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Spongiform change is a cardinal feature in transmissible spongiform encephalopathies, including Creutzfeldt-Jakob disease (CJD) and bovine spongiform encephalopathy (BSE). It is characterized by swelling of the neuronal processes and vacuolization of the neuropil, leading to increased intraneuronal water content. The present study examines, by gel electrophoresis and Western blotting, the expression levels of the water channels aquaporin 1 (AQP1) and aquaporin 4 (AQP4) in the frontal cortex (area 8) homogenates of sporadic CJD cases (six men, four women; seven cases with methionine/methionine at codon 129 and PrP type 1; two cases with valine/valine at codon 129 and PrP type 2, and one case methionine/valine at codon 129 and PrP type 1) compared with age-matched controls, and cases with Alzheimer's disease (AD, stage VI of Braak and Braak) and diffuse Lewy body disease (DLB). AQP1 and AQP4 protein levels were also studied in the cerebral cortex of BSE-infected bovine-PrP transgenic mice (BoPrP-Tg110 mice) examined at 60, 150, 210 and 270 days post-inoculation (dpi) compared with healthy brain-inoculated control mice. Quantitative densitometry of AQP bands normalized for beta-actin was analyzed using Statgraphics plus 5.0 software from ANOVA and LSD statistical tests. Significant increased expression levels of AQP1 (as revealed with two different antibodies) and AQP4 were seen in CJD, but not in advanced AD and DLB cases when compared with controls. Immunohistochemistry revealed that AQP1 and AQP4 were expressed in astrocytes in diseased cases. No modifications in the expression levels of AQP1 and AQP4 were observed in BSE-infected bovine-PrP transgenic mice at 60, 150 and 210 dpi. However, a significant increase in the expression levels of AQP1 and AQP4 was found in mice at 270 dpi, the time corresponding with the appearance of PrP(res) immunoreactivity in Western blots and typical spongiform lesions in the brain. Together, these findings show increased expression of water channels in the brain in human and animal prion diseases. These modifications may have implications in the regulation of water transport in astrocytes and may account for an imbalance in water and ion homeostasis in prion diseases.

This report describes the incidence, location and histopathological and immunohistochemical features of 30 canine meningiomas, of which 22 were intracranial, three were retrobulbar and five were located in the spinal canal. Nine types of meningioma were diagnosed: transitional (9), meningothelial (5), psammomatous (3), anaplastic (3), fibroblastic (2), angioblastic (2), papillary (2), microcystic (1) and meningiomas arising from the optic nerve (3). One of the optic nerve tumours had a granular cell component. All tumours were examined immunohistochemically with antibodies against vimentin, S100, neuron-specific enolase (NSE), cytokeratin (CK) and glial fibrillary acidic protein (GFAP). Vimentin was demonstrated in all tumours, and concentric whorls of cells showed more intense labelling than did bundles of fibroblastic cells. S100 labelling was detected in all tumours except a single angioblastic meningioma. The intensity of labelling for S100 was lower than that for vimentin, and bundles of fibroblastic cells showed particularly strong positivity. NSE labelling was highly variable, but most tumours displayed moderate positivity. CK expression was observed in five of the 30 meningiomas, and was stronger in areas of microcystic differentiation. Most of the tumours were GFAP-negative, but two fibroblastic meningiomas were strongly positive.

Scrapie is a prion disease in small ruminants that manifests itself with neurological clinical signs amongst which are ataxia and tremors. These signs can be explained partially by an imbalance in central inhibitory innervation. The study of the brain's inhibitory neuronal GABAergic populations and of their extracellular matrix has been used to define, in part, the pathogenesis of human prion diseases and scrapie models in rodents. The brain's distribution of neuronal GABAergic subpopulations has been monitored carefully using, as markers, antibodies against the calcium binding proteins parvalbumin and calbindin D-28K. The distribution of this perineuronal net marker was evaluated by means of affinity histochemistry with W. floribunda agglutinin. These techniques were performed on the brains of nine scrapie-positive sheep and on four infection-free sheep. These animals had undergone previously a clinical follow-up as well as a lesion profile and an immunohistochemical profile of the scrapie-associated prion protein deposition in the brain. The study of calcium-binding proteins revealed an alteration of the parvalbumin positive GABAergic neuronal subpopulation. In scrapie-positive cases, a reduction in stained neuronal perykaria was observed, along with a marked reduction of neurite labelling. This finding was noticeable in regions such as the neocortex, particularly the motor frontal cortex, and was concomitant with a moderate PrPsc deposition and a mild degree of lesion. No changes were observed in the extracellular matrix study. The results of the present study provide a partial explanation for the mechanisms of scrapie clinical signs due to a disturbance of the parvalbumin-positive inhibitory neuronal population.

An immunohistochemical and histochemical study was carried out on the brains of nine cases of BSE-diagnosed cattle as part of the surveillance plan in Catalonia, Spain. The animals had no clinical symptoms reported and were thus at early stages of the disease. The first part of the study consisted of a characterization of PrP(BSE) deposits throughout the encephalon. The behaviour of the different immuno-labelling patterns was analysed and tropism of some patterns towards certain brain areas was described. This tropism is principally directed to the brain stem region; however, an association of the stellate pattern was found with areas where PrP(BSE) is deposited less abundantly, such as the cerebral cortex. Secondly, distinct pathogenesis mechanisms that take place in the early stages of BSE, which would include these cases were investigated. This study describes the glial response to the presence of PrP(BSE) (using antibodies against astrocytic glial fibrillary acidic protein and lectin from Griffonia simplicifolia to identify microglia), the presence of mild oxidative stress phenomena (antibodies against metallothioneins I and II and against nitrated aminoacidic residues: nitrotyrosine), the apparent absence of apoptotic cellular death (cleaved caspase 3) and the preservation of synaptic proteins synaptophysin and small synaptosome-associated 25 kDa protein immuno-labelling. Finally, no alteration of the extra-cellular matrix was detected with the use of Wisteria floribunda agglutinin, a marker for perineuronal nets.

A 7-month-old, male European cat was examined because of weakness and inappetence. The cat was dehydrated, polypnoeic and severely weak. Severe, generalised muscle atrophy was present. Spinal reflexes were all decreased to absent. Blood analysis and urinalysis showed several abnormalities, including intermittent hyperoxaluria. The L-gliceric acid concentration was remarkably increased. Electrodiagnostic tests of the peripheral nervous system were abnormal. At necropsy, generalised muscle atrophy was observed. Microscopically, both kidneys showed intraluminal birefringent oxalate crystals. Motor neuron degeneration and accumulation of neurofilaments were observed in the axons of the spinal motor neurons.

A meningioma with a significant component of granular cells is described in the left ocular orbit of a 5-year-old male Golden retriever dog that presented with exophthalmos. The neoplastic mass surrounded the optic nerve. Microscopically, the tumour was characterized by nests of large, round to polygonal cells, variable in size, with eccentric nuclei and abundant eosinophilic cytoplasm, containing PAS-positive granules. In focal areas, cells were smaller and occasionally formed whorl-like structures. Immunohistochemical analysis revealed that neoplastic cells reacted positively for vimentin and, with less intensity, for neuron specific enolase and S-100, whereas they were negative for glial fibrillary acidic protein and cytokeratins. Metastatic growths, formed by similar cells, were seen in the lung and heart.

Neuronal intranuclear inclusion disease (NIID) is reported in a 16-year-old Pure Spanish breed female horse suffering from progressive ataxia and motor deficiencies. The neuropathological study revealed NIIs throughout the central nervous system, although mainly in the brain stem and spinal cord. This distribution did not correlate with neuron loss, which was marked in the hippocampus and moderate in the neocortex, particularly in the occipital cortex. As in humans, NIIs in the horse were hyaline autofluorescent inclusions composed of non-membrane-bound aggregates of filaments and fine granules. NIIs were stained with anti-ubiquitin and anti-clusterin antibodies. In addition, NIIs were stained with antibodies raised against subunits of the 19S and PA28, but not of the 20S, components of the proteasome. These observations indicate similarities between NIID in humans and horses, and suggest that clusterin and abnormal ubiquitin-proteasomal expression participate in NII formation.

Inflammatory myopathies (IMs) occur relatively frequently in dogs, and, with the exception of masticatory muscle myositis (MMM), have not been characterized. This study analyzed the distribution and types of cellular infiltrates in 21 cases of generalized IM, 3 cases of focal IM (MMM), and 1 case with features of both generalized and focal IM, using a panel of monoclonal antibodies to cell surface markers. In generalized IM, mononuclear cells showed an endomysial and perimysial distribution with invasion of non-necrotic fibers similar to human IM. T lymphocytes with T-cell receptor (TCR)alphabeta predominated. Distinct differences were seen in MMM including prominent B-cell infiltration, dendritic cells and macrophages in greater numbers than T cells, and numerous T cells with TCRgammadelta. Thus, generalized IM and MMM appear to be distinct diseases with different mechanisms. Canine generalized IM may be an important animal model for human IM.

The sigma-1 (sigma(1)) receptors can bind different psychotropic drugs and have been implicated in schizophrenia, depression and dementia. The cloning of the sigma(1)-receptor has allowed to obtain specific antibodies and, in a recent immunohistochemical study, we demonstrated that, in addition to neurons, the sigma(1)-receptor is located in oligodendrocytes [Brain Res. 961 (2003) 92.]. In the present study using in vivo and in vitro techniques, we demonstrate the localization of the sigma(1)-receptor in Schwann cells. Double immunofluorescence studies showed that sigma(1)-receptor co-localized with S100 protein, a specific marker of Schwann cells, in both rat sciatic nerve Schwann cells and Schwann cells in cultures. The sigma(1)-receptor immunoreactivity was seen in the cytoplasm and paranodal region formed by these cells, but not in myelin itself. The presence of sigma(1)-receptor in oligodendrocytes and Schwann cells is discussed on the basis on recent findings involving this receptor in lipid metabolism, compartmentalization and transport to the plasma membrane, thus suggesting a role for sigma(1)-receptor signaling in myelination.

A neuropathological study of Holstein-Friesian calves with spinal muscular atrophy (SMA) demonstrated decreased numbers of motor neurons in the brachial and lumbo-sacral regions of the spinal cord, together with swelling and accumulation of phosphorylated neurofilaments, and neuronophagia in most of the remaining motor neurons. The pyramidal tracts, motor cortex and thalamus were not affected. Synaptophysin immunohistochemistry revealed a marked reduction of punctate terminals but only around swollen neurones, suggesting loss of terminal afferents on motor neurons at advanced stages of the degenerative process. An immunohistochemical study of proteins linked with cell death and cell survival demonstrated reduced expression of Fas, Fas-L, Bcl-2 and Bax in swollen motor neurons. Punctate cytochrome C immunoreactivity, consistent with mitochondrial localization, was detected in the soma of normal motor neurons, but not in swollen motor neurons. Finally, no labelling of motor neurons with antibodies to cleaved (active) caspase-3 (17kD) was detected, suggesting a lack of involvement of the apoptotic pathways in motor neuron death. Taken together, the present findings point to necrosis as a major cause of motor neuron death in the advanced stages of SMA in Holstein-Friesian calves.

Disturbances of the gamma-aminobutyric acid (GABA) neurotransmitter system have been implicated in chronic degenerative neurological disease. Cognitive dysfunction and neuron loss are features in older dogs. GABAergic neurons also show immunoreactivity for specific calcium-binding proteins. Immunohistochemistry was used to study the neuronal expression of calbindin D-28k and parvalbumin in different areas of the brain in 13 dogs, aged between 2 and 13.5 years. Calbindin expression was found only in the cerebellum. There were significant differences in the quantity and distribution of neurons expressing these proteins between geriatric and adult brains. Parvalbumin- and calbindin-expressing neurons are relatively sensitive to degeneration in the cerebellum of older dogs. Parvalbumin labelling was associated with dystrophic structures that are commonly associated with ageing., (Copyright 2002 Elsevier Science Ltd.)

Reduced expression of synaptophysin p38, synaptic-associated protein of molecular weight 25,000 (SNAP-25), syntaxin-1, synapsin-1, and alpha- and beta-synuclein, matching the distribution of spongiform degeneration, was found in the neurological phase of scrapie-infected mice. In addition, synaptophysin and SNAP-25 were accumulated in isolated neurons, mainly in the thalamus, midbrain and pons, and granular deposits of alpha- and beta-synuclein were present in the neuropil of the same areas. No modifications in the steady state levels of Bcl-2, Bax, Fas and Fas ligand were observed following infection. Yet antibodies against the c-Jun N-terminal peptide, which cross-react with products emerging after caspase-mediate proteolysis, recognize coarse granular deposits in the cytoplasm of reactive microglia. In situ end-labeling of nuclear DNA fragmentation showed positive nuclei with extreme chromatin condensation in the thalamus, pons, hippocampus and, in particular, the granular layer of the cerebellum. More importantly, expression of cleaved caspase-3, a major executioner of apoptosis, was seen in a few cells in the same regions, thus indicating that cell death by apoptosis in scrapie-infected mice is associated with caspase-3 activation. The present findings support the concept that synaptic pathology is a major substrate of neurological impairment and that caspase-3 activation may play a pivotal role in apoptosis in experimental scrapie. However, there is no correlation between decreased synaptic protein expression and caspase-3-associated apoptosis, which suggests that in addition to abnormal prion protein deposition, there may be other factors that distinctively influence synaptic vulnerability and cell death in murine scrapie.

Dystrophic axons in a 2-year-old male Rottweiler with neuroaxonal dystrophy have shown synaptophysin, synapsin-I, synaptosomal-associated protein of 25 kDa (SNAP-25), Rab 3a, and alpha-synuclein immunoreactivity. Similar findings have been observed in isolated dystrophic axons in the nuclei gracillis and cunneatus in five dogs aged between 14 and 18 years. Abnormal expression of integral synaptic vesicle, synaptic vesicle-associated presynaptic plasma membrane and cytosolic proteins, which participate in the trafficking, docking and fusion of the synaptic vesicle to the plasma membrane, suggest severe disruption of axonal transport in dystrophic axons in canine neuroaxonal dystrophy.

Electrophysiologic assessment of the blink reflex test and the muscle-evoked potentials evoked by stimulation of the facial nerve were performed in 15 healthy adult Beagles before and after supraorbital (trigeminal) and facial anesthetic nerve blocks performed by lidocaine injections. Unilateral electrical stimulation of the supraorbital nerve elicited 2 ipsilateral (R1 and R2) and a contralateral (Rc) reflex muscle potential in orbicularis oculi muscles. Electrical stimulation of the facial nerve elicited 2 muscle potentials (a direct response [D] and a reflex faciofacial response [RF]) in the ipsilateral orbicularis oculi muscle. Anesthetic block of the left supraorbital nerve resulted in bilateral lack of responses upon left supraorbital nerve stimulation, but normal responses in right and left orbicularis oculi muscles upon right supraorbital stimulation. Right facial anesthetic block produced lack of responses in the right orbicularis oculi muscle regardless the side of supraorbital nerve stimulation. Results of this study demonstrate that the blink reflex can be electrically elicited and assessed in dogs. Reference values for the blink reflex responses and for the muscle potentials evoked by direct facial nerve stimulation in dogs are provided. The potential usefulness of the electrically elicited blink reflex test in the diagnosis of peripheral facial and trigeminal dysfunction in dogs was demonstrated.

An eight-year-old, male Siberian husky cross was referred with a history of an acute onset of pelvic-limb ataxia and paraparesis. Radiography and subsequent myelography of the spine revealed an extradural compression of the spinal cord at the level of the 13th thoracic (T13) to first lumbar (L1) vertebrae. Hemilaminectomy resulted in the successful removal of an extradural cystic lesion. The morphological diagnosis based on histopathology was a synovial cyst with chondromatosis. There were no postoperative complications, and the dog's condition improved markedly. At two years postoperatively, the animal remains normal on both physical and neurological examination. To the authors' knowledge, this article is the first report of an intraspinal synovial cyst in a dog.

Neuronal DNA fragmentation, as revealed with the method of in situ end-labeling of nuclear DNA fragmentation (TUNEL), has been reported in both the canine and human brains in normal ageing, and in some human age-related neurodegenerative diseases. These results have suggested that apoptosis plays an important role in age-related neuronal loss. It is not clear, however, whether the TUNEL method is highly specific for apoptosis, as DNA fragmentation also occurs in the late stages o necrosis. In this study we have examined 27 dogs aged from 8 to 18 years, to investigate the occurrence of nuclear DNA fragmentation. An autolysis index based on current histological criteria was assigned to each animal to evaluate the effects of autolysis on nuclear DNA integrity. Our results have shown that neuronal nuclear DNA fragmentation is frequent in aged dogs, although it is not accompanied by apoptotic morphology. Yet, a positive relation between TUNEL labelling and the degree of tissue autolysis was observed. In contrast, no TUNEL labelling was detected in young control dogs despite autolysis indices being similar to those in aged dogs. Taken together, these results suggest that neuronal nuclear DNA fragmentation is an age-related phenomenon, not due to apoptosis, whenever other factors render neuronal DNA more susceptible to autolytic fragmentation. We confirm the effect of autolysis in a subpopulation of neurons in the aged canine brain, inducing nuclear DNA fragmentation.

Objective: To reassess reference values for the components of the electrically induced blink reflex, document reference values for facial motor nerve conduction velocity, and demonstrate usefulness of the blink reflex as a diagnostic tool in peripheral facial and trigeminal nerve dysfunction in horses., Animals: 10 healthy adult horses (8 males, 2 females) without neurologic abnormalities., Procedure: Blink reflex tests were performed by electrical stimulation of the supraorbital nerve and facial (auriculopalpebral) nerve. Reflex and direct muscle-evoked potentials of the orbicularis oculi muscles were recorded from concentric needle electrodes inserted bilaterally in these muscles. Supraorbital and auriculopalpebral nerve blocks were performed by lidocaine hydrochloride injections., Results: Supraorbital nerve stimulation elicited 2 or 3 ipsilateral and 1 contralateral reflex muscle potential in the orbicularis oculi muscles. Auriculopalpebral nerve stimulation elicited a direct and a reflex potential in the ipsilateral orbicularis oculi muscle. After left supraorbital nerve block, no responses could be elicited ipsilaterally or contralaterally upon stimulation of the blocked nerve, but bilateral responses were obtained upon stimulation of the right supraorbital nerve. After right auriculopalpebral nerve block, no responses were recorded from the right orbicularis oculi muscle upon stimulation of left or right supraorbital nerves., Conclusions and Clinical Relevance: Reference values for the components of the blink reflex and facial motor nerve conduction velocity will allow application of these tests to assist in the diagnosis of equine neurologic disorders involving the trigeminal and facial nerves, the brainstem, and the cranial end of the cervical segment of the spinal cord. This study reveals the usefulness of the blink reflex test in the diagnosis of peripheral trigeminal and facial nerve dysfunction in horses.

Neuronal vacuolation, involving the cerebellar roof nuclei, Purkinje cells, selected nuclei of the brain stem, thalamus, Clarke's column, anterior and posterior horns of the spinal cord, visceral autonomic ganglia and myenteric plexus, as well as axonal degeneration of the white matter of the brain stem, cerebellar pedunculi, dorsolateral columns of the spinal cord and ventral roots of the spinal cord, were observed in two young Rottweiler dogs which were clinically afflicted with hind limb weakness progressing to paraparesia, ataxia, intention tremor, and difficulty in swallowing and barking. The absence of modifications in Bcl-2 and Bax immunoreactivity, a lack of strong c-Jun/AP-1 (N) immunoreactivity in vacuolated cells, and the absence of DNA breaks, as seen with the method of in situ end-labeling of nuclear DNA fragmentation, all suggest that there is no involvement of the apoptotic pathway in vacuolated cells in this new neurodegenerative disorder.

A case of bilateral encephalomalacia in a pig related to latent Aujeszky's disease virus infection is reported. The pig was experimentally inoculated with the NIA-3 strain and survived the infection after showing intense central nervous system disease. Abnormal behaviour was observed up to the date of death. The pig was demonstrated to be latently infected with the virus by polymerase chain reaction (PCR). The main microscopic lesion was a bilateral encephalomalacia which involved structures related to the limbic system. A complete description of lesions observed and their relation to abnormalities shown by the pig are exposed.

The clinical and neuropathological findings of spinal muscular atrophy (SMA) in Holstein-Friesian calves are described in four females and one male from a dairy farm composed of 150 cows and 2 breeding bulls. Locomotion difficulties started at the age of 15 days, and progressed to paraparesis and tetraparesis in 2 weeks. Signs consistent with denervation were revealed with electromyography. The neuropathological examination showed degeneration and loss of motor neurons in the spinal cord, together with astrocytosis. Among the remaining motor neurons were ghost cells and neurons filled with accumulations of straight filaments measuring 10-12 nm in diameter, which were strongly immunoreactive with antibodies produced against phosphorylated neurofilaments. Degenerating cells in SMA did not stain with the method of in situ labelling of nuclear DNA fragmentation and did not show c-Jun immunoreactivity. This feature contrasts with the in situ labelling of DNA breaks of apoptotic cells and with the strong c-Jun immunoreactivity restricted to dying cells during the whole process of naturally occurring cell death in the developing central nervous system. These features suggest that cell death in SMA differs from programmed cell death during normal development, and that pathological cell death in SMA should not be considered as a mere persistence or reactivation of normally occurring developmental cell death.

A Pekingese dog with hemivertebrae, rib malformations and spinal cord dysraphism without spina bifida was presented. Two types of hemivertebrae were seen: bilateral and unilateral. Thoracic hemivertebrae were associated with fused ribs and rudimentary ribs. Spinal dysraphism consisted of polycavitary syringomyelia in the dorsal and lateral funiculi, hydromyelia and anomalies of the dorsal median septum and median fissure, associated to lumbar and sacral hemivertebrae. Cauda equina agenesia was also present. To conclude, the dog showed two malformations from different embryonic origins. Vertebral and rib malformations are of mesodermic origin and spinal dysraphism is of ectodermic origin. A possible common mechanism responsible for both anomalies is discussed.

Masticatory muscle myositis (MMM) is presumed to be an immunologically mediated canine myopathy but is of unknown origin. Severe atrophy and degeneration of masticatory muscle fibres, infiltration of eosinophilic granulocytes, and proliferation of the fibrous interstitial tissue are the hallmarks of MMM. Transforming growth factor-beta (TGF-beta) is a multifunctional regulatory peptide controlling myogenesis, inflammation and tissue repair. We investigated immunocytochemically the expression of TGF-beta 1 and latent transforming growth factor-beta binding protein (LTBP), a TGF-beta modulator protein, in cases of MMM. The study demonstrated the presence of TGF-beta and LTBP in muscle fibres. infiltrating leucocytes and extracellular matrix in MMM, and suggested that TGF-beta and LTBP play a role in muscle tissue repair, inflammation and fibrogenesis in MMM.

Intraneuronal vacuoles have been observed in the motor trigeminal nucleus of the medulla oblongata of two dogs which showed neurological deficits. Its significance and possible relation with the same lesions observed in other animal species are discussed.

Two cases of naturally occurring fatal disease in eagles (a booted eagle and a buzzard) are reported. Both eagles showed anorexia, weight loss, weakness, and inability to fly. Microscopically, stained liver sections showed wide non-zonal coagulation necrosis and eosinophilic intranuclear inclusion bodies in hepatocytes adjacent to the edges of necrotic regions. Ultrastructural studies of hepatocytes revealed multiple enveloped viral particles in the cytoplasm, focal paracrystalline arrays of virions within the nuclei, and some budding particles bound by a membrane, located in an evagination of nuclear membrane. The size and morphology of all of these particles were consistent with herpesvirus. To our knowledge, this is the first report of naturally occurring field cases of herpesvirus hepatitis in eagles (Accipitridae).

Degeneration of the central white matter is described in old dogs. The presence of ubiquitin-immunoreactive free granules and intracytoplasmic globules in glial cells and macrophages, together with galacerebroside-immunoreactive precipitates and lipofusion storage, point to the likelihood of a primary myelin degeneration with deposits of non-degraded ubiquitin-protein conjugates and complex galactolipids.

We present a case of a young dog exhibiting internal hydrocephalus, associated with parasitic granulomas within the ventricular system, inflammatory changes in the periventricular brain tissue and stenosis of the mesencephalic aqueduct. Reference is made to possible causes of these lesions in animals and man.

Immunohistological (S-100, cIg) and enzyme histochemical (ANAE/ANBE, beta-glu, ATPase, AcP) investigations were carried out to identify lymphocyte and reticular cell subpopulations "in situ", in pig lymphoid tissue (lymph node, spleen, and thymus) of a 6 months old group, and a 6-9 days old one. By means of immunohistological techniques, in the 6 month old pigs we could detect S-100 protein (PAP), chiefly in T-areas lymphocytes, but we also found some S-100 positive lymphocytes in spleen follicles. Also S-100 protein were detected at Follicular Dendritic Cells (FDC) in lymph node and spleen; and Reticular Fibroblastic Cells (RFC) only in the first one. Finally, S-100 were noted in Hassall corpuscles (thymus), nervous fibres, and endothelial cells too. Using PAP (IgG, IgM) and IPI (IgA) techniques we could detect lymphocyte cytoplasmatic surface immunoglobulins (cIg) in lymphocytes, lymphoblastoid and plasmacytoid cells in nearly all tissue compartments. By means of histochemical techniques we could identify T-area lymphocytes ANAE/ANBE and beta-glu positives (cytoplasmatic spots) and B-area lymphocytes ATPase positive; macrophages, and polymorphonuclear eosinophiles PHNE being ANAE/ANBE and beta-glu positives (diffuse cytoplasmic stain); and Hassall corpuscles ANAE/ANBE and AcP positives. Concerning to reticular cells, we found FDC and RFC in lymphoid follicles, and Interdigitating Reticular Cells (IDC) in lymphoid diffuse tissue, with enzyme activity (all the enzymes studied) in nearly all the cases. In piglets, the immunohistological and histochemical pattern was nearly the same.