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Transient expression of selected catecholaminergic traits in cranial sensory and dorsal root ganglia of the embryonic rat.

We describe the transient expression of catecholaminergic traits in cranial sensory and dorsal root ganglia of the embryonic rat in vivo. Isolated cells expressing tyrosine hydroxylase (T-OH) immunoreactivity were initially detected in trigeminal (V) ganglion anlages as early as gestational Day 10.5 (E10.5; 18-22 somites). Neurofilament (NF) protein was also evident in V at these early stages. By E11.5 (27-30 somites) clusters of T-OH-positive cells were visible in V. Many of these cells were bipolar; others sent processes into the primitive brainstem. In addition, cells expressing T-OH were apparent in primordia of sensory ganglia serving the glossopharyngeal (IX) and vagal (X) cranial nerves. By this stage (E11.5) all cranial sensory ganglia were rich in NF protein, but immunoreactivity was confined to cellular processes rather than perikarya. By E12 (35-37 somites), only a few, faintly positive T-OH-containing cells were evident in V. However, DBH- and T-OH-positive cells were visible within the more caudal nodose and petrosal ganglia. Furthermore, isolated bipolar cells expressing T-OH were detected in rostral dorsal root ganglia at this stage. Catecholamine fluorescence could not be detected in any sensory ganglia even after maternal treatment with inhibitors of monoamine oxidase. Catecholaminergic cells were not seen at any stage in anlages of the acousticovestibular nucleus. Immunoreactive T-OH was undetectable in all ganglia by E13.5 (46-48 somites). These findings highlight the fact that transient expression of the catecholamine phenotype during development is a widespread phenomenon, evident in a variety of cell types of diverse embryonic origin.

Age Factors↗

The dynamics of dopamine metabolism in the rat superior cervical, coeliac and mesenteric ganglia.

Dopamine (DA) metabolism was compared in rat superior cervical ganglion, coeliac ganglion, mesenteric ganglion and adrenal medulla. Substantial amounts of DA, 3-4 dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were found in all the above structures. The proportion of DA metabolites over total adrenergic compounds increased from the superior cervical (22 +/- 2.2%) to the mesenteric ganglia (37 +/- 1.4%) and was much higher in ganglia (30 +/- 1.6%) than in adrenal medulla (1.1 +/- 0.3%). The turnover rates of DOPAC and HVA were calculated in sympathetic ganglia after pargyline (75 mg/kg i.p.) or probenecid (200-500 mg/kg i.p.). After pargyline, the DOPAC levels decreased faster than HVA levels in all ganglia. The corresponding half-lives and calculated turnover rates were: about 4 and 10 min and 100 and 40 pmol/mg protein per h for DOPAC and HVA respectively. No differences were observed between the three ganglia. After probenecid, DOPAC accumulated in all the ganglia in a dose-dependent way; HVA accumulated in the superior cervical and coeliac ganglia but not in the mesenteric ganglion. As in central areas, the turnover rates of DOPAC and HVA calculated on the basis of the greatest accumulation of acidic levels after probenecid were much smaller than those obtained after pargyline. Probenecid increased DOPAC levels in adrenal medulla, but the concomitant changes in DA and epinephrine (E) amounts suggest that probenecid was able to enhance adrenomedullary activity.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗

Herpes simplex virus type-2 infection by a footpad route results in neuronal death in mouse spinal ganglia.

We have examined the effects of herpes simplex virus type 2 (HSV-2) infection on neuron numbers in mouse dorsal root ganglia (DRG) following unilateral hind footpad inoculation. One month following HSV-2 strain MS inoculation, tissue sections of decalcified spine containing the paired 4th and 5th lumbar DRGs were stained with cresyl violet. Neuronal numbers, somal areas and ganglion volumes were determined for ganglia ipsilateral and contralateral to both HSV-2 and medium inoculations. One month following HSV-2 infection, 47-88% of neurons disappeared in the ipsilateral ganglia. The somal areas of the remaining neurons in these ganglia fell within the range of the uninfected population. Ganglionic shrinkage did not occur as a result of HSV-2 infection; neurons were replaced by large numbers of inflammatory cells. Neuron numbers in the contralateral control ganglia of the HSV-2 inoculated mice appeared slightly decreased. Mice inoculated with medium contained similar numbers of neurons in ipsilateral and contralateral ganglia. These results show that, in addition to other previously described host alterations, infection with HSV-2 strain MS results in neuronal death in the affected host ganglia. This is the first in vivo quantitative documentation of neuronal death induced by herpes simplex virus infection.

Animals↗

Immunohistochemical studies of substance P, cholecystokinin-octapeptide and somatostatin in dorsal root ganglia of the rat.

Immunofluorescence histochemistry was used to determine the distribution of substance P, somatostatin and cholecystokinin-octapeptide-immunoreactive perikarya in C6, T6, T10, L2 and S1 dorsal root ganglia of rat. Five different categories of immunoreactive primary afferent neurons were distinguished on the basis of cell size, cytology and peptide immunoreactivities. The population of small cells (diameter less than 20 microns) included three groups which were identified as containing somatostatin, substance P, or substance P + cholecystokinin-octapeptide. Two groups of cells were identified in an intermediate size range (diameter 21-43 microns) as containing cholecystokinin-octapeptide or cholecystokinin-octapeptide + substance P. These categories may reflect four distinct populations of primary afferent neurons. The relative abundance of dorsal root ganglion cells containing substance P, cholecystokinin-octapeptide or somatostatin immunoreactivities was significantly different within segmental levels. More neurons were immunoreactive for cholecystokinin-octapeptide than substance P in ganglia C6, T6 and T10. Somatostatin-containing cells were fewest in number regardless of level. The number of immunoreactive cells also varied among spinal ganglia. L2 contained the greatest number of immunoreactive cells; S1 contained the fewest. These studies are relevant to our understanding of dorsal root ganglia in two ways. Firstly, the data document significant variation in the distribution of peptide-containing neurons among spinal ganglia associated with various cord levels. The variation in peptide-containing cell populations among spinal ganglia may reflect differences in populations of modality-specific primary afferent fibers as well as in populations of somatic and visceral primary afferent fibers at each level. Furthermore, the data indicate that the relative abundance of a population of peptide-containing primary afferent neurons cannot be extrapolated from the examination of spinal ganglia from a single level. Secondly, substance P and cholecystokinin-octapeptide did not co-exist in all spinal ganglion cells as previously reported. In conjunction with immunostaining characteristics and cell size, the differential distribution of the two peptides defined four cell types, raising the possibility that each cell type may mediate a different modality.

Animals↗

Peptide-immunoreactive neurons and nerve fibres in lumbosacral sympathetic ganglia: selective elimination of a pathway-specific expression of immunoreactivities following sciatic nerve resection in kittens.

The distributions of peptide-immunoreactive nerve fibres and cell bodies in lumbosacral paravertebral sympathetic ganglia of young cats were analysed with antibodies to calcitonin gene-related peptide, enkephalin, neurotensin, somatostatin, substance P, galanin, neuropeptide Y and vasoactive intestinal polypeptide. Fairly dense networks of nerve fibres showing enkephalin-, neurotensin-, somatostatin- or substance P-like immunoreactivity were observed in the ganglia. Double-staining experiments revealed that enkephalin- and somatostatin-immunoreactive nerve fibres preferentially surrounded calcitonin gene-related peptide- and/or vasoactive intestinal polypeptide-immunoreactive cell bodies. Neurotensin- and substance P-immunoreactive nerve fibres were mainly associated with neurons showing neuropeptide Y and/or galanin-like immunoreactivity. Occasional nerves containing calcitonin gene-related peptide-, galanin-, neuropeptide Y- or vasoactive intestinal polypeptide-like immunoreactivity were observed. These fibres did not seem to have any direct regional distribution within the ganglia. In kittens surviving for three months after early postnatal sciatic nerve resection, no calcitonin gene-related peptide-immunoreactive cell bodies could be detected in ganglia ipsilateral to the operation. In contrast, vasoactive intestinal polypeptide-like immunoreactivity, which partly co-exists with calcitonin gene-related peptide, was observed to the same extent as in control ganglia. Furthermore, almost all of the somatostatin-immunoreactive varicose nerve fibres had disappeared, whereas a fairly dense network of calcitonin gene-related peptide-immunoreactive nerve fibres could be observed. This change was paralleled by an increased content of nerve fibres that were immunoreactive to antibodies against the growth-associated protein GAP-43 (also known as B-50). The present findings suggest that experimental perturbations where postganglionic neurons are separated from their target areas by axotomy, not only induce differential changes in neurotransmitter expression in the principal ganglion cells, but also in preganglionic sympathetic neurons projecting to the ganglia. One possible explanation for the occurrence of an axotomy-induced network of calcitonin gene-related peptide-immunoreactive nerve fibres, is that extrinsic sensory nerve fibres grow into the ganglia after the sciatic nerve lesion. Thus, these findings seem to suggest one additional possibility with regard to the question of a possible interaction between sympathetic and sensory neurons after peripheral nerve injury.

Animals↗

Development and distribution of serotonin in the central nervous system of Manduca sexta during embryogenesis. II. The ventral ganglia.

The distribution of serotonin (5-HT) immunoreactive cells and their projections was mapped in the ganglia of the ventral nerve cord of the tobacco hornworm, Manduca sexta, during embryonic development, using an antiserum to 5-HT. Immunoreactive cells were first seen at 60% development. By 75% of embryonic development, a total of 94 immunoreactive cells were found in the ventral ganglia, including the suboesophageal ganglion. This number decreased to 80 neurons by 100% of development. About 50% of these cells were arranged in the abdominal ganglia and the rest were located in both the suboesophageal and thoracic ganglia. The suboesophageal ganglion exhibited immunoreactive segmental interneurons in areas corresponding to the mandibular, maxillary and labial neuromeres. Two pairs of immunoreactive interneurons were also observed to occur bilaterally in each of the thoracic and abdominal ganglia, with the exception of the prothoracic ganglion. This ganglion contained three pairs of bilaterally arranged immunoreactive neurons as early as 60% of embryonic development. Serotonin immunoreactivity was also found in a number of efferent neurons in the mandibular and labial neuromeres of the suboesophageal ganglion and in the prothoracic, mesothoracic and posterior abdominal ganglia. The occurrence of 5-HT in these efferent neurons suggests an involvement of serotonin in fore- and hindgut function via its effect on the visceral muscles. Immunoreactive lateral longitudinal fibers extended along the entire length of the ventral nerve cord together with dense segmental arborizations. The latter had regressed by the time the embryo was fully developed. This regression of the arborizations in the ganglia at the end of embryonic development indicates that a reorganization of 5-HT innervation occurs to support new larval functions. The time of appearance of 5-HT immunoreactive cells and fibers suggests that serotonin may play a role in the development of the ventral nerve cord.

Animals↗

Considerations on the phrenic ganglia.

UNLABELLED: The phrenic ganglion is described as a small ganglion located at the junction of the right phrenic nerve and branches of the celiac plexus, on the diaphragm. The descriptions of this ganglion are few and incomplete and justify the present study which has been performed macroscopically by dissection and microscopically using silver stained (the method of Bielschowsky) drawn pieces. Dissections of 10 human adult specimens showed one or more ganglia located at the level of the terminal division of the right diaphragmatic artery; these ganglia belong to a trunk linking the right phrenic nerve and the celiac ganglion. In some specimens that nervous trunk was replaced by a ganglionated plexus. That trunk--the diaphragmatic nerve--attaches to a distinctive projection of the celiac ganglion; it may be double, but there is one ganglionated component. No left phrenic ganglia were detected. The macroscopic phrenic ganglia are distributed as follows: the lower to the adrenal gland and the upper to the diaphragm. Microscopically, the ganglia had autonomic characteristics; intrinsic microganglia were also detected within the diaphragmatic nerve. Moreover, periadventitial nervous cells were detected on the right inferior phrenic artery. IN CONCLUSION: (1) the phrenic ganglia seem to be constant structures on the right-hand side; (2) their number is variable--it may be the result of individual fragmentation or coalescence during development; (3) these ganglia may be either adrenal vasomotor or diaphragmatic vasomotor, and functionally belong to the celiac plexus; (4) intrinsic neural and periarterial locations are also possible for macroscopically undetectable populations of autonomic nervous cells.

Adult↗

ASIC3-immunoreactive neurons in the rat vagal and glossopharyngeal sensory ganglia.

ASIC3-immunoreactivity (ir) was examined in the rat vagal and glossopharyngeal sensory ganglia. In the jugular, petrosal and nodose ganglia, 24.8%, 30.8% and 20.6% of sensory neurons, respectively, were immunoreactive for ASIC3. These neurons were observed throughout the ganglia. A double immunofluorescence method demonstrated that many ASIC3-immunoreactive (ir) neurons co-expressed calcitonin gene-related peptide (CGRP)- or vanilloid receptor subtype 1 (VRL-1)-ir in the jugular (CGRP, 77.8%; VRL-1, 28.0%) and petrosal ganglia (CGRP, 61.7%; VRL-1, 21.5%). In the nodose ganglion, however, such neurons were relatively rare (CGRP, 6.3%; VRL-1, 0.4%). ASIC3-ir neurons were mostly devoid of tyrosine hydroxylase in these ganglia. However, some ASIC3-ir neurons co-expressed calbindin D-28k in the petrosal (5.5%) and nodose ganglia (3.8%). These findings may suggest that ASIC3-containing neurons have a wide variety of sensory modalities in the vagal and glossopharyngeal sensory ganglia.

Acid Sensing Ion Channels↗

Role of basal ganglia-brainstem pathways in the control of motor behaviors.

Here we review a role of a basal ganglia-brainstem (BG-BS) system throughout the mesopontine tegmentum in the control of various types of behavioral expression. First the basal ganglia-brainstem system may contribute to an automatic control of movements, such as rhythmic limb movements and adjustment of postural muscle tone during locomotion, which occurs in conjunction with voluntary control processes. Second, the basal ganglia-brainstem system can be involved in the regulation of awake-sleep states. We further propose the possibility that the basal ganglia-brainstem system is responsible for the integration of volitionally-guided and emotionally-triggered expression of motor behaviors. It can be proposed that dysfunction of the basal ganglia-brainstem system together with that of cortico-basal ganglia loop underlies the pathogenesis of behavioral disturbances expressed in basal ganglia dysfunction.

Basal Ganglia↗

Information processing, dimensionality reduction and reinforcement learning in the basal ganglia.

Modeling of the basal ganglia has played a major role in our understanding of this elusive group of nuclei. Models of the basal ganglia have undergone evolutionary and revolutionary changes over the last 20 years, as new research in the fields of anatomy, physiology and biochemistry of these nuclei has yielded new information. Early models dealt with a single pathway through the nuclei and focused on the nature of the processing performed within it, convergence of information versus parallel processing of information. Later, the Albin-DeLong "box-and-arrow" model characterized the inter-nuclei interaction as multiple pathways while maintaining a simplistic scalar representation of the nuclei themselves. This model made a breakthrough by providing key insights into the behavior of these nuclei in hypo- and hyper-kinetic movement disorders. The next generation of models elaborated the intra-nuclei interactions and focused on the role of the basal ganglia in action selection and sequence generation which form the most current consensus regarding basal ganglia function in both normal and pathological conditions. However, new findings challenge these models and point to a different neural network approach to information processing in the basal ganglia. Here, we take an in-depth look at the reinforcement driven dimensionality reduction (RDDR) model which postulates that the basal ganglia compress cortical information according to a reinforcement signal using optimal extraction methods. The model provides new insights and experimental predictions on the computational capacity of the basal ganglia and their role in health and disease.

Animals↗

Laterality, somatotopy and reproducibility of the basal ganglia and motor cortex during motor tasks.

We investigated the basal ganglia, motor cortex area 4, and supplementary motor area (SMA) using functional magnetic resonance imaging (fMRI) and five motor tasks: switching between finger and toe movements, writing, finger tapping, pronation/supination, and saccadic eye movements. We found reliable activation in the caudate nucleus and putamen in single subjects without the need for inter-subject averaging. Percent signal changes in basal ganglia were smaller by a factor of three than those in SMA or motor cortex (1% vs. 2.5-3%). There was a definite foot-dorsal, hand-ventral basal ganglia somatotopy, similar to prior data from primates. Saccadic eye movements activated the caudate nucleus significantly more than the other tasks did. Unilateral movements produced bilateral activation in the striatum even when motor cortex activation was unilateral. Surprisingly, bilateral performance of the tasks led, on average, to consistently smaller basal ganglia activation than did unilateral performance (P<0.001), suggesting less inhibition of contralateral movements during bilateral tasks. Moreover, there was a striking dominance pattern in basal ganglia motor activation: the left basal ganglia were more active than the right for right handers, regardless of the hand used. This lateralization appears much stronger than that previously reported for motor cortex. Comparisons of inter-subject and intra-subject reproducibility indicated a much larger variability in basal ganglia and SMA compared to motor cortex, in spite of similar percent signal changes in the latter two structures.

Adult↗

Hypothalamic digoxin related membrane Na+-K+ ATPase inhibition and familial basal ganglia calcification.

The isoprenoid pathway produces three key metabolites-digoxin (membrane sodium-potassium ATPase inhibitor and regulator of intracellular calcium-magnesium ratios), dolichol (regulator of N-glycosylation of proteins) and ubiquinone (free radical scavenger). The pathway was assessed in a rare and specific type of familial basal ganglia calcification described. The family had a coexistence of basal ganglia calcification (six out of 10 cases), schizophrenia, Parkinson's disease, Alzheimer's disease, rheumatoid arthritis, systemic tumours and syndrome X and were all right hemispheric dominant. The isoprenoid pathway was also studied for comparison in right hemispheric dominant, bihemispheric dominant and left hemispheric dominant individuals. The isoprenoid pathway was upregulated with increased digoxin synthesis in familial basal ganglia calcification. Membrane sodium-potassium ATPase inhibition can lead on to increase in intracellular calcium and calcification of the basal ganglia. There was increase in tryptophan catabolites and a reduction in tyrosine catabolites. There was also an increase in dolichol and glycoconjugate levels with reduced lysosomal stability in these patients. The ubiquinone levels were low and free radical levels increased. The cholesterol-phospholipid ratio was increased and glycoconjugate level of the RBC membrane reduced in these group of patients. No significance difference was noted in family members with and without basal ganglia calcification. This findings were correlated with the pathogenesis of syndrome X, immune mediated diseases, degenerations, tumours and psychiatric disorders noted in the familial basal ganglia calcification described. The biochemical patterns obtained in familial basal ganglia calcification correlated with those in right hemispheric dominance.

Adult↗

Quantitation of changes in gene expression of norepinephrine biosynthetic enzymes in rat stellate ganglia induced by stress.

Enzymes involved in catecholamine synthesis are present in the highest concentration in the adrenal medulla, however they were found also in other, mainly nervous tissues. The aim of our study was to quantify the exact concentration of tyrosine hydroxylase (TH) and dopamine-ss-hydroxylase (DBH) mRNA in rat stellate ganglia under control conditions and at different intervals after exposure to immobilization stress (IMO). In rats immobilized once for 2h, we determined TH and DBH mRNA in different time intervals up to 22 h after the end of the stress stimulus. TH immunoreactive protein levels were also determined in stellate ganglia. TH and DBH mRNA levels were quantified by RT-competitive-PCR. In stellate ganglia, the concentration of TH mRNA was 17+/-1.6 amol/microg of total RNA, which is approximately 30-times lower than in the adrenal medulla. The concentration of DBH mRNA in the stellate ganglia was 2601+/-203 amol/microg of total RNA, which is the concentration similar to adrenal medulla, but is 150-times higher than concentration of TH mRNA in stellate ganglia. After a single 2-h immobilization the highest elevation of TH and DBH mRNA levels was measured 22 h after the termination of the stress stimulus. Repeated immobilization (7 days, 2h daily) did not produce further increase in TH and DBH mRNA levels compared to already elevated levels in adapted control group (immobilized for 6 days, 2h daily and decapitated 22 h later). Levels of TH protein were significantly changed only after the repeated immobilization. This study compared for the first time the precise amounts of TH and DBH mRNA in rat stellate ganglia under control conditions and after immobilization stress, and indicates large differences in their concentration. TH and DBH mRNA concentrations in stellate ganglia are markedly elevated for a prolonged period of time after termination of the stress stimuli.

Animals↗

Basal ganglia motor function in relation to Hallervorden-Spatz syndrome.

Hallervorden-Spatz syndrome (HSS) is a degenerative neurologic disorder associated with progressive rigidity, dystonia, impaired voluntary movement, dysarthria, and mental deterioration. Pathologically, there is iron deposition in the basal ganglia, with destruction of basal ganglia output neurons. Recent advances in the understanding of basal ganglia functional anatomy and physiology make it possible to hypothesize how specific neural mechanisms relate to specific clinical manifestations of HSS. Experimental lesions of the basal ganglia output nucleic cause involuntary muscle contractions, similar to contractions observed in dystonia. A model of selection and suppression of competing motor patterns by the basal ganglia is presented in relation to the manifestations of damage to basal ganglia output neurons. It is hypothesized that the dystonia and other motor abnormalities seen in HSS can be attributed to degeneration of basal ganglia output neurons.

Basal Ganglia↗

MR volumetric analysis of the human basal ganglia: normative data.

RATIONALE AND OBJECTIVES: The authors undertook this study to identify a precise, semiautomated, reproducible magnetic resonance (MR) imaging technique for measuring the basal ganglia, to establish normative volumetric data, and to verify the presence of previously reported asymmetries. MATERIALS AND METHODS: Twenty-eight healthy adults underwent cranial MR examination. The volumes of the various components of the basal ganglia were measured by means of a combination of thresholding and manual tracing techniques performed with specialized software. The validity of these measurements was assessed by fashioning, imaging, and measuring a practical basal ganglia phantom. Measurement accuracy was also established by means of inter- and intrarater reliability indexes. Normalized volumes were statistically analyzed with analysis of variance and paired t tests. RESULTS: The absolute values of the various components of the basal ganglia varied widely even though the volumes were normalized to differences in intracranial volume. The right caudate nucleus volume was significantly (P < .000001) larger than the left in both men and women and in both right-handed and non-right-handed subjects. This asymmetry led to an increase in the overall volume of the basal ganglia on the right. CONCLUSION: The authors have defined a precise, reproducible technique for measuring various components of the basal ganglia and have established normative data. The basal ganglia, similar to other brain structures, exhibit hemispheric lateralization.

Adult↗

Nicotinic acetylcholine receptors in autonomic ganglia.

Although alpha3beta4 subunit combination is clearly prevalent in the nAChRs of autonomic ganglia neurons, the ganglia are strikingly different in the ratio of neurons containing each particular nAChR subunit, as found with immunohistochemical methods and from the analysis of the effects of nAChR subunit-specific antibodies on the ACh-induced membrane currents. In particular, the number of neurons containing alpha3, alpha4, alpha5 or alpha7 subunits is by about three times higher in sympathetic ganglia than in parasympathetic ganglia. This difference may explain why the parasympathetic and sympathetic ganglia markedly differ in their pharmacology. Still, alpha7 subunit makes the highest contribution to ACh-induced membrane current. No correlation between the physiological functions of the ganglia and subunit composition of their nAChRs has been found as yet. High permeability for Ca2+ should permit the nAChRs with alpha7 subunits to influence a variety of Ca2+-dependent events in autonomic neurons. As found with biochemical methods and site-directed mutagenesis, the ACh binding site is formed in the alpha/beta subunits interface by multiple loops containing cysteine, tyrosine and tryptophan amino residues as important for ACh binding. Likewise, both alpha and beta subunits are important for the effects of blocking agents on nAChRs. As found by electrophysiological methods, each neuron of sympathetic and parasympathetic ganglia, as a rule, possesses nAChRs of two groups, "fast" and "slow", with the mean duration of the burst of single channel openings ranging approximately from 5 to 10 and from 25 to 45 ms, respectively. These groups of channels differ from each other with their pharmacology. The burst-like activity of autonomic nAChRs channels is possible only if the disulfide bonds are left intact, otherwise only single openings of the channel are observed. The ionic channel of a nAChRs pentamer is formed by M2 transmembrane segments arranging glutamate, serine, threonine, leucine, and valine rings critical for channel conductance and ionic selectivity. In particular, the mutations V251T and E237A, and insertion of proline or alanine, convert a cation-selective channel into an anion-selective one. The open-channel blockers bind to the nAChR channel at the level where the channel diameter is nearly 12 A, both for "fast" and "slow" channel groups.

Animals↗

Cadherin-1, -2 and -4 expression in the cranial ganglia and lateral line system of developing zebrafish.

Cadherins are cell adhesion molecules that play important roles in development of a variety of tissues and organs including the nervous system. In this study we analyzed expression patterns of three zebrafish classical (type I) cadherins (cadherin-1, -2, and -4) in the embryonic zebrafish cranial ganglia and lateral line system using in situ hybridization and immunohistochemical methods. All three cadherins exhibit distinct spatiotemporal patterns of expression during cranial ganglia and lateral line system development. cadherin-1 message was detected in the trigeminal and facial ganglia, in the lateral line ganglia, and in most of neuromasts in the lateral lines. Cadherin-2 mRNA and protein were expressed by the majority of the cranial ganglia and lateral line system. Both cadherins were found in embryos younger than 24 hours post fertilization as well as in 2-3-day old embryos and larvae. In contrast, cadherin-4 mRNA and protein expression was detected in embryos older than 30 hours post fertilization and limited to the trigeminal, statoacoustic, and vagal cranial ganglia, and the lateral line ganglia of older embryos and larvae.

Animals↗

Muscarinic inhibitory transmission in mammalian sympathetic ganglia mediated by increased potassium conductance.

Slow muscarinic inhibition may be a powerful influence on membrane properties in the peripheral and central nervous system. But the location of the muscarinic receptors in sympathetic ganglia, either on interneurones or on the postganglionic membrane, and the underlying mechanism of the inhibitory response, remains controversial. In mammalian sympathetic ganglia synaptic activation of muscarinic receptors located on inhibitory interneurones was thought to release catecholamines leading to a membrane hyperpolarization called the slow inhibitory postsynaptic potential, or s.-i.p.s.p.. However, the s.-i.p.s.p. in parasympathetic ganglia and in amphibian sympathetic ganglia is due to direct monosynaptic activation of muscarinic receptors, accompanied by an increased potassium conductance (but see ref. 11), and is not mediated by catecholamines. The situation is less clear in mammalian sympathetic ganglia and monosynaptic s.-i.p.s.ps observed in other ganglia could be exceptions to the hypothesis. We showed earlier that the s.-i.p.s.p. in rabbit superior cervical ganglia is not affected by catecholamine antagonists. We now show that the s.-i.p.s.p. in a mammalian sympathetic ganglion is due to the monosynaptic activation of muscarinic receptors, probably by an increase in potassium conductance.

Acetylcholine↗