[Prevalence of psychiatric disorders in prisoners with a short imprisonment: results from a prison in north Germany]. / Die Prävalenz psychischer Erkrankungen bei Gefängnisinsassen mit Kurzzeitstrafe.

OBJECTIVE: The aim of the study was to determine the prevalence of mental disorders among prisoners with a short prison term. METHODS: We investigated 102 participants with the Structured Clinical Interview for DSM Disorders (SCID I and II) and the Symptom Check List (SCL-90). RESULTS: We found a lifetime-prevalence of mental disorders (axis I) of 83 %. 80 % of the participants showed at least one personality disorder. CONCLUSIONS: These results indicate that short-term prisoners are a population which is highly troubled in a psychiatric sense and shows a need of treatment in prison.

Anti-AGEing defences against Alzheimer's disease.

Accumulation of insoluble protein deposits and their cross-linking by AGEs (advanced glycation end products) in the brain is a feature of aging and neurodegeneration, especially in AD (Alzheimer's disease). In AD, two types of fibrillar protein aggregates are present: extracellular deposits (plaques) consisting mainly of Abeta (beta-amyloid peptide), and intracellular deposits (tangles) composed predominantly of microtubule-associated protein tau. Both plaques and tangles are modified by AGEs, which occurs particularly at lysine and arginine residues. Interaction of a synthetic amyloid plaque (fibrillar Abeta) with microglia leads to a strong pro-inflammatory response, indicating that priming of immune cells with beta-amyloid potentiates their response to secondary stimuli such as AGE and cytokines such as interferon-gamma. Formation of hyperphosphorylated and cross-linked microtubule-associated protein tau aggregates, especially tau dimers as the first step in tangle formation, can be induced in vitro by the combination of okadaic acid, a PP2A phosphatase inhibitor, and methylglyoxal. These results suggest that excess production of reactive carbonyl compound ("carbonyl stress") and subsequent AGE formation can contribute to cross-linking of protein fibrils and to pathological pro-inflammatory signalling, which all contribute to pathological changes and dementia progression in AD. However, the human brain has developed the glyoxalase system, a most effective defence system to scavenge small dicarbonyl compounds such as glyoxal and methylglyoxal. Very importantly, this system needs GSH as a rate-limiting cofactor. Since GSH is limited under conditions of oxidative stress and inflammation, supplementation with antioxidants such as lipoic acid, vitamin E or flavonoids could indirectly strengthen the anti-glycation defence system in AD. In addition, synthetic carbonyl scavengers and anti-inflammatory drugs could also be valuable drugs for the "anti-glycation" treatment of AD.

Advanced glycation endproducts co-localize with inducible nitric oxide synthase in Alzheimer's disease.

Advanced glycation endproducts (AGEs), protein-bound oxidation products of sugars, have been shown to be involved in the pathophysiological processes of Alzheimer's disease (AD). AGEs induce the expression of various pro-inflammatory cytokines and the inducible nitric oxide synthase (iNOS) leading to a state of oxidative stress. AGE modification and resulting crosslinking of protein deposits such as amyloid plaques may contribute to the oxidative stress occurring in AD. The aim of this study was to immunohistochemically compare the localization of AGEs and beta-amyloid (Abeta) with iNOS in the temporal cortex (Area 22) of normal and AD brains. In aged normal individuals as well as early stage AD brains (i.e. no pathological findings in isocortical areas), a few astrocytes showed co-localization of AGE and iNOS in the upper neuronal layers, compared with no astrocytes detected in young controls. In late AD brains, there was a much denser accumulation of astrocytes co-localized with AGE and iNOS in the deeper and particularly upper neuronal layers. Also, numerous neurons with diffuse AGE but not iNOS reactivity and some AGE and iNOS-positive microglia were demonstrated, compared with only a few AGE-reactive neurons and no microglia in controls. Finally, astrocytes co-localized with AGE and iNOS as well as AGE and were found surrounding mature but not diffuse amyloid plaques in the AD brain. Our results show that AGE-positive astrocytes and microglia in the AD brain express iNOS and support the evidence of an AGE-induced oxidative stress occurring in the vicinity of the characteristic lesions of AD. Hence activation of microglia and astrocytes by AGEs with subsequent oxidative stress and cytokine release may be an important progression factor in AD.

Expression of endothelial and inducible NOS-isoforms is increased in Alzheimer's disease, in APP23 transgenic mice and after experimental brain lesion in rat: evidence for an induction by amyloid pathology.

The nitric oxide-synthesizing enzyme nitric oxide synthase (NOS) is present in the mammalian brain in three different isoforms, two constitutive enzymes (i.e., neuronal, nNOS, and endothelial eNOS) and one inducible enzyme (iNOS). All three isoforms are aberrantly expressed in Alzheimer's disease giving rise to elevated levels of nitric oxide apparently involved in the pathogenesis of this disease by various different mechanisms including oxidative stress and activation of intracellular signalling mechanisms. It still is a matter of debate, however, whether the abnormal expression of NOS isoforms has some primary importance in the pathogenetic chain and might thus be a potential therapeutic target or only reflects a secondary effect that occurs at more advanced stages of the disease process. To tackle this question, we analysed the expression of both eNOS and iNOS in patients with sporadic AD, in transgenic mice expressing human amyloid precursor protein (APP) with the Swedish double mutation under control of the Thy1 promotor (APP23 mice), and after electrolytic cortical lesion in rat, an experimental paradigm associated with elevated expression of APP. In all three conditions, an astrocytosis was induced accompanied by a strong increase of both iNOS and eNOS. Both NOS isoforms were frequently though not always colocalized. Thus, based on the expression pattern of NOS isoforms three types of astrocytes, expressing only one of the two isoforms or both together could be distinguished. In both AD and transgenic mice eNOS-expressing astrocytes exceeded iNOS-expressing astrocytes in number. Astrocytes with elevated levels of iNOS or eNOS were constantly seen in direct association with Abeta-deposits in AD and transgenic mice and were found in the vicinity of the lesion site in the rat cortex. The results of the present study show that expression of both iNOS and eNOS is increased in activated astrocytes under experimental conditions associated with elevated expression of APP (electrolytic brain lesion) or Abeta-deposition (APP23 transgenic mice). Therefore, it is suggested that altered expression of these NOS isoforms being part of AD pathology is secondary to the amyloid pathology and might not be primarily involved in the pathogenetic chain though it might contribute to the maintenance, self-perpetuation and progression of the neurodegenerative process.

Aberrant expression of nNOS in pyramidal neurons in Alzheimer's disease is highly co-localized with p21ras and p16INK4a.

Aberrancies of growth and proliferation-regulating mechanisms might be critically involved in the processes of neurodegeneration in Alzheimer's disease (AD). Expression of p21ras and further downstream signalling elements involved in regulation of proliferation and differentiation as, for example, MEK, ERK1/2, cyclins, cyclin-dependent kinases and their inhibitors such as those of the p16INK4a family, are elevated early during the course of neurodegeneration. Activation of p21ras can also directly be triggered by nitric oxide (NO), synthesized in the brain by various isoforms of nitric oxide synthase (NOS) that might be differentially involved into the pathomechanism of AD. To study the potential link of NO and critical regulators of cellular proliferation and differentiation in the process of neurofibrillary degeneration, we analyzed the expression pattern of NOS-isoforms, p21ras and p16INK4a compared to neurofibrillary degeneration in AD. Additionally to its expression in a subtype of cortical interneurons that contain the nNOS-isoform also in normal brain, nNOS was detected in pyramidal neurons containing neurofibrillary tangles or were even unaffected by neurofibrillary degeneration. Expression of nNOS in these neurons was highly co-localized with p21ras and p16INK4a. Because endogenous NO can activate p21ras in the same cell which in turn leads to cellular activation and stimulation of NOS expression [H.M. Lander, J.S. Ogiste, S.F.A. Pearce, R. Levi, A. Novogrodsky, Nitric oxide-stimulated guanine nucleotide exchange on p21 ras, J. Biol. Chem. 270 (1995) 7017-7020], the high level of co-expression of NOS and p21ras in neurons vulnerable to neurofibrillary degeneration early in the course of AD thus provides the basis for an autocrine feedback mechanism that might exacerbate the progression of neurodegeneration in a self-propagating manner.

Activated mitogenic signaling induces a process of dedifferentiation in Alzheimer's disease that eventually results in cell death.

Neurodegeneration in Alzheimer's disease (AD) is associated with the appearance of dystrophic neuronal growth profiles that most likely reflect an impairment of neuronal reorganization. This process of morphodysregulation, which eventually goes awry and becomes a disease itself, might be triggered either by a variety of life events that place an additional burden on the plastic capability of the brain or by genetic pertubations that shift the threshold for decompensation. This paper summarizes recent evidence that impairment of the p21ras intracellular signal transduction, which is is mediated by a hierarchy of phosphorylation signals and eventually results in loss of differentiation control and an attempt of neurons to re-enter the cell-cycle, is critically involved in this process. Neurodegeneration might thus be viewed as an alternative effector pathway of those events that in the dividing cell would lead to cellular transformation. This hypothesis might be of heuristic value for the development of a therapeutic strategy.

Crosslinking of alpha-synuclein by advanced glycation endproducts--an early pathophysiological step in Lewy body formation?

An excess of reactive carbonyl compounds (carbonyl stress) and their reaction products, advanced glycation endproducts (AGEs), are thought to play a decisive role in the pathogenesis of neurodegenerative disorders and Parkinson's disease (PD) in particular. Accumulation of AGEs in various intracellular pathological hallmarks of PD, such as Lewy bodies, densely crosslinked intracellular protein deposits formed from neurofilament components and alpha-synuclein, have already been described in patients in advanced stages of the disease. There is, however, no indication of the involvement of AGE-induced crosslinking of alpha-synuclein in very early stages of the disease. In this study, we observed that AGEs and alpha-synuclein are similarly distributed in very early Lewy bodies in the human brain in cases with incidental Lewy body disease. These cases might be viewed as pre-Parkinson patients, i.e. patients who came for autopsy before the possible development of clinical signs of PD. AGEs are both markers of transition metal induced oxidative stress as well as, inducers of protein crosslinking and free radical formation by chemical and cellular processes. Thus, it is likely that AGE promoted formation of Lewy bodies reflects very early causative changes rather than late epiphenomenons of PD.

Co-expression of APP with cNOS but not iNOS after cortical injury in rat.

Alterations in the expression of both the beta-amyloid precursor protein (APP) and nitric oxide synthase (NOS) might be involved in neurodegenerative conditions and/or in the neuronal response to injury. We have investigated the relationship between the increased expression of beta-amyloid precursor protein (APP) and the reactive changes in the expression of isoforms of nitric oxide synthase (NOS) in neurons and glial cells after small electrolytic lesions placed to the cerebral cortex. An increase in the expression of APP in both neurons and glial cells was detected 4 days post-operation. The inducible NOS (iNOS) was observed in macrophages or glial cells surrounding the lesion site. No major changes in constitutive NOS (cNOS) were found. APP immunoreactivity was not co-localized with either iNOS or cNOS at this survival time. At longer survival times (8 and 12 days post-lesion), a reactive increase in the expression of cNOS in cortical pyramidal neurons was seen in addition to the elevated expression of iNOS in astrocytes. The reactive expression of cNOS was confined to a subset of neurons also showing a high expression of APP. The present results suggest a relationship between reactive changes in the expression of APP and cNOS during the neuronal response to injury.

Ultrastructural demonstration of constitutive nitric oxide synthase (cNOS) in neocortical glial cells and glial perisynaptic sheaths.

We investigated the localization of the constitutive isoform of nitric oxide synthase (cNOS) in the rat visual cortex by electron microscopy, using a pre-embedding immunohistochemical method. NOS-immunoreactivity was demonstrated in very few somata, dendrites and axon terminals of nerve cells, and also in a few glial cells. The morphological characteristics of labelled glial cells enabled us to identify them as astrocytes. In comparison to the enzyme activity in neurons, the glial cells show a very weak reactivity which was not detectable at the light microscopical level. Immunoreactivity was located in the perikaryon and in the processes of astrocytes. Qualitative analyses with the electron microscope indicate that NOS-positive astroglial cells constitute a very small proportion in the rat visual cortex, whereas the great majority of astrocytes is NOS-negative. An unexpected observation was the localization of NOS immunoreactivity in astroglial sheath-like structures around some synaptic junctions. These results suggest that NO may act very locally at some synapses, and that specialized glial cells are involved in the NO-mediated mechanisms.

Distribution patterns of Wisteria floribunda agglutinin binding sites and parvalbumin-immunoreactive neurons in the human visual cortex: a double-labelling study.

Extracellular lattic-like coatings--known as perineuronal nets (PNs)--ensheath certain types of neurons in the mammalian neocortex. PNs and densely stippled zones in some cortical layers contain proteoglycans stainable e.g. with several plant lectins. The present study is focused on the binding sites of the plant lectin Wisteria floribunda agglutinin (WFA) and on its relationship to parvalbumin-immunoreactive (PARV-ir) neuronal constituents in the human visual cortical fields 17 and 18. Size and numbers of PNs varied not only between these two areas, but also between its layers. In area 17 the PNs appeared accumulated in two conspicuous bands which included layer IV, particularly layer IVb, and layer VI. Layer IVc of area 17 contained numerous small faintly stained PNs. In area 18 a two-tiered organization of PNs in layers IIIb-c and layer V was emphasized. The neuropil staining by WFA was much more intense in layers IIIb-c of area 18 than of area 17. In areas 17 and 18 the vast majority of PNs was associated with sub-populations of PARV-ir cells resembling several classes of GABAergic cortical interneurons. Among PARV-negative cells surrounded by PNs, only exceptionally pyramide-like neurons were detected. The patterns of lectin-labelling in the human visual primary and association cortex resembled those of macaque monkeys and differed from those in the visual cortex of rat and gerbil. These differences between mammals representing divergent modes of visual specialization may support the view that such extracellular matrix components in these occipital cortical areas are involved in visual information processing subserving fast inhibitory interneuronal actions.

Postnatal development of NADPH-diaphorase/nitric oxide synthase positive nerve cells in the visual cortex of the rat.

The postnatal development of NADPH-diaphorase (NADPH-d)/nitric oxide synthase (NOS) positive nerve cells was studied in the visual cortex of rats on postnatal day 1, 5, 10, 15, 20, 30 and at the age of 1 year. NADPH-d was demonstrated enzymhistochemically and NOS immunohistochemically using a polyclonal antibody. NADPH-d is localized in nerve cell somata, dendrites, axons and blood vessels, whereas NOS immunoreactivity is only detectable in nerve cells. The identity of NADPH-d cells with those which contain NOS was proved in double labelling experiments in the cortex of rats on postnatal day 5, 15 and at the age of 1 year. The results of these experiments have shown that in the cortex of rats NADPH-d positive cells are identical with NOS-positive cells in the different stages. Therefore we have used NADPH-d histochemistry in all other postnatal stages as a marker for neurons which contain NOS. NOS positive nerve cells appear very early on postnatal day 1 in the intermediate (white matter) and subplate (layers V and VI) region as small undifferentiated neurons. During the following postnatal differentiation these neurons reached their typical morphology in the second week and appeared in all layers. Neurons in layers V and VI preceded those in the superficial layers. Nerve cells in the white matter seem to have their own differentiation pattern because they showed characteristic features of immaturated varicose dendrites for a longer time. The investigation of soma size with the computerized "Kontron Videoplan" system (Zeiss, Germany) showed the largest cell bodies on postnatal day 20 which then decreased towards adulthood. Between postnatal day 10 and 20 some NOS-positive neurons especially in the deep layers displayed symptoms of degeneration, like shrunken cell bodies, corkscrew and twisted dendrites. Furthermore, NOS-positive neurons in layer I are not detectable in adult neocortex. These observations could suggest that some NOS-positive cells in the cerebral cortex of rats may occur only transiently. Also in the neuropil some alterations in the localization of NOS positive axonal boutons were observed. On postnatal day 10 NOS negative cell somata were shadowy surrounded by boutons. During the further development from postnatal day 20 until adulthood this particular position was no longer visible. Beside the NOS cells which played a transient role, the majority of these cells survived to adulthood and are a morphological (Martinotti-cells with ascending axons) and chemical (GABAergic, NADPH-d/NOS positive, peptide containing cells) defined cell type in the neuronal network of the cortex of the rat.

On the structure of the pretectal nuclei of the rat: an immunocytochemical and tracer study.

We have studied the distribution of the calcium-binding proteins parvalbumin, calbindin and calretinin, the NADPH diaphorase activity and the morphology of the commissural neurons, revealed by the stereotactic applications of fluorogold in the pretectal complex of the rat. The histochemical differentiation of the pretectal complex shows a complementary pattern of parvalbumin and calbindin containing cells. Only a few of the neurons in the pretectal complex contain calbindin. Calretinin immunoreactivity is scant and diffuse. The NADPH-diaphorase activity is restricted to neurons and terminals in the nucleus of the optic tract and the dorsal terminal nucleus. Due to numerous active fibers which traverse these nuclei they display a reticular appearance. Commissural neurons constitute 20% of the cell number of the pretectal complex and are restricted to the dorsal and lateral terminal nuclei.

Morphological analyses of NADPH-diaphorase/nitric oxide synthase positive structures in human visual cortex.

Human visual cortex was studied using NADPH-diaphorase histochemistry and nitric oxide synthase immunohistochemistry. Large, strongly stained, sparsely spined non-pyramidal cells (average soma diameter: 16 x 16 microns) occur in layers II-VI, but are commonest in layers II-III. Small weakly stained multipolar cells (average soma diameter 3.6 x 4 microns, stellate like cells) in layers II-VI are concentrated in layer IV of areas 17 and 18. The density of these cells, measured with a computer assisted microscopy system is less in area 18 than 17. Large, strongly stained, predominantly horizontal cells (average soma diameter 12 x 19 microns) are localized in the underlying white matter. Axons of the large, strongly NADPH-diaphorase positive cells are thin and unbranched with fine boutons. These axons ascend to layer I. The large, strongly stained cells in layers II-VI we identify as Martinotti neurons. In layer I parallel unbranched positive fibres with some fine boutons run horizontally and build dense axonal plexuses together with the axons of Martinotti neurons. Axons of presumed extrinsic origin are morphologically different from NADPH-diaphorase positive intrinsic fibres. They show thick varicosities running in different directions and forming a network in layers III-VI. Basket like formations of these fibres were frequently observed in layers IV, V and VI. Other fibres seem to innervate blood vessels. Nitric oxide synthase was also demonstrated immunohistochemically by a polyclonal rabbit nitric oxide synthase antiserum. The morphology and distribution of the immunostained cells correspond with those seen with NADPH-diaphorase histochemistry. Double labelling experiments confirm the colocalization of NADPH-diaphorase and nitric oxide synthase in all demonstrated cells. Immunohistochemical demonstration of glial fibrillary acidic protein has shown that astrocytes are not involved in the NADPH-diaphorase/NOS system in the human visual cortex.

The calcium-binding protein calretinin is localized in a subset of interneurons in the rat cerebral cortex: a light and electron immunohistochemical study.

The distribution of the calcium binding protein, calretinin (CR) has been investigated immunohistochemically in the cerebral cortex of albino rats by light- and electron microscopy. At the light microscopical level the pattern of CR-immunoreactivity (ir) appeared very similar in all regions of the rat cerebral cortex. CR-immunoreactive cells were found sparsely in layer I to layer VI, and frequently also in the white matter of the corpus callosum. All CR-ir neurons revealed morphological characteristics of local interneurons. The calretinin positive interneurons could be grouped according to their laminar occurrence, dendritic arborization and the soma size into 5 cell type classes. Quantitative measurements were performed only in the visual cortex. CR-ir neurons were more frequent in the superficial layers II and III. In all other layers, CR-ir cells are sparsely distributed with no preferential laminar localization. At the electron microscopical level, CR-ir axonal boutons formed frequently symmetrical axo-dendritic contacts. In all animals we observed CR-ir axons forming also synaptses of asymmetrical type. In summary calretinin labelled an interneuronal subpopulation of the rat cerebral cortex, which seemed not to overlap in its distribution and labelled structures to those, containing the related calcium binding proteins parvalbumin and calbindin D-28k.

Light- and electron microscopic localization of parvalbumin, calbindin D-28k and calretinin in the dorsal lateral geniculate nucleus of the rat.

The localization of parvalbumin, calbindin D-28k and calretinin have been investigated in the dorsal lateral geniculate nucleus (d lgn) of the rat at the light and electron microscopical level. Parvalbumin and calretinin positive sites are restricted to nerve fibres, whereas calbindin is present in fibres as well as in nerve cells showing morphological characteristics of interneurons. Ultrastructurally parvalbumin immunoreactivity is found in large terminals surrounded by glial lamellae containing round vesicles and making asymmetric contacts on dendrites. These morphological characteristics are typical for retinal endings of type 2a. Another kind of parvalbumin positive presynaptic terminals are seen on the surface of unstained nerve cell bodies and features symmetrical contacts. We conclude that this type represents axonal terminals of GABAergic neurons of the thalamic reticular nucleus. Calbindin positive nerve cells in the d lgn occur in the latero-dorsal part and according to morphological characteristics, belong to interneurons. Calbindin positive nerve cells receive synaptic terminals deriving from different kind of unstained presynaptic profiles. Calretinin immunoreactivity is localized in small to medium sized presynaptic endings with round vesicles, pale mitochondria and Gray-type 1 contacts on dendrites of relay- and interneurons. Some calretinin positive terminals are located in triads or in complex encapsulated regions. Therefore we identify calretinin positive terminals as the retinal inputs of type 2b. Our results demonstrate the expression of the three calcium binding proteins in morphologically, physiologically and biochemically different structures within the d lgn of the rat. The distribution differs from that found in the d lgn of the cat or monkey.

Soybean lectin binding neurons in the visual cortex of the rat contain parvalbumin and are covered by glial nets.

We carried out qualitative and quantitative studies on the distribution of soybean agglutinin-labelled cells in the visual cortex of the rat. Lectin-positive nerve cells mostly showed the morphological characteristics of small and large multipolar basket cells. Only a few cells appeared to be bipolar with a vertical or horizontal orientation. By light microscopy, soybean agglutinin binding sites were seen as discontinuous, punctate perineuronal staining (or pericellular nets) on the surface of about 9% of cortical neurons. Lectin-positive cells were predominantly localized in layers IV and V (16.9 and 12.4% of all neurons), where the intensity of staining was also the strongest. Combining lectin- and immunohistochemistry on cryo semithin sections, lectin-positive cells were shown to contain parvalbumin. Nerve cells in the visual cortex containing the related calcium binding-proteins, calbindin or calretinin were never soybean agglutinin-positive. Some glial cells and their processes were also soybean agglutinin-positive. The structure of the soybean agglutinin-positive pericellular nets was similar to that of glial nets visualized with the Golgi-method. Electron microscopy revealed that lectin binding sites were localized on the membranes and cytoplasm of glial processes ensheathing the axon terminals that impinged upon neurons and their proximal dendrites. Synaptic clefts and axon terminals were never reactive, thus explaining the discontinuous punctate labelling of the neuronal surface. Lectin binding sites were also found on the trans-face of the Golgi-complex of some lectin positive neurons suggesting that N-acetylgalactosamine-containing glycoconjugates, which are selectively detected by the lectin, are synthesized, at least partly, within the labelled neurons. We therefore consider possible the existence of specific interactions between parvalbumin positive basket cells and the glial network surrounding them, by which the neuron may determine the conditions of its own microenvironment.

Morphology of neurons in the rat basal forebrain nuclei: comparison between NADPH-diaphorase histochemistry and immunohistochemistry of glutamic acid decarboxylase, choline acetyltransferase, somatostatin and parvalbumin.

Transversal sections through the basal forebrain of 11 adult male rats were immunostained for glutamic acid decarboxylase (GAD), choline acetyltransferase (ChAT), somatostatin (SOM) and parvalbumin (PARV). Immunohistochemistry of ChAT, PARV, and SOM was combined with histochemistry of NADPH-diaphorase (NADPH-d) to obtain information on the colocalization of various neuroactive substances and this enzyme and to facilitate the recognition of morphological details of double-stained neurons. The distribution patterns of GAD- and PARV-immunoreactive cells were only in part congruent in basal forebrain nuclei in the rat. In the medial septal nucleus (MS) and the vertical limb of the diagonal band (vDB) PARV-immunopositive neurons were homogeneously scattered inside the nucleus, whereas the GAD-immunoreactive cells were much more numerous in the lateral part of this nuclear complex. In the horizontal limb of the diagonal band (hDB) and the nucleus preopticus magnocellularis (NPM), where GAD-immunoreactive cells occurred in high number, only very few cells contained PARV-immunoreaction product. In the substantia innominata-nucleus basalis Meynert complex (SI-NB) and in the ventral pallidum (VP) the neuropil was heavily stained with the GAD-immunoreaction product. The number of GAD-positive cells appeared low in the SI-NB, but much higher in the VP. In this nucleus GAD- and PARV-immunoreactive cells seem to be identical. PARV-positive neurons are very sparse in the SI-NB. Double-staining of PARV-immunoreactivity and NADPH-d was not registered. These nuclei were the only ones in which some cells with SOM-like immunoreactivity were observed. Among ChAT-positive neurons those double-stained with NADPH-d occurred in moderate number, but with obvious regional differences. In MS-vDB and the marginal zone of hDB the two neuron groups were intermingled, but only in the innermost part of the hDB ChAT-single-immunostained cells form aggregates, which were also typical of the zone in the SI-NB that surrounds and infiltrates the globus pallidus (GP). Double-labelled cells were more frequent in the lateral aspect of the NPM and SI-NB. Cells single-stained for NADPH-d were frequent in the MS-vDB along the border toward the lateral septal nuclei, but low in number in the NPM, VP and SI-NB. The functional aspects of the occurrence of GAD-immunoreactive cell aggregates in the lateral preoptic area (LP) and the lateral hypothalamic area (LH) were discussed with special regards to extrinsic GABAergic input in the dorsal SI-NB.(ABSTRACT TRUNCATED AT 400 WORDS)

[Gabaergic NADPH-diaphorase-positive Martinotti cells in the visual cortex in rats]. / GABAerge NADPH-diaphorase-positive Martinottizellen im visuellen Cortex der Ratte.

NADPH-diaphorase positive cells were described in the visual cortex of the rat in layers II-VI and in the white matter. Their somata were large or medium-sized, oval or elongated, and their cytoplasm was accumulated at the poles. Some proximal thickened coarse dendrites formed a bitufted dendritic field. These features showed a cell type impregnated with the Golgi-Kopsch-method and a Golgi-deimpregnation-method described as Martinotti cell (sparsely spined polarized neurons with ascending axons). The immunocytochemical evidence of GABA in NADPH-diaphorase positive neurons (double labeling) showed the GABA ergic nature of these cells, but an attempt for a double labelling of NADPH-diaphorase and Parvalbumin was negative.

[Dendrite-free GABAergic neurons of the visual system in the rat]. / Spinefreie GABAerge Neuronen im visuellen Cortex der Ratte.

Spinefreie GABAergic neurons in the visual cortex of the rat were studied with the Golgi-Kopsch-method and immunohistochemical methods against GABA. They show differences of their axonal arborizations, axonal surfaces and of their axonal terminal formations. We found large spinefree neurons, spinefree neurons with strictly axonal fields, spinefree neurons with dense axonal fields, spinefree neurons with axons forming arcades, spinefree neurons with columnar axons and spinefree neurons with clewded axonal terminals.