Apoptosis as a mechanism of maxillary sinus mucosa injury in rats after experimental transection of the maxillary nerve.

Transection of the maxillary nerve initiates apoptosis of the maxillary sinus mucosa cells in rats. Significant activation of apoptosis and proapoptotic factor p53 was found in the epithelium during week 1 after nerve transection. In delayed period after injury, apoptotic cells predominated in the submucosa against the background of Bcl-2 hypoexpression.

[Age-related changes in the nervous apparatus of the blood vessels in the brain and spinal cord].

This work was designed to study changes in the nervous apparatus of the blood vessels in the brain and spinal cord with a view to developing methods for the determination of the biological age in man. Pial and intramedullary vascular systems of the brain and spinal cord were examined in different periods of postnatal ontogenesis (between the age of 1 and 90 years) using histological, fluorescent-histochemical, and immunohistochemical methods as well as by ink injections into the blood vessels, scanning and transmission electron microscopy. The data obtained on the age-related rearrangement of the nervous apparatus of the arterial vessels in the brain and spinal cord have not only theoretical significance but can also be used for the solution of practical problems encountered in the practical work of forensic medical experts.

[Innervation of the brain: what is innervated by what].

In the pia mater, brain substance and ependyma, peripheral nerves with sensory and effector axons and two types of neurons are located: (1) afferent pseudounipolar and bipolar cells and (2) efferent vegetative Dogiel type I neurons. Together, these nerves and neurons form the intramedullary part of the autonomous nervous system, innervating blood vessels, ependyma and perivascular connective tissue.

The role of nitric oxide in the apoptosis of neurons in the retina of the human fetal eye.

The locations of NADPH-diaphorase (NADPH-d), inducible NO synthase (iNOS), and TUNEL-immunoreactive neurons in the retina of human fetuses collected during the first to third trimesters of pregnancy were studied. High levels of NADPH-d activity were seen in the inner segments of light-sensitive cells, amacrine cells, and ganglion cells. The population of NADPH-d-positive amacrine cells included three types of neuron. Type 1 neurons were large and had sparse dendritic fields occupying the inner nuclear and outer retinal layers. Small type 2 neurons were located in the inner retinal layer. Ectopic amacrine cells, type 3, were located in the outer part of the ganglion layer. A high density of NADPH-d-positive neurons was seen in the central part of the retina, surrounding the central fovea and optic disk area. NADPH-d activity increased progressively during ontogenesis and correlated with the appearance of immunoreactive iNOS in neurons. iNOS labeled a subpopulation of amacrine and ganglion cells, which appeared at 20-21 weeks of development and reached a peak of immunoreactivity by the end of the third trimester. TUNEL-immunopositive neuron nuclei with signs of apoptotic destruction were seen at 30-31 weeks of pregnancy. The greatest apoptotic index was seen in the ganglion and amacrine cell populations. These data identify NO as a factor mediating apoptosis of neurons during the critical period of differentiation of interneuronal connections in the human retina.

[Neurogliaform cells: neurochemistry, spatial arrangement, and their role in the neocortical inhibitory system].

The neurogliaform cells (NGFC) localized in area 4 of the human motor cortex were found to express choline acetyl transferase (ChAT), GABA, and calbindin. ChAT-positive neurons were located in cortical layer II. Their dendrites lay in a close proximity to those of pyramid cells, neighbouring neurogliaform cells, and bodies and dendrites of other cortical neurons. The NGFCs revealed by Golgi staining fell into two groups. Cells of the first group had locally (within cortical layer II) spreading axons, while those of the second group had axons extending into the adjacent layers. Neurochemical heterogeneity of NGFCs is discussed in the context of information processing in cortical modules and interaction of excitatory and inhibitory interneurons.

[Role of nitric oxide in apoptosis of retinal neurons in human fetuses].

The localization of NADPH-diaphorase (NADPH-d), inducible NO-synthase (iNOS) and TUNEL-immunoreactive neurons was studied in the retina of human fetuses in the I-III trimesters of pregnancy. High NADPH-d activity was found in internal segments of photosensory cells, amacrine and ganglion cells. The population of NADPH-d-positive amacrine cells included three types of neurons. Neurons of the 1st type had large size and scarce dendritic field, occupying the inner nuclear and outer plexiform layers. Small neurons of the 2nd type were located in the inner plexiform layer. Ectopic amacrine cells of 3rd type could be found in the outer part of the ganglion cell layer. High density of the NADPH-d-positive neurons was detected in the central portion of retina surrounding fovea centralis and the optic disk area. The activity of NADPH-d was found to grow progressively in ontogenesis and to correlate with the appearance of immunoreactive iNOS in neurons. Immunoreactive iNOS marked a subpopulation of amacrine and ganglion cells which appeared in weeks 20-21 of gestation and attained maximal immunoreactivity by the end of the III trimester. TUNEL-immunoreactive nuclei of the neurons with the signs of the apoptotic destruction were found in weeks 30-31 of gestation. The highest apoptotic index was found in the population of ganglion cells. The data obtained strongly suggest that NO is a factor, mediating the neuronal apoptosis during the critical period of a differentiation of interneuronal connections in the human retina.

Induction of NO synthase and glial acidic fibrillary protein in astrocytes in the temporal cortex of the rat with audiogenic epileptiform reactions.

The localizations of NADPH-diaphorase (NADPH-d), inducible NO synthase (iNOS), and glial acid fibrillary protein (GFAP) in astrocytes of the temporal cortex were studied in Krushinskii-Molodkina rats, which are genetically predisposed to audiogenic convulsive seizures. Convulsive reactions were induced in rats by three exposures to acoustic stimuli. Controls consisted of Wistar rats and Krushinskii-Molodkina rats not subjected to acoustic stimulation, these not developing convulsive reactions. The neocortex of animals with audiogenic convulsions consistently showed foci of brain tissue damage. Foci, of diameter 300-400 microm, were located in layers III-V and were groupings of NADPH-d-positive astrocytes; these were seen in both hemispheres. Astrocytes in foci of damage expressed iNOS and had elevated GFAP levels. The numbers of GFAP-immunopositive cells were increased by 25-37% in damage foci as compared with levels in controls and undamaged areas of the cortex. The induction of NO synthase and GFAP in astrocytes seen here indicates the involvement of glia in compensatory NO-dependent mechanisms formed in damage foci in response to audiogenic convulsive seizures.

[Induction of NO-synthase and glial fibrillary acidic protein in astrocytes of the temporal cortex in rats with audiogenic epileptiform reaction]. / Induktsiia NO-sintazy i glial'nogo kislogo fibrilliarnogo belka v astrotsitakh visochnoi kory krys s audiogennoi épileptiformnoi reaktsiei.

The localization of NADPH-diaphorase (NADPH-d), inducible NO-synthase (iNOS) and glial fibrillary acidic protein (GFAP) was studied in the astrocytes of the temporal cortex in rats of Krushinsky-Molodkina strain which are genetically prone to audiogenic seizures. The seizure was evoked by thrice-repeated acoustic stimulation. Wistar rats and acoustically untreated seizure-free Krushinsky-Molodkina rats were used as a control. The foci of brain damage were consistently found in the neocortex of the animals with audiogenic seizures. Epileptic foci, 300-400 microm in diameter, were localized in layers III-V; they were found to consist of the clusters of NADPH-d-positive astrocytes and to be present in both hemispheres. In the foci of cortical damage astrocytes expressed iNOS and an elevated level of GFAP. The number of GFAP-immunopositive astrocytes in the foci of damage was increased by 25-37% compared to the control and to undamaged areas of the cortex. Astrocyte NOS and GFAP induction found in this work, suggests the participation of glia in compensatory NO-dependent mechanisms, that are formed in the damage foci of neocortex during the audiogenic seizures.

Induction of NO-synthase and acetaldehyde dehydrogenase in neurons of human cerebellar cortex during chronic alcohol intoxication.

Induction of NO-synthase and acetaldehyde dehydrogenase in Purkinje cells, basket-like neurons, and microvascular endothelium of human cerebellar cortex was detected in patients with chronic alcohol intoxication. It was hypothesized that the neuromodulating effect of NO is associated with mechanisms protecting neurons from toxic effects of ethanol and acetaldehyde.

Ethanol-oxidizing and NO-synthesizing enzymes in monoaminergic nuclei of human brain.

Serotonin-, dopamine-, and noradrenergic nuclei in human brainstem were examined histochemically for alcohol dehydrogenase, aldehyde dehydrogenase, and NADPH diaphorase. The findings indicate that monoaminergic centers are characterized by different repertoire of NO-ergic and ethanol-oxidizing enzymes, whose distribution correlates with the transmitter specialization of neurons.

[Significance of nitric oxide function in development of cardiac hypertrophy under condition of experimental renal hypertension]. / Znachenie oksida azota v razvitii gipertrofii serdtsa v usloviiakh éksperimental'noi pochechnoi gipertenzii.

The development of cardiac hypertrophy was studied under condition of experimental renal hypertension on the rat. The number of cardiac nitric oxide synthase (NOS)-positive neurones increased simultaneously with the increase in NOS-activity in these neurones. A connection was found between the development of cardiac hypertrophy and the activity of NOS in cardiomiocytes. The involvement of NO in the development cardiac hypertrophy as auto- and paracrine regulator is supposed.

[Nitric oxide formation by chromaffinocytes of respiratory system and its importance for catecholamine exocytosis]. / Obrazovanie okisi azota khromaffinotsitami organov dykhaniia i ee znachenie dlia ékzotsitoza katekholaminov.

Chromaffinocytes (both single and within paraganglia) located in larynx, trachea, extrapulmonary bronchi and lungs possess NADPH-diaphorase/NO-synthase activity. Chromaffinocytes and paraganglia are anatomically associated with the vagus, autonomous ganglia and the walls of small blood vessels. NO-synthase agonists, acethylcholine and Ca ionophore A23217, after intrapleural injection increase the enzyme activity, that is accompanied with the decrease of luminescence intensity and a reduction of monoamine content in cell cytoplasm. It is concluded that NO is involved in the mechanism of catecholamine release.

[Nitric oxide synthase in neurons of the vagal nucleus dorsalis and ganglion nodosum and its changes following acetylcholine inhalation in the norm and in experimental bronchial asthma]. / Nitrooksidsintaza neironov zadnego iadra i uzlovatogo gangliia bluzhdaiushchego nerva i ee izmeneniia pri ingaliatsiiakh atsetilkholina v norme i pri éksperimental'noi bronkhial'noi astme.

The expression NADPH-diaphorase and inducible NO-synthase (NOS) was studied in vagal nucleus dorsalis and ganglion nodosum neurons following acethylcholine inhalation in healthy rats and rats with ovalbumin-induced experimental bronchial asthma (BA). It was found that NOS activity regulation is mediated by cholinoreceptors; functioning of this mechanism is disturbed in hypoxic state. It is shown that both in conditions of physiological norm and in experimental BA, changes in NOS activity are determined by its constitutive, neuronal isoform.

Dynamics of NADPH diaphorase activity in raphe neurons during chronic treatment with opiates.

Systemic administration of diacetylmorphine considerably reduced the number of NADPH diaphorase-positive (NO-synthesizing) neurons in rat brain raphe nuclei. This effect was blocked by naloxone. In animals with the withdrawal syndrome NO-ergic activity in raphe neurons increased and surpassed the normal.

[Nitric oxidergic neurons of the respiratory organs]. / Nitrooksidergicheskie neirony organov dykhaniia.

Using histochemical NADPH-diaphorase reaction NO-ergic neurons distribution in human tracheobronchial tree was studied in man and mammals. Psedounipolar sensory neurons forming microganglia mark in adventitia of the trachea posterior surface from superior border up to trachea bifurcation. It was suggested that protoneurons are the constant structural formations of respirator organs. Their capacity to exert effector influence on the tissue through axon-reflex mechanism, apart from their sensory function is under discussion.

[Nitric oxide production by normal and injured neurons of Nodose ganglion and Nucleus dorsalis of Vagus nerve]. / Obrazovanie oksida azota normal'nymi i povrezhdennymi neironami uzlovatogo gangliia i dorsal'nogo iadra bluzhdaiushchego nerva.

Nodosum ganglion and nucleus dorsalis contain from 19.2 to 22.65% of NO-positive neurons. Their amount increases up to almost 77.4 and 68.8% in the ganglion and the nucleus dorsalis, respectively, in the damaged nervus vagus due to i-NOS transcription. It has been shown that NO participates in desorganization and recovery of the traumatic neuron, as auto- and paracrine regulator.