. Using a direct in situ PCR the EHV-4 genome was localized in the nuclei of neurons and in the bronchiolar as well as alveolar epithelium of the lung. In none of these tissues could infectious virus or viral antigens be detected. Applying the more sensitive liquid RT-PCR, however, an acute infection was demonstrated in one of the trigeminal ganglia by amplification of viral transcripts coding for glycoprotein B. The failure to detect these transcripts in the other trigeminal ganglia and the lung indicates a latent infection. This report formally proves that, like other members of the Alpha-herpesvirinae, EHV-4 establishes latency in the trigeminal ganglia.

Animals↗
PubMed2006

Competition and complementation between thymidine kinase-negative and wild-type herpes simplex virus during co-infection of mouse trigeminal ganglia.

Laboratory strains of herpes simplex virus lacking thymidine kinase (TK) cannot replicate acutely to detectable levels in mouse trigeminal ganglia and do not reactivate from latency. However, many pathogenic clinical isolates that are resistant to the antiviral drug acyclovir are heterogeneous populations of TK-negative (TK(-)) and TK-positive (TK(+)) viruses. To recapitulate this in vivo, mice were infected with mixtures of wild-type virus and a recombinant TK(-) mutant in various ratios. Following co-infection, the replication, number of latent viral genomes and reactivation efficiency of TK(+) virus in trigeminal ganglia were reduced in a manner related to the amount of TK(-) virus in the inoculum. TK(+) virus did not always complement the acute replication or increase the number of latent viral genomes of TK(-) mutant in mouse ganglia. Even so, TK(+) virus could still confer the pathogenic phenotype to a TK(-) mutant, somehow providing sufficient TK activity in trans to permit a TK(-) mutant to reactivate from latently infected ganglia.

Animals↗
PubMed1984

Effect of eight antiviral drugs on the reactivation of herpes simplex virus in explant cultures of latently infected mouse trigeminal ganglia.

The effect of several antiviral drugs on the reactivation of herpes simplex virus type 1 in explant cultures of latently infected mouse trigeminal ganglia was investigated. Phosphonoacetate and phosphonoformate, which act directly on the virus-induced DNA polymerase, require a drug concentration of 400 micrograms/ml for the inhibition of virus reactivation in latently infected ganglia. Arabinosyladenine and arabinosyladenine monophosphate, which are phosphorylated to triphosphates by cellular enzymes and inhibit virus synthesis either by blocking the DNA polymerase or by incorporation into viral DNA, require a concentration of only 100 micrograms/ml for the inhibition of the reactivation process. Drugs that are phosphorylated by the virus-induced thymidine kinase, such as acyclovir, arabinosylthymine, bromovinyldeoxyuridine, and three fluorinated pyrimidine nucleosides require the lowest drug concentrations for complete inhibition of virus reactivation in latently infected ganglia explant cultures. Our data suggest that the inhibition of virus reactivation is dependent not only on drug concentration, but also on the number of latently infected neurons in the ganglia.

Acyclovir↗
PubMed2006

Serotonin in trigeminal ganglia of female rodents: relevance to menstrual migraine.

OBJECTIVES: We examined changes in the serotonin system across the estrous cycle in trigeminal ganglia of female rodents to determine which components are present and which are regulated by the variations in levels of ovarian steroids that occur during the estrous cycle. BACKGROUND: Migraine is 2-3 times more prevalent in women than in men and attacks are often timed with the menstrual cycle, suggesting a mechanistic link with ovarian steroids. Serotonin has been implicated in the pathogenesis of migraine, and the effectiveness of triptans, selective 5HT-1B/D/F agonists, has provided further support for this concept. It is not known whether serotonin, its rate-limiting enzyme tryptophan hydroxylase (TPH), or its receptors are regulated by ovarian steroids in trigeminal ganglia. METHODS: We used reverse transcription-polymerase chain reaction to examine gene expression in cycling mice, Western blots to examine protein expression, double-labeling immunohistochemistry using markers of nociceptors and nonnociceptors and confocal microscopy to identify specific types of neurons, and primary tissue culture to examine effects of estrogen on trigeminal neurons in vitro. RESULTS: In C57/BL6 mice mRNA levels of TPH-1, the rate-limiting enzyme in serotonin synthesis, were over 2-fold higher and protein levels were 1.4-fold higher at proestrus, the high estrogen stage of the cycle than at diestrus, the low estrogen stage. TPH protein also was present in primary trigeminal cultures obtained from female Sprague-Dawley rats, but levels were not affected by 24-hour treatment with physiological levels (10(-9) M) of 17beta-estradiol. Gene expression of 5HT-1B and 5HT-1D receptors in trigeminal ganglia was not regulated by the estrous cycle. Serotonin was present in trigeminal neurons containing CGRP, a potent vasoactive neuropeptide, peripherin, an intermediate filament present in neurons with unmyelinated axons, neurofilament H, which is present in neurons with myelinated axons, and in neurons binding IB4, a marker of nonpeptidergic nociceptors. Serotonin was also present in neurons containing 5HT-1B. The serotonin-positive population was significantly larger in diameter than the serotonin-negative population. Conclusions.-Expression of the rate-limiting enzyme required for serotonin synthesis is regulated during the natural estrous cycle, and serotonin is present in larger trigeminal neurons of all the major subtypes. Colocalization of serotonin with 5HT-1B suggests that this receptor functions as an autoreceptor to regulate serotonin release. Cyclical changes in serotonin levels in trigeminal ganglia could contribute to the pathogenesis of menstrual migraine.

Animals↗
PubMed2001

Prevalence of HSV-1 LAT in human trigeminal, geniculate, and vestibular ganglia and its implication for cranial nerve syndromes.

Herpes simplex virus type 1 (HSV-1) enters sensory neurons and can remain latent there until reactivation. During latency restricted HSV-1 gene expression takes place in the form of latency-associated transcripts (LAT). LAT has been demonstrated to be important not only for latency but also for reactivation, which may cause cranial nerve disorders. Tissue sections of the trigeminal ganglia (TG), geniculate ganglia (GG), and the vestibular ganglia (VG) from seven subjects were examined for the presence of LAT using the in situ hybridization technique. LAT was found on both sides in allTG (100%), on both sides of five subjects (70%) in the GG, and in none of the VG. Using a second more sensitive detection method (RT-PCR), we found LAT in the VG of seven of ten other persons (70%). This is the first study to demonstrate viral latency in the VG, a finding that supports the hypothesis that vestibular neuritis is caused by HSV-1 reactivation. The distribution of LAT in the cranial nerve ganglia indicates that primary infection occurs in the TG and GG and subsequently spreads along the faciovestibular anastomosis to the VG.

Adult↗
PubMed1984

Monoclonal antibodies suppress replication of herpes simplex virus type 1 in trigeminal ganglia.

The effect of monoclonal antibodies on the growth of herpes simplex virus type 1 in trigeminal ganglia was investigated. Four-week-old mice were infected on an abrased cornea with herpes simplex virus type 1. Forty-eight hours after infection, trigeminal ganglia ipsilateral with infected eyes were removed and placed in culture. Incubation of infected ganglia in the presence of a pool of nonneutralizing monoclonal antibodies specific for glycoproteins of gB and gE suppressed virus growth by greater than 90%. This was comparable to the amount of suppression observed when infected ganglia were incubated in hyperimmune serum. Individual monoclonal antibodies were less efficient, being able to inhibit virus growth by only two- to threefold. The mechanism of suppression was examined. Reduction in virus growth was observed under conditions in which all susceptible ganglion cells were infected in vitro before nonneutralizing monoclonal antibody was added. Similar results were obtained in tests with virus-infected neuroblastoma cells. Furthermore, suppression of infectious progeny was seen in the absence of complement and immunologically reactive cells. Thus, neither virus neutralization nor immunocytolysis could account for the effects of antibody on virus growth. Rather, the data suggest that antibody can bind to herpes simplex virus type 1-infected neuronal cells and suppress intracellular virus replication.

Animals↗
PubMed1988

Detection and preliminary characterization of herpes simplex virus type 1 transcripts in latently infected human trigeminal ganglia.

RNA extracted from human trigeminal ganglia was examined for the presence of herpes simplex virus type 1 (HSV-1) transcripts by Northern hybridization (RNA blot) analysis. By using cloned DNA and single-stranded RNA probes, two abundant colinear HSV-1 transcripts (1.85 and 1.35 kilobases) were detected in ganglia from 9 of 17 individuals. These RNAs overlap the 3' end of the transcript for immediate-early gene ICP0 but are transcribed from the opposite strand; thus, they are antisense relative to the ICP0 mRNA. We also report evidence by in situ hybridization that these latently infected ganglia contain HSV-1 RNA homologous to the BamHI SP region of the genome which is transcribed in the same direction as the other latency transcripts. In Vero cells productively infected with laboratory strain HSV-1 KOS and in cultures infected with different low-passage clinical isolates, only the 1.85-kilobase transcript was detected, and there was variation in the size of this larger latency transcript. These novel transcripts may play a role in maintaining HSV-1 latency in human ganglia.

Animals↗
PubMed1988

RNA complementary to herpes simplex virus type 1 ICP0 gene demonstrated in neurons of human trigeminal ganglia.

Recent studies with mice have demonstrated abundant RNA transcripts which are complementary (antisense) to the herpes alpha gene ICP0 in latently infected ganglia. We investigated the situation in unselected human trigeminal ganglia. Strand-specific 2.7-kilobase herpes simplex virus type 1 (HSV-1) ICP0 RNA probes were prepared, and their sense was determined in productively infected cells. Although in situ hybridization demonstrated ICP0 antisense RNA transcripts in the nuclei of neurons in 46% of the ganglia, ICP0 messenger RNA was not found in any of the ganglia. We conclude that HSV-1 antisense ICP0 RNA is present in humans during ganglionic latency.

Adult↗
PubMed1993

Induction of reactivation of herpes simplex virus in murine sensory ganglia in vivo by cadmium.

Herpes simplex viruses maintained in a latent state in sensory neurons in mice do not reactivate spontaneously, and therefore the factors or procedures which cause the virus to reactivate serve as a clue to the mechanisms by which the virus is maintained in a latent state. We report that cadmium sulfate induces latent virus to reactivate in 75 to 100% of mice tested. The following specific findings are reported. (i) The highest frequency of induction was observed after two to four daily administrations of 100 micrograms of cadmium sulfate. (ii) Zinc, copper, manganese, or nickel sulfate administered in equimolar amounts under the same regimen did not induce viral reactivation; however, zinc sulfate in molar ratios 25-fold greater than those of cadmium induced viral replication in 2 of 16 ganglia tested. (iii) Administration of zinc, nickel, or manganese prior to the cadmium sulfate reduced the incidence of ganglia containing infectious virus. (iv) Administration of cadmium daily during the first week after infection and at 2-day intervals to 13 days after infection resulted in the recovery from ganglia of infectious virus in titers 10- to 100-fold higher than those obtained from animals given saline. Moreover, infectious virus was recovered as late as 11 days after infection compared with 6 days in mice administered saline. (v) Administration of cadmium immediately after infection or repeatedly after establishment of latency did not exhaust the latent virus harbored by sensory neurons, inasmuch as the fraction of ganglia of mice administered cadmium and yielding infectious virus was similar to that observed in mice treated with saline. We conclude that induction of cadmium tolerance precludes reactivation of latent virus. If the induction of metallothionein genes was the sole factor required to cause reactivation of latent virus, it would have been expected that all metals which induce metallothioneins would also induce reactivation, which was not observed. The results therefore raise the possibility that in addition to inducing the metallothionein genes, cadmium inactivates the factors which maintain the virus in latent state.

Animals↗