Neuronal Connections between the Auricular Skin and the Sympathetic Pre- and Postganglionic Neurons of the Dog as Studied by Using Pseudorabies Virus

Pseudorabies virus (PrV) as a neuronal tracer was Pseudorabies virus (PrV ) as a neuronal tracer was microinjected into the concave surface of the puppy's left pinna to establish the morphological basis of somato- visceral linkage. The virus infected neurons were detected by FITC conjugated with polyclonal swine anti-PrV serum. Labelled neurons were localized in: (1) the trigeminal, geniculate and superior vagal ganglia; ( 2) the subnucleus caudalis of the spinal trigeminal nucleus; (3) the intermediolateral column (IML) of the thoracolumbar segments and (4) the sympathetic chain ganglia. Present results suggest that when injected into the peripheral nerves, PrV was retrogradely transported to the nerve cell bodies located in the respective sensory ganglia. From the first order sensory neurons, the virus would self-replicate and was transported trans- synaptically via the brainstem nuclei and IML to reach the neurons in the sympathetic ganglia

Microglial Distribution and Apoptosis in Fetal Rat Brain

By histochemical and immunocytochemical techniques, this study aimed to determine the possible involvement of apoptosis in regulating the microglial distribution in fetal rat brain. While microglial cells were labeled with the isolectin Griffonia simplicifolia (GSA I-B4), apoptotic cells were detected by using terminal transferase-mediated dUTP nick end- labeling (TUNEL). TUNEL-labeled cells occurred mainly in the dorsal midline along its rostral-caudal axis of the brain where lectin-labeled microglia were also observed. Occasional TUNEL-labeled cells were observed in the intermediate zone lateral to the striatum (IZS) where lectin- labeled microglia were common from embryonic day 16 ( E16) onwards. Some of lectin-labeled microglia showing different morphological forms ingested TUNEL-labeled bodies. In contrast, lectin-labeled microglia showing signs of apoptosis appeared to be lacking: These results clearly demonstrated that lectin-labeled microglia were distributed in areas with and without the occurrence of a large concentration of TUNEL-labeled cells. Our studies suggest that microglia in fetal rat brain will undergo differentiation and activation rather than apoptotic death to govern their population. (C) 2002 Elsevier Science B.V. All rights reserved

Melatonin Restores the Cytochrome Oxidase Reactivity in the Nodose Ganglia of Acute Hypoxic Rats

This study aimed to elucidate whether melatonin would exert beneficial effects on the neuronal functions of the nodose ganglion (NG) following acute hypoxic insult. The cytochrome oxidase (COX) and the nicotinamine adenine dinucleotide phosphate diaphorase (NADPH-d) histochemistry along with the nitric oxide synthase (NOS) immunofluorescence were used to examine the metabolic stage and nitric oxide production in nodose neurons respectively. Adult rats were injected intraperitoneally with melatonin at 5 or 100 mg/kg. Hypoxia was achieved by placing the rats into an altitude chamber ( PO2 = 43 torr) for 4 hr. The results show that in normal untreated rats, nearly all and about 43% of the NG neurons displayed COX and NOS/NADPH-d reactivities with various staining intensities respectively. However, COX reactivity was drastically decreased while NOS/ NADPH-d reactivity was significantly upregulated following hypoxia treatment. In melatonin pretreated rats, the hypoxia-induced reduction of COX reactivity was obviously prevented and the augmentation of NOS/NADPH-d reactivity was successfully suppressed. The deficit in the metabolic stage and the over-activation of NOS would contribute to the generation of oxidative stress. By effectively preventing the metabolic disruption, melatonin may have potential utility in therapeutic treatment of neuronal dysfunctions where oxidative stress is a participant

Evidence of neuroanatomical connection between the superior cervical ganglion and hypoglossal nerve in the hamster as revealed by tract-tracing and degeneration methods

Previous studies have shown the existence of a sympathetic component in some cranial nerves including the hypoglossal nerve. In this study, the horseradish peroxidase (HRP) tract-tracing retrograde technique and experimental degeneration method were used to elucidate the possible neuroanatomical relationship between the superior cervical ganglion (SCG) and the hypoglossal nerve of hamsters. About 10% of the SCG principal neurons were HRP positive following the tracer application to the trunk of hypoglossal nerve. Most of the HRP-labelled neurons were multipolar and were randomly distributed in the ganglion. When HRP was injected into the medial branch of the hypoglossal nerve, some of the SCG neurons were labelled, but they were not detected when HRP was injected into the lateral branch. The present findings suggest that postganglionic sympathetic fibres from the SCG may travel along the hypoglossal nerve trunk via its medial branch to terminate in visceral targets such as the intralingual glands. By electron microscopy, the HRP reaction product was localised in the neuronal somata and numerous unmyelinated fibres in the SCG. In addition, HRP-labelled axon profiles considered to be the collateral branches of the principal neurons contained numerous clear round and a few dense core vesicles. Besides the above, some HRP-labelled small myelinated fibres, considered to be visceral afferents, were also present. Results of experimental degeneration following the severance of the hypoglossal nerve showed the presence of degenerating neuronal elements both in the hypoglossal nucleus and the SCG. This confirms that the hypoglossal nerve contains sympathetic component from the SCG which may be involved in regulation of the autonomic function of the tongue

Ultrastructural localisation of NADPH-d/nNOS expression in the superior cervical ganglion of the hamster

This study examined NADPH-d and nNOS expression in the SCG of hamsters. By light microscopy, numerous NADPH-d/NOS positive processes were widely distributed in the ganglion. Ultrastructurally, the NADPH-d reaction product was associated with the membranous organelles of neuronal soma, dendrites, myelinated fibres, small granular cells, and axon profiles bearing agranular vesicles. The NOS immunoreaction product, on the other hand, was localised in the cytoplasm of principal neurons and dendrites. Some of the NADPH-d/NOS labelled processes formed junctional contacts including synapses or zonulae adherentia. Compared with the neurons, the nonneuronal cells in the ganglion, namely, macrophages, satellite cells and endothelial cells were labelled by NADPH-d but devoid of nNOS immunoreaction product. The results suggest that the NADPH-d/NOS positive fibres in the SCG originate not only from the projecting fibres of the lateral horns of thoracic spinal cord, but also from the principal neurons and small granular cells; some may represent visceral afferent fibres. Electron microscopic morphometry has shown that about 67% of the principal neurons contain NADPH-d reaction product, and that the majority were small to medium sized neurons based on cross-sectional areas in image analysis. On the basis of the present morphological study, it is concluded NO is produced by some local neurons and possibly some nonneuronal cells in the SCG as well as some fibres of extrinsic origin. In this connection, NO may serve either as a neurotransmitter or neuromodulator

Misdiagnosis as steatohepatitis in a family with mild glycogen storage disease type 1a

The manifestations of glycogen storage disease type 1a (GSD 1a) are usually so prominent in childhood that it is readily diagnosed by pediatricians. However, a mild form of the disease may only become apparent during adolescence or adulthood. We observed a brother and sister with subtle manifestations of the disease, which was discovered after the brother's son was diagnosed with typical GSD 1a. The adult siblings never suffered from hypoglycemia, had normal fasting blood glucose and liver transaminases at the time of diagnosis, and were taller than average for Chinese. Their only notable disease manifestations were recurrent gouty arthritis associated with hyperuricemia and hyperlipidemia during adolescence. When diagnosed, the brother had multiple benign and malignant hepatic tumors, and died of fulminant metastatic hepatocellular carcinoma 6 months after liver transplantation. p.M121V/p.R83H and p.M121V/p.M121V genotypic constellations of the G6PC gene were identified in this family. Both siblings were homozygous for the newly identified p.M121V mutation. The infant had compound heterozygous mutations, p.R83H and p.M121V. We recommend that mild GSD should be considered in the adolescents with unexplained hyperuricemia and hyperlipidemia, despite the presence of normal blood glucose levels. This report also reminds us that hepatocellular carcinoma could develop even in very mild GSD 1a patients