Degenerative axonopathy associated with copper deficiency in pigs / Axonopatia degenerativa associada com deficiência de cobre em suínos

The epidemiological, clinic and morphological (pathological and ultrastructural) aspects of four outbreaks of copper deficiency affecting 21- to 90-day-old pigs in the Northeast region of Brazil are reported. Clinical signs began with paraparesis and ataxia and progressed to flaccid or spastic paralysis of the pelvic and thoracic limbs, followed by sternal and/or lateral recumbence. In addition, some animals showed dog-sitting position and intention tremors. The clinical manifestation period was 5-20 days. Significant gross lesions were not observed; however, microscopically, symmetrical degeneration of the white matter with ballooned myelin sheaths containing occasional macrophages was observed, mainly in the spinal cord. Two pigs presented with necrosis ad loss of Purkinje cells and ectopic Purkinje cells in the granular layer and cerebellar white matter. A ultrastructural analysis showed different degrees of damage of myelinated axons in the spinal segments, including an absence of the axoplasm structures with only axonal residues remaining. The myelin sheaths were degenerated and often collapsed into the space previously occupied by the axon. These results suggest that myelin degeneration is secondary to the axonal lesion. Finally, the concentration of copper in the liver was determined using atomic absorption spectrophotometry and was found to be low (ranging from 2.2 to 10.8 ppm). In conclusion, in the Brazilian semiarid region, Cu deficiency occurs in 21 to 90-day-old pigs that ingested different types of waste in their food.(AU)

São relatados os achados epidemiológicos, clínicos e morfológicos (patológicos e ultraestruturais) de quatro surtos de deficiência de cobre em suínos afetados entre 21 e 90 dias de idade na região Nordeste do Brasil. Os sinais clínicos iniciaram com paraparesia e ataxia, que progrediu a paralisia flácida ou espástica dos membros pélvicos e torácicos, seguido de decúbito esternal e/ou lateral. Além disso, alguns animais apresentaram posição de cão sentado e tremores de intenção. O período de manifestação clínica variou de 5-20 dias. Não foram observadas lesões macroscópicas significativas; no entanto, microscopicamente, foi observada degeneração simétrica da substância branca com fragmentação das bainhas de mielina, contendo ocasionais macrófagos, principalmente na medula espinal. Dois suínos apresentaram necrose e perda de células de Purkinje e células de Purkinje ectópicos na camada granular da substância branca cerebelar. A análise ultraestrutural mostrou diferentes graus de lesões em axônios mielinizados em segmentos da medula espinhal, incluindo o desaparecimento de estruturas do axoplasma, restando apenas restos axonais. A bainha de mielina encontrava-se degenerada e muitas vezes, colapsada dentro do espaço previamente ocupado pelo axônio. Esses resultados sugerem que a degeneração da mielina é secundária à lesão axonal. Finalmente, a concentração do cobre no fígado foi determinada usando espectrometria de absorção atômica e revelou baixos valores (variando de 2,2-10,8ppm). Conclui-se que na região semiárida do Brasil ocorre deficiência de cobre em suínos de 21 a 90 dias de idade alimentados com diferentes tipos de resíduos.(AU)

Caracterização do papel da célula de Schwann no processo de neurodegeneração do neurônio motor na esclerose lateral amiotrófica no modelo animal transgênico e no nervo periférico de pacientes: estudo in vitro / Characterization of Schwann cell role in the motor neuron neurodegeneration process in amyotrophic lateral sclerosis in the transgenic animal model and in the peripheral nerve of patients: in vitro study

A Esclerose Lateral Amiotrófica (ELA) é uma doença neurodegenerativa progressiva de evolução rápida, caracterizada pela perda seletiva dos neurônios motores (NM) superiores e inferiores. Recentemente, as células gliais centrais (astrócito, microglia e oligodendrócito) mostraram-se tóxicas aos NM, porém os detalhes moleculares não estão completamente elucidados. Em relação às células gliais periféricas, alterações eletrofisiológicas no nervo ciático do modelo animal da ELA na idade pré-sintomática foram reportadas pelo nosso grupo e os achados de denervação precoce tanto no modelo animal quanto em pacientes sugerem a participação das células de Schwann (CS) na morte neuronal retrógrada na ELA, teoria conhecida como dying back. Nesse contexto, as CS mostraram-se capazes de induzir a retração axonal e a denervação das junções neuromusculares, eventos precoces na doença, ocorrendo possivelmente na fase présintomática. O objetivo deste trabalho foi verificar a influência das CS do modelo experimental na fase pré-sintomática e do paciente com evolução recente da forma esporádica da ELA, na sobrevida e no tamanho dos prolongamentos dos NM in vitro e entender a natureza molecular do fenômeno. Culturas de CS altamente purificadas foram obtidas a partir do nervo ciático do camundongo modelo animal e do nervo periférico de pacientes com ELA. Os NM da medula espinal de camundongos neonatos foram co-cultivados com as CS. A neurodegeneração foi avaliada pela presença do marcador Fluoro-Jade C (FJC). Os NM também foram tratados com o meio condicionado das culturas de CS do modelo animal ou dos pacientes com ELA. Os motoneurônios tiveram os seus prolongamentos contados e a morte neuronal foi identificada pela presença do FJC. Diversos fatores neurotróficos foram quantificados no meio condicionado das culturas de CS pela técnica de ELISA. A reação em cadeia da polimerase quantitativa (do inglês, quantitative polymerase chain reaction - qPCR) foi realizada para...

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterized by the selective loss of upper and lower motor neurons (MN). Recently, central glia (astrocytes, microglias and olygodendrocytes) were toxic to the MN, but the molecular aspects have not fully described. In relation to the peripheral glia, electrophysiological changes in the sciatic nerve of ALS animal model in the presymptomatic stage have been reported by our group and early denervation findings in both animal models and patients suggests the participation of Schwann cells (SC) in the retrograde neuronal death of ALS , theory known as dying back. In this context, the SC proved to be able to induce axonal retraction and denervation of the neuromuscular junctions, early events in the disease, possibly occurring in the pre-symptomatic phase. The aim of this thesis was to investigate the influence of SC of pre-symptomatic experimental model and from patient with recent evolution of ALS sporadic form, in the survival and axonal length of MN in vitro and understand the molecular nature of the phenomenon. Highly purified SC cultures were obtained from the sciatic nerve of the animal model and from ALS patient's peripheral nerve. MN from the newborn mouse spinal cord were co-cultured with SC and the neurodegeneration was assessed by the presence of the marker Fluoro-Jade C (FJC). MN were also treated with conditioned medium from cultures of SC of the animal model or ALS patients. MN had their neuronal length measured and neuronal degeneration was identified by the presence of the FJC. Several neurotrophic factors were measured in conditioned medium of mice and ALS patient's SC cultures by ELISA. The chain reaction quantitative polymerase (qPCR) was performed to detect changes in the SC and peripheral nerve that could be related with dysfunction in the functional unit SC/MN. The MN co-cultured with ALS SC showed a greater number of neurodegenerative...

Structural analysis of a ligatured rat sciatic nerve in the ex vivo state using synchrotron small-angle X-ray scattering (SAXS)

BACKGROUND: To understand the fundamentals of neural tissue injury, experiments on the nano-structured nerve system of animals are essential. This study was designed to reveal the nanostructure changes of an isolated ligatured rat sciatic nerve using the synchrotron small-angle X-ray scattering (SAXS) technique. METHODS: Male Sprague-Dawley rats (weighing approximately 250 grams) were used in this study. The SAXS patterns of 1 week after ligatured nerves (N = 5) and the normal sciatic nerves (N = 5) for the control were acquired after extracted approximately 15 mm before the experiment. Experiments were conducted at the 4C1 beam line at the Pohang Accelerator Laboratory in Korea. The exposure time was 60 sec, and 8 to 12 images per sample were acquired in 0.5 mm intervals, including the regions above, around and below the ligatured position. RESULTS: The periodic peaks of the myelin sheath and the interfibrillar space of collagen completely disappeared at the ligatured position. Farther from the ligatured point, weak and quite different SAXS patterns were observed for the myelin sheath and interfibrillar space. However, the collagen fiber peaks appeared at all positions, although they were weaker near the ligatured position. CONCLUSIONS: The ligature treatment totally destroyed the myelin sheath and interfibrillar space of collagen. In addition, retrograde degeneration developed 2 mm above the ligatured site. The myelin sheath and interfibrillar space of collagen were damaged 6 mm below the ligatured site. However, the collagen fiber structure was not significantly affected by the ligature, indicating a much different structural organization.

Diabetes-induced prefrontal nissl substance deficit and the effects of neem-bitter leaf extract treatment / Diabetes inducida por déficit prefrontal de sustancia de nissl y el efecto del tratamiento con extracto de hoja de neem amargo

Cognitive dysfunction is reportedly associated with poorly-managed diabetes mellitus. In this study, we report the effect of oral treatment with combined leaf extract (CLE) of neem and bitter leaf on the prefrontal cortex of diabetic Wistar rats. Adult male Wistar rats were randomized to one of the following groups: control, diabetic (STZ-induced), STZ + CLE, STZ + metformin and CLE only. At euthanasia, paraffin sections of the prefrontal cortex were stained with cresyl fast violet; while malondialdehyde (MDA) and glutathione peroxidase (GPx) were assayed in prefrontal homogenates. Oral CLE produced normoglycemia in the treated hyperglycaemic rats. Besides, Nissl-stained prefrontal sections showed no morphologic deficits in all the groups except the untreated diabetic rats. In the latter, there was weak Nissl staining, while prefrontal MDA was significantly high at euthanasia, compared with the control and CLE-treated rats (P<0.05). This study showed that untreated diabetes mellitus is associated with prefrontal Nissl body deficit and oxidative stress in Wistar rats. The absence of these deficits in CLE-treated rats suggests a neuroprotective effect of the extract in streptozotocin-induced diabetic rats. This may improve the cognitive function of the prefrontal cortex in diabetes mellitus.

La disfunción cognitiva es presuntamente asociada con un mal manejo de la diabetes mellitus. En este estudio, se presenta el efecto del tratamiento oral combinado con extracto de hoja (CLE) de hoja de neem amarga sobre la corteza prefrontal de ratas Wistar con diabetes. Las ratas Wistar adultas fueron asignadas al azar a uno de los siguientes grupos: control, diabetes (STZ inducida), STZ + CLE, STZ + metformina y CLE. Después de la eutanasia, los cortes de parafina de la corteza prefrontal se tiñeron con violeta de cresil rápido, mientras que el malondialdehído (MDA) y la glutatión peroxidasa (GPx) fueron analizadas en homogenizados prefrontales. El CLE produce normoglucemia en las ratas hiperglucémicas tratadas. Además, las secciones prefrontales teñidas para Nissl no muestran ningún déficit morfológico en todos los grupos excepto en las ratas diabéticas sin tratamiento. En este último caso, hubo una tinción de Nissl débil, mientras que la MDA prefrontal fue significativamente más alta en comparación con los grupos de ratas control y las tratadas con CLE (p <0,05). Este estudio mostró que la diabetes mellitus no tratada se asocia con déficit prefrontal de cuerpos de Nissl y estrés oxidativo en ratas Wistar. La ausencia de estos déficits en las ratas tratadas CLE, sugiere un efecto neuroprotector del extracto en ratas diabéticas inducidas por estreptozotocina. Esto puede mejorar la función cognitiva de la corteza prefrontal en la diabetes mellitus.

Number changes and axonal sprouting of neuropeptide Y interneurons in the hippocampus of pilocarpine-induced rats / 中南大学学报(医学版)

OBJECTIVE@#To investigate the role of neuropeptide Y(NPY) positive interneurons in the generation and compensation of temporal lobe epilepsy.@*METHODS@#Pilocarpine-induced rat model was founded. Immunohistochemistry was used to observe the number changes and axonal sprouting of NPY interneurons at different time points in the hippocampus of rats.@*RESULTS@#After lithium-chloride and pilocarpine administration, 92.9% rats were induced status epilepticus (SE) successfully, and the mortality rate was 19.2%. In the experimental group, the number of NPY positive neurons decreased in the hilus of the hippocampus, and was least on 7 d after the SE (P0.05) except the loss of them in CA3 area on 7 d after the SE (P>0.05). Increased NPY positive fibers could be seen in the molecular layer of the dentate gyrus on 30 d after the SE.@*CONCLUSION@#NPY interneurons have different sensitivities to the injuries induced by seizures at different time points and domains. Loss of NPY interneurons plays an important role in the generation of temporal lobe epilepsy, while axonal sprouting of them may play a significant role in the compensation of temporal lobe epilepsy.

Ganglion Cell Death in Rat Retinaby Persistent Intraocular Pressure Elevation

Glaucoma is characterized by loss of retinal ganglion cells (RGCs) and their axons. Retrograde axoplasmic transport blockade and excitotoxicity were proposed to be a major cause of RGC apoptosis. We conducted this study to characterize the episcleral vessel cauterization glaucoma model in the rat with respect to decreased retrograde axoplasmic flow and subsequent apoptotic RGC death. After episcleral vessels were cauterized in Sprague-Dawley rats, Fluorogold was injected into their superior colliculi by stereotactic method. Retrograde axoplasmic flow and TUNEL-stained apoptotic dead cells were observed microscopically. Elevated intraocular pressure was maintained for up to 6 weeks during follow-up. Retrograde axoplasmic flow to the rat retina was significantly decreased. Apoptotic RGC was selectively TUNELstained in the retina, especially at the ganglion cell layers. We concluded that elevated intraocular pressure caused apoptotic RGC death through retrograde axoplasmic flow blockage. Further studies will elucidate the neuroprotection strategies in glaucoma patients.

Striatal injection of 6-hydroxydopamine induces retrograde degeneration and glial activation in the nigrostriatal pathway

PURPOSE: The effect of a highly selective 6-hydroxydopamine (6-OHDA)-induced lesion of the nigrostriatal system on the astroglial and microglial activation was analysed in adult Wistar rats after an unilateral striatal injection of the neurotoxin. METHODS: Male rats received an unilateral stereotaxical injection of the 6-OHDA in the left side of the neostriatum and were sacrificed 22 days later. Control animals received the injection of the solvent. The rotational behaviour was registered by a rotometer just before the sacrifice. Immunohistochemistry was employed for visualization of the tyrosine hydroxylase (TH) positive dopamine cells, glial fibrillary acidic protein (GFAP) immunolabeled astrocytes and OX42 immunoreactive microglia. Stereological method employing the optical disector was used to estimate the degree of the changes. RESULTS: The striatal injection of the 6-OHDA induced a massive disappearance (32 percent of control) of the TH immunoreactive terminals in a defined area within the striatum surrounding the injection site. A disappearance (54 percent of control) of dopamine cell bodies was observed in a small region of the ipsilateral pars compacta of the substantia nigra (SNc). The GFAP and OX42immunohistochemistry revealed astroglial and microglial reactions (increases in the number and size of the cells) in the ipsilateral neostriatum and SNc of the 6-OHDA injected rats. CONCLUSIONS: The striatal injection of 6-OHDA leads to retrograde degeneration as well as astroglial and microglial activation in the nigrostriatal dopamine pathway. Modulation of activated glial cells may be related to wound repair and to the trophic paracrine response in the lesioned nigrostriatal dopamine system.

Experimental Study of Changes of beta-catenin, PCNA, Substance P after Peripheral Nerve Compression in Rat / 체질인류학회지

The ultrastructural changes of sciatic nerve and immunohistochemical changes of beta-catenin, PCNA, substance P were studied at the proximal segment of rat sciatic nerve after compression injury. We used 90 Sprague Dawley rats and the sciatic nerve compressed using silicon tube. We divided experimental groups which were the compression group for 1 hour (1C), for 2 hours (2C), and for 3 hours (3C), the release group for 1 day (1C1R) and 3 days (1C3R) after the compression for 1 hour, the release group for 1 day (2C1R) and 3 days (2C3R) after the compression for 2 hours, the release group for 1 day (3C1R) and 3 days (3C3R) after the compression for 3 hours. The rats were sacrified and took the sciatic nerve specimen. The specimens were investigated under the light microscope after hematoxylin & eosin, toluidin blue, and immunohistochemical stainings. In the H & E finding, the axon of the 1C disappeared, but recovered at the 1C3R. The part of nerve fibers at the 2C were swollen, but began to be partially recovered at 2C3R. Most nerve fibers were enlarged at the 3C, but markedly decreased at the 3C1R. The beta-catenin reaction disappeared at the 1C, but almost recovered at the 1C3R. This reaction of the 2C disappeared in the large fibers, but began to be recovered in the small fibers at the 2C1R. This reaction of the 3C disappeared in the large fibers, but began to be recovered at the 3C1R and 3C3R. The PCNA reaction prominently appeared at the 1C3R and 2C3R, the more prominent reaction at the 3C1R, and markedly increased reaction at the 3C3R. The substance P reaction of the 1C1R was mild positive, and the 2C1R and 3C1R were strong positive. In the toluidin blue staining, the myelin sheaths near the perineurium began to be thickened at the 1C, but almost recovered at the 1C3R. Many myelin sheaths became to be very thickened at the 2C and 3C, but almost recovered at the 2C3R and 3C3R. In the electron microscopic findings, the myelin sheaths of the 1C underwent the demyelination with the separated lamellae and the increase microtubules. At the 1C3R, the axolemma was attached on the myelin sheath and the axon was recovered. the myelin sheaths of the 2C underwent the demyelination with the separated axolemma. At the 2C1R, the myelin sheath was recovered by the developing Schwann cells, many intraaxonal mitochondria of demyelinated nerve fibers. At the 2C3R, the myelin sheath tended to be recovered by the increased rough endoplasmic reticulum and mitochondria of Schwann cells, many intraaxonal mitochondria of demyelinated nerve fibers. The myelin sheaths of the 3C began to be underwent severe demyelination from the middle portion of the sheath and the vacuolization of intraaxonal mitochondria. At the 3C1R, the myelin sheaths were recovered and contained many extended microtubules, mitochondria, and small granules. At the 3C3R, severe demyelinated nerve fibers were recovered by increasing microtubules. The proximal retrograde degeneration of sciatic nerve by the acute compression appeared the loss of the axons and the swelling of nerve fibers. The beta-catenin reaction was disappeared by the compression, but recovered by releasing. This reaction may be played a important role of the recover of demyelination. The PCNA reaction of Schwann cells was increased by the nerve compression. In the substance P finding, the pain after the compression appeared at the 1 day after releasing. Electron microscopic changes after sciatic nerve compression were the demyelination, the separated lamellae and the increase of intraaxonal microtubules. After releasing, the nerve fibers were recovered by developing Schwann cell, the intraaxonal mitochondria, and the transported granules through extending microtubules.

The Behavioral Changes and the Patterns of Dopamine NeuronalDegeneration after Intrastriatal 6-hydroxydopamine Injection in Rat

BACKGROUND: The terminal destruction of the striatal dopaminergic axon can produce the retrograde degeneration of nigral dopaminergic neurons. An analyses of the postsynaptic dopamine D1 & D2 receptors and the DOPAC/DA level, revealed that this model mimics the early course of Parkinson's disease in humans. We evaluated the time course of the retrograde dopaminergic neuronal degeneration and the pattern of dopaminergic neuronal loss in the substantia nigra after various doses of 6-hydroxydopamine (6-OHDA) injections in the striatum of rats. METHODS: Different doses of 6- OHDA (0.0, 1.25, 2.5, 5, 10 ug/ul in 3.5 ul of saline) were unilaterally injected into the right striatum of rats using a stereotaxic frame. Structural and functional deficits were quantified and compared using apomorphine-induced rotations and tyrosine hydroxylase-immunoreactive (TH-IR) cell numbers in the substantia nigra pars compacta (SNpc) at 3, 6, 9 weeks after lesioning. RESULTS: Striatal 6-OHDA lesions produced dose-dependent decreases in TH-IR cell numbers in SNpc at 3 weeks (-3.8%, 17.9%, 41.2%, 58.5%, 69.9% cell loss compared with the contralesional side respectively), where the ventrolateral portion of the SNpc were more affected. As time progressed, nigral cell loss was significantly increased in all dosage groups and the lesion extended to the medial side of the SNpc and the ventral tegmental area. Apomorphine-induced rotations did not correlate well with nigral TH-IR cell loss. CONCLUSIONS: Intrastriatal injections of 6-OHDA, results in time-dependent and dose-dependent progressive degeneration of nigral dopaminergic neurons. We conclude that this rat model can be useful for the evaluation of further neuroprotective and neurotrophic therapies.

Electrodiagnostic Study of Retrograde Degeneration in Carpal Tunnel Syndrome

OBJECTIVE: We investigated the useful electrodiagnostic indicators and the extent of retrograde degeneration (RD) in carpal tunnel syndrome (CTS). METHOD: We measured median mixed nerve action potentials (MMNAP) in 26 CTS and 37 normal hands by recording at the elbow and stimulating 0, 3, 6 and 9 cm proximal to the distal wrist crease. The 3 MMNAP parameters such as amplitude, latency and conduction velocity were compared between CTS and control group. The most useful indicator was compared between subgroups of CTS (mild and severe) and control group. RESULTS: The amplitudes of all MMNAPs in CTS group, except stimulating 9 cm proximal to the wrist (MA9), were significantly smaller than those in control group (p<0.05). MA9 in severe CTS subgroup, not mild subgroup, was significantly smaller than that in control group (p<0.05). CTS and control group were not significantly different in the MMNAP latencies, except stimulating 9 cm proximal to the wrist (p<0.05), and in the MMNAP conduction velocity, except stimulating in 0 cm to 3 cm segment proximal to the wrist. CONCLUSION: The amplitude of MMNAP in forearm can be the most useful indicator of RD in CTS, and the conduction velocity, a less useful indicator. We believe that RD progresses as the severity of CTS increases, and dose beyond 9 cm proximal to the distal wrist crease.

Median Nerve Conduction Velocity of Forearm Segment in Carpal Tunnel Syndrome

OBJECTIVE: To find out the incidence of reduced median conduction velocity of forearm (MNCV-F) in carpal tunnel syndrome (CTS) and to compare clinical and electrophysiologic characteristics of CTS with reduced MNCV-F and to observe the changes of reduced MNCV-F after carpal tunnel release. METHOD: One hundred and fifty nine hands with CTS are divided into two groups; MNCV-F of 50 m/sec and above as group I and that of below 50 m/sec as group II. For the electrophysiologic comparison, median sensorimotor distal latency, peak-to-peak amplitudes and abnormal spontaneous activity of abductor pollicis brevis were observed and for clinical comparison, sensorimotor symptoms, Phalen and Tinel sign were observed. Twenty four hands which had successful carpal tunnel release were examined for the changes of MNCV-F. RESULTS: The hands with reduced MNCV-F were 29 among 159 hands. Sensorimotor distal latency were significantly prolonged and sensorimotor amplitudes also significantly reduced in group II. Sensory change and Phalen signs were more frequently observed in group II. MNCV-F in group I had not changed after carpal tunnel release, but MNCV-F in group II was improved significantly. The changes MNCV-F in group II were much delayed than the improvement of parameters of distal conduction studies. CONCLUSION: The incidence of reduced MNCV-F in CTS was 18.24%. Patients with reduced MNCV-F had more severe CTS both electrophysiologically and clinically. Reduced MNCV-F had improved significantly, but there was significant time gap between the electrophysiologic improvements of distal and proximal portions of nerve. This findings may suggest that retrograde degeneration may play a partial role in reduced forearm motor nerve conduction velocity of the median nerve in CTS.

Retrograde Changes of Median-Nerve Fibers in Carpal Tunnel Syndrome

Slowing in forearm median nerve conduction in patients with carpal tunnel syndrome(CTS) has been described. But the cause of slowing is still unclear whether it is related to a technical artifact on electrodiagnostic appr oach or pathophysiologic changes in the proximal segment of median nerve. To investigate the possible retrograde degeneration of median nerve in the forearm segment(wrist to elbow) in patients with known carpal tunnel syndrome, the median nerve conduction studies were performed in 23 normal persons as control and 25 patients with carpal tunnel syndrome. To evaluate the median nerve conductions in the forearm, the recording bar-electrode were placed at the volar aspect of the wrist and stimulating electrodes were applied at the elbow area. The mixed nerve action potentials and conduction velocities were measured. The median mixed nerve action potential(FNAP) amplitudes recorded at the wrist and motor nerve conduction velocity(MMCV) in patients with carpal tunnel syndrome patients were significantly reduced compared to those of control group(p<0.05). However, the median mixed nerve conduction velocity(FNCV) was not reduced significantly. The median mixed nerve action potential amplitudes demonstrated positive correlation with the decrease of motor and sensory action potential amplitudes and velocities. This result suggests that the retrograde degeneration progresses as the carpal tunnel syndrome progresses and the retrograde degeneration may play a major role in reduced motor nerve conduction velocity of the median nerve in the forearm. We propose that FNAP amplitude and MMCV might be used to evaluate the severity of retrograde degeneration in patients with carpal tunnel syndrome.

Topographical representation of the teeth of the upper jaw in the trigeminal ganglion in cat

Twenty one cats were sacrificed. Three animals were used as a control group. The remaining animals were classified into three groups. The incisors of the upper jaw were extracted from the first group: three animals from their right side and three from their left side. The canines were removed from the second group while the premolars and molars were removed from the last group following the ame numbers and sides as the first group. After 3 weeks, the corresponding trigeminal ganglia were dissected, processed and stained with ordinary haematoxylin and eosin and with silver stain. The topographical representation of the teeth in the trigeminal ganglion was studied. The nerve cells supplying the incisors were found randomly distributed throughout the ganglion but more located in its center. On the other hand, the neurons supplying the canines were found more distributed in the posterior part of the ganglion. while the neurons supplying the premolars and molars were situated anteriorly

Experimental Optic Nerve Atrophy in Rabbits

After general anesthesia with intra-venous pentothal sodium, half of the optic nerve was sectioned on both sides with special care to preserve vessels of the optic nerve. To observe retrograde degeneration of the optic nerve, the animals were sacrifised 1, 2, 3, 4, and 5 weeks after nene section. Eye ball and optic nerve was removed and fixed in 10% formalin solution. Eye baIl and optic nerve was cut and stained with Hematoxylin Eosin and Luxol Fast Blue stain for light microscopic examination. Until 2 weeks. no significant pathologic changes were observed. Specimens 3 weeks after optic nerve section showed decreased retinal ganglion cell numbers and gliosis and myelin loss in optic nerve and these changes were intensified on 4th and 5th weeks specimens. So, I observed the followings: 1. Retrograde degeneration of the optic nerve occurred simultaneously through out the length of the nerve fibers instead progressively from the cut end toward the ganglion cell. 2. The retrograde degeneration of the optic nerve started 3 weeks after section.