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PubMed1989

Neuroanatomically selective down-regulation of beta adrenergic receptors by chronic imipramine treatment: relationships to the topography of [3H]imipramine and [3H] desipramine binding sites.

The down-regulation of beta adrenergic receptors by chronic imipramine treatment was investigated with high resolution autoradiography of [125I]pindolol binding to brain sections. Neuroanatomically selective down-regulation of [125I]pindolol binding was found after chronic imipramine treatment. Subdivisions of the amygdala and hippocampus and discrete cortical regions were differentially affected. In the hippocampus, reduction of [125I]pindolol binding was observed in imipramine-treated rats in the CA-1 stratum radiatum and dentate molecular layer, but not in the CA-3 stratum radiatum. In the amygdala, the basolateral nucleus exhibited reduced [125I]pindolol binding after imipramine treatment but the central and medial nuclei were not affected. Chronic imipramine treatment was also associated with reduced [125I]pindolol binding in layer 1 of the cingulate cortex and layer 3 of the piriform cortex. In contrast, no effect on [125I]pindolol binding was apparent in the ventrolateral thalamic nucleus, caudate-putamen, lateral hypothalamus or layers 2 and 3 of the somatosensory cortex. In order to determine if regional variation in binding sites for imipramine, or its pharmacologically active metabolite desipramine, was responsible for the observed neuroanatomically selective reduction in [125I]pindolol binding, the binding of [3H]imipramine and [3H]desipramine was investigated. In some brain regions that exhibited high densities of [3H]imipramine and [3H]desipramine binding sites, [125I]pindolol binding was reduced after chronic treatment with imipramine. However, other regions that contained high densities of binding sites for antidepressant drugs did not show a reduction in [125I]pindolol binding after chronic imipramine treatment. Thus, regional binding of [3H]imipramine or [3H]desipramine cannot fully explain the neuroanatomical specificity of imipramine-induced beta adrenergic receptor down-regulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2000

Dorsal hippocampal kindling produces long-lasting changes in the origin of spontaneous discharges in the piriform versus perirhinal cortex in vitro.

In an in vitro slice preparation of the amygdala-piriform-perirhinal cortex (A-P area), it was shown previously (McIntyre, D.C., Plant, J. R., 1993. Long-lasting changes in the origin of spontaneous discharges from amygdala-kindled rats: piriform vs. perirhinal cortex in vitro, Brain Res. 624, 268-276) that the infrequent spontaneous field potentials that initially originated in or near the perirhinal (PRh) cortex of slices from control rats began instead in the piriform (Pir) cortex of amygdala-kindled rats. This change in onset was only observed in the A-P area ipsilateral to the kindled amygdala. In the present experiment, we determined whether similar changes in activity were evident following kindling from a different limbic site, the dorsal hippocampus (DH). Kindling of the DH resulted in changes in the origin of the spontaneous discharges in the A-P area similar to amygdala kindling but, importantly, the changes involved both hemispheres. In addition, the origin of spontaneous discharges in slices from partial kindled rats (those that received as many hippocampal afterdischarges as the fully kindled rats but had not developed generalized convulsive responses) initially were similar to control tissue, but, during 0 Mg(2+) perfusion, changed more quickly than control tissue to mimic the profile of generalized kindled rats. The enduring changes in A-P area excitability caused by previous generalized kindling highlights the importance of the A-P area in convulsive generalization of limbic-kindled seizures.

Animals↗

PubMed2001

Olfactory-evoked regional cerebral blood flow in Alzheimer's disease.

Olfaction is impaired in Alzheimer's disease (AD). It was hypothesized that AD would reduce olfactory-evoked perfusion in mesial temporal olfactory (piriform) cortex, where neuropathology begins. Seven AD patients and 8 elderly controls (ECs) underwent olfactory threshold and identification tests and olfactory stimulation during positron emission tomography. Odor identification was impaired in AD, but threshold was not. Olfactory stimulation in ECs activated right and left piriform areas and right anterior ventral temporal cortex. AD patients had less activation in right piriform and anterior ventral temporal cortex but not in the left piriform area. Although orbital cortex did not activate in ECs, there was a significant between-groups difference in this area. Right piriform activation correlated with odor identification. Impaired odor identification likely reflects sensory cortex dysfunction rather than cognitive impairment. Given olfactory bulb projections to the mesial temporal lobe, olfactory stimulation during functional imaging might detect early dysfunction in this region.

Aged↗

PubMed1984

Somatostatin in the brain of the turtle Testudo hermanni Gmelin. An immunohistochemical mapping study.

An immunohistochemical mapping study in the brain and upper spinal cord of the turtle Testudo hermanni Gmelin revealed a wide distribution of somatostatin perikarya and fibres. Within the telencephalon, somatostatin perikarya are present in the anterior olfactory nucleus, in the medial, dorsomedial and dorsal cortex, in the pallial thickening, in the piriform cortex, paleostriatum augmentatum, in the dorsoventricular ridge, core nucleus of the dorsoventricular ridge, in area c and d, and in the amygdala. In the diencephalon, the periventricular nucleus of the hypothalamus contains many somatostatin perikarya. Cerebrospinal fluid contacting somatostatin perikarya of the infundibular nucleus terminate with club-like endings in the ventricular cavity. Some somatostatin perikarya are present in the nu. reuniens of the thalamus and in the lateral habenular nucleus of the epithalamus. Within the mesencephalon somatostatin perikarya are located in the interpeduncular nucleus, area tegmentalis ventralis and in the nu. reticularis isthmi. In the rhombencephalon, somatostatin perikarya are encountered in the nu. raphe superior, nu. reticularis magnus, periventricular grey matter, bed nucleus of the fasciculus longitudinalis medialis and in the nu. solitarius-vagus complex. Somatostatin fibres form a circular band in the olfactory bulb. In the telencephalon, dense aggregations of somatostatin fibres are present in the anterior olfactory nucleus, in the pallial thickening, in the parahippocampal gyrus, cortex medialis, dorsomedialis, dorsalis and piriformis, in the dorsal ventricular ridge, paleostriatum augmentatum, area c and d, in the septum, nu. diagonalis of Broca, in the amygdala and in the anterior commissure. In the diencephalon, somatostatin fibres terminate at the vessels of the organum vasculosum of the lamina terminalis. A dense band of somatostatin fibres surrounds the rostral third ventricle. Somatostatin fibres terminate in the infundibulum at portal capillaries, and in the neural lobe. Somatostatin fibres are found in the periventricular, ventromedial and lateral nucleus of the hypothalamus. In the thalamus, the area triangularis, the dorsomedial and dorsolateral area and the nu. reuniens contain somatostatin fibres. Somatostatin fibres are very dense in the lateral habenular nucleus. At the mesencephalic level, somatostatin fibres are found in the pretectal nucleus, in the deep layers of the tectum, in the nu. tori semicircularis lateralis, in the interpeduncular nucleus, area tegmentalis ventralis, nu. ruber, substantia nigra and periventricular grey.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1986

Connections of the lateral cortex in the lizard Podarcis hispanica.

The connections of the lateral cortex of the lizard Podarcis hispanica have been traced using horseradish peroxidase transport techniques. After injections, restricted to the lateral cortex, labelled neurons can be observed bilaterally in the main olfactory bulbs and the diagonal band, contralaterally in the lateral cortex and ipsilaterally in the nucleus of the lateral olfactory tract, the ventral amygdaloid nucleus and also in the area triangularis. An efferent has also been shown on the ipsilateral medial cortex. This pattern of connections supports the hypothesis that the reptilian lateral cortex is comparable to the entorhinal and piriform cortex of mammals.

Animals↗

PubMed1992

Regionally specific and rapid increases in brain-derived neurotrophic factor messenger RNA in the adult rat brain following seizures induced by systemic administration of kainic acid.

In situ hybridization techniques were used to analyse the spatiotemporal pattern of brain-derived neurotrophic factor messenger RNA elevation associated with kainic acid-induced seizure activity in the rat. Pronounced increases in hippocampal brain-derived neurotrophic factor messenger RNA levels were observed as early as 30 min following the onset of behavioral seizures. The greatest increase (10-fold) occurred in the dentate granule cell layer, while pyramidal layers CA1, CA3, and CA4 exhibited increases of two- to six-fold. Peak elevation of brain-derived neurotrophic factor messenger RNA in CA1 hippocampal region was evident at 4 h in CA3, and in the dentate granule layer at 30 min postseizure. Elevations persisted in the dentate and hilar regions to four days, while the increases in CA1 and CA3 returned to control levels by 16 h following seizure. Significant increases in brain-derived neurotrophic factor messenger RNA were also observed in the superficial layers of cortex (II and III) and in the piriform cortex which reached peak elevations by 8 h. No detectable changes were observed in the dorsomedial thalamus. Although histologically defined pyramidal and granule cell layers displayed relatively uniform increases in brain-derived neurotrophic factor messenger RNA in response to kainate, a closer examination of the labeling patterns using emulsion autoradiography revealed discrete areas of high grain densities overlapping uniform, moderate hybridization densities in the dentate granule cell layer and CA3, suggesting that the capacity to upregulate brain-derived neurotrophic factor messenger RNA in these regions may differ among individual neurons. In conclusion, our studies revealed that brain-derived neurotrophic factor messenger RNA induction in response to systemic kainate administration differs in hippocampal and cortical areas, in magnitude, time of onset and duration. The observed temperospatial pattern does not correspond in a simple way to increases in metabolic or electrical activity associated with seizures or neuronal vulnerability coincident with the seizures.

Animals↗

PubMed2002

Parvalbumin neuron circuits and microglia in three dopamine-poor cortical regions remain sensitive to amphetamine exposure in the absence of hyperthermia, seizure and stroke.

The dopamine-releasing and depleting substance amphetamine (AMPH) can make cortical neurons susceptible to damage, and the prevention of hyperthermia, seizures and stroke is thought to block these effects. Here we report a 2-day AMPH treatment paradigm which affected only interneurons in three cortical regions with average or below-average dopamine input. AMPH (six escalating doses/day ranging from 5 to 30 mg/kg for 2 days) was given at 17-18 degrees C ambient temperature (T) to adult male rats. During the 2-day AMPH treatment, peak body T stayed below 38.9 degrees C in 40% of the AMPH treated rats. In 60% of the rats, deliberate cooling suppressed (<39.5 degrees C) or minimized (<40.0 degrees C) hyperthermia. Escalation of stereotypes to seizure-like behaviors was rare and post-mortem morphological signs of stroke were absent. Neurons labeled with the anionic, neurodegeneration-marker dye Fluoro-Jade (F-J) were seen 1 day after dosing, peaked 3 days later, but were barely detectable 14 days after dosing. Only nonpyramidal neurons in layer IV of the somatosensory barrel cortex and in layer II of the piriform cortex and posterolateral cortical amygdaloid nucleus were labeled with Fluoro-Jade. Isolectin B-labeled activated microglia were only detected in their neighborhood. F-J labeled neurons were extremely rare in cortical regions rich in dopamine (e.g. cingulate cortex), and were absent in cortical regions with no dopamine (e.g. visual cortex). Parvalbumin was seen in some Fluoro-Jade-labeled neurons and parvalbumin immunostaining in local axon plexuses intensified. This AMPH paradigm affected fewer cortical regions, and caused smaller reduction in striatal tyrosine hydroxylase (TH) immunoreactivity than previous 1-day AMPH regimens generating seizures or severe (above 40 degrees C) hyperthermia. Correlation between peak or mean body T and the extent of neurodegeneration or microgliosis was below statistical significance. Astrogliosis (elevated levels of the astroglia-marker, glial fibrillary acidic protein (GFAP)) was detected in many brain regions. In the striatum and midbrain, F-J labeled neurons and activated microglia were absent, but astrogliosis, decreased TH immunolabel, and swollen TH fibers were detected. In sum, after this AMPH treatment, cortical pyramidal neurons were spared, but astrogliosis was brain-wide and some interneurons and microglia in three cortical regions with average or below-average dopamine input remained sensitive to AMPH exposure.

Amphetamine↗

PubMed1998

Tracing of axonal connectivities in a combined slice preparation of rat brains--a study by rhodamine-dextran-amine-application in the lateral nucleus of the amygdala.

In preparation for electrophysiological studies, the fiber pathways within the amygdala of rats have been examined using a combined Nissl- and silver-staining method (Bielshowsky) in horizontal sections of the amygdala. To determine if fibers in the lateral nucleus of the amygdala are in functional connection with other brain regions, an anterograde and retrograde axonal tracing method (application of rhodamine-dextran-amine) was performed. Horizontal slices containing some nuclei of the amygdala (lateral nucleus, basolateral nucleus, central nucleus, medial nucleus), as well as the entorhinal cortex, the hippocampus and parts of the piriform cortex were used. Crystals of rhodamine-dextran-amine were placed in the lateral nucleus. Intra-amygdaloid connections as well as connections to other brain regions were preserved in this preparation. The connectivities of the lateral nucleus with other nuclei of the amygdala (basolateral, medial, central) correspond with the findings made by tracer applications in-vivo. The use of a tracer that is transported in both the antero- and retrograde direction shows the whole spectrum of efferent and afferent fibers which are involved in the projection pattern of the lateral nucleus. To test the usefulness of this preparation for electrophysiological studies, extracellular field potentials were recorded.

Amygdala↗

PubMed1997

Morphofunctional effects of moderate forebrain ischemia combined with short-term hypoxia in rats--protective effects of Cerebrolysin.

Morphofunctional effects of combined moderate forebrain ischemia due to permanent bilateral carotid artery ligation and short-term systemic hypoxia in rats were investigated. Moreover, a putative effect of brain protection by Cerebrolysin (Cerebrolysin, EBEWE, Austria), a brain tissue hydrolysate containing a mixture of 85% free amino acids and 15% small peptides (MW < 10,000), was studied. Eighty-seven adult Wistar rats (24 Cerebrolysin treated and 63 controls) were subjected to chronic moderate forebrain ischemia by permanent bilateral carotid artery ligation for 7 days. Twenty-four hours after the onset of ischemia, 56 of them underwent an additional hypoxic hypoxia (FiO2 = 0.08) of 15 min. A first group (19 out of 56 animals) received Cerebrolysin (every dose 2.5 ml/kg body weight s.c.) after ligation, after hypoxia and then daily. A second group (6 out of 56 animals) received an equal volume of physiological saline after ligation and Cerebrolysin the first time after hypoxia and then once a day. An untreated control group (31 out 56 animals) received physiological saline. Changes in behavior were scored and electrophysiological activity was quantified by spectral ECoG analysis before carotid artery ligation, before and after hypoxia, and once a day during the following 7 days. On the 7th day after hypoxia, the animals were sacrificed and the grade of histological damage was quantified by morphometry. After permanent carotid artery ligation, 20 out of 63 (31.7%) untreated control animals died within 24 h but only 4 out of 20 (16.7%) Cerebrolysin treated animals. However, Cerebrolysin had not detectable effect on mortality after the additional acute hypoxia. Within 24 h after hypoxia, ECoG power of the higher frequency ranges remained low (p < 0.05). Surviving animals showed a significantly higher ECoG power during and 15 min after hypoxia than those animals that died within 48 h after hypoxia (p < 0.05). All animals showed reduced behavioral activity (p < 0.01) 20 min after hypoxia, however, basal reflex responses were not altered. The major patterns of neuronal damage were coagulation necrosis and general sponginess of the neuropil which is a sign of brain edema. These changes occurred predominantly within the superolateral convexities of the parietal cortex, in the entorhinal and in the piriform cortex as well as in the CA1 and CA4 region and in the dentate gyrus of the hippocampus. The striatum and the origin nuclei of the brain nerves were also affected. We did not observe a relationship between behavior, ECoG depression and the extent of morphological damage after hypoxia nor did we find any protective effects of Cerebrolysin on these parameters. Rather it is suggested that the degree of ECoG depression immediately after hypoxic hypoxia could be a predictor for prognosis of animal survival. Cerebrolysin reduced the amount of early mortality which was caused by moderate global forebrain ischemia. However, no protective influences of the amount of brain tissue damage could be shown.

Amino Acids↗

PubMed2002

Tin-protoporphyrin prevents experimental superficial siderosis in rabbits.

Superficial siderosis of the human central nervous system is caused by small continuous or recurrent subarachnoid hemorrhages that lead to the destructive deposition of hemosiderin. The excessive tissue iron derives from heme that is oxidized in a rate-limiting step by the enzyme heme oxygenase (HO), and especially the inducible form, HO-1. We postulated that competitive inhibition of HO by tin-protoporphyrin IX (SnPP) could prevent experimental superficial siderosis. Since synthetic metalloporphyrins do not cross the blood-brain barrier, SnPP was delivered directly into the cisterna magna. Rabbits received weekly intracisternal injections of washed autologous red blood cells (RBC) over a period of 1 to 16 wk. In companion experiments, SnPP was added to the suspension of RBC, or SnPP was injected without RBC. All injections caused increased HO-1 immunoreactivity in the Bergmann glia of the cerebellar cortex and in superficial astrocytes of the piriform cortex. The injections of RBC or RBC with added SnPP also generated a vigorous microglial response. The metalloporphyrin entered the tissue in inhibitory amounts and greatly reduced the accumulation of histochemically detectable iron. It did not alter the microglial response. The observations allowed the conclusion that SnPP suppressed heme oxidation but did not affect other steps in the pathogenesis of superficial siderosis.

Animals↗

PubMed1997

The telencephalon of tetrapods in evolution.

Numerous scientists have sought a homologue of mammalian isocortex in sauropsids (reptiles and birds) and a homologue of sauropsid dorsal ventricular ridge in mammals. Although some of the proposed theories were enormously influential, alternative theories continued to coexist, primarily because the striking differences in pallial organization between adult mammals, sauropsids, and amphibians enabled different authors to enlist different subsets of similarity data in support of different hypotheses of putative homology. A phylogenetic analysis based on parsimony cannot discriminate between such alternative hypotheses of putative homology, because sauropsids and mammals are sister groups. One solution to this dilemma is to include embryological patterns of telencephalic organization in the comparative analysis. Because early developmental stages in different taxa tend to resemble each other more than the adults do, the embryological data may reveal intermediate patterns of organization that provide unambiguous support for a single hypothesis of putative homology. The validity of this putative homology may then be supported by means of a phylogenetic analysis based on parsimony. A comparative analysis of pallial organization that includes embryological data suggests the following set of homologies. The lateral cortex in reptiles is homologous to the piriform cortex in birds and mammals. The anterior dorsal ventricular ridge in reptiles is probably homologous to the neostriatum and ventral hyperstriatum in birds and to the endopiriform nucleus in mammals. The posterior dorsal ventricular ridge in reptiles is most likely homologous to the archistriatum in birds and to the pallial amygdala in mammals. The pallial thickening in reptiles is probably homologous to the dorsal and intercalated portions of the hyperstriatum in birds and to the claustrum proper in mammals. Finally, the dorsal cortex in reptiles is probably homologous to the accessory hyperstriatum and parahippocampal area in birds and to the isocortex in mammals. These hypotheses of homology imply relatively minor evolutionary changes in development but major changes in neuronal connections. Most significantly, they imply the independent elaboration of thalamic sensory projections to derivatives of the lateral and dorsal pallia in sauropsids and mammals, respectively. They also imply the independent evolution of lamination in the pallium of birds and mammals.

Animals↗

PubMed1997

5-HT2A receptor-mediated regulation of brain-derived neurotrophic factor mRNA in the hippocampus and the neocortex.

The influence of 5-HT receptor agonists on the expression of BDNF in brain was determined. Administration of a hallucinogenic 5-HT2A /2C receptor agonist, but not a 5-HT1A receptor agonist, resulted in a significant but differential regulation of BDNF mRNA levels in hippocampus and neocortex. In the hippocampus, the 5-HT2A /2C receptor agonist significantly decreased BDNF mRNA expression in the dentate gyrus granule cell layer but did not influence expression of the neurotrophin in the CA subfields. In parietal cortex and other neocortical areas, but not piriform cortex, the 5-HT2A /2C receptor agonist dramatically increased the expression of BDNF mRNA. The effect of the 5-HT2A /2C receptor agonist on BDNF mRNA in both the hippocampus and the neocortex was blocked by pretreatment with a selective 5-HT2A, but not 5-HT2C, receptor antagonist. The expression of BDNF mRNA in the hippocampus is reported to be decreased by stress, raising the possibility that the 5-HT2A receptor mediates this effect. Pretreatment with ketanserin, a 5-HT2A /2C receptor antagonist, significantly blocked the stress-induced downregulation of BDNF mRNA in hippocampus, in support of this hypothesis. The results of this study raise the possibility that regulation of BDNF expression by hallucinogenic 5-HT2A receptor agonists leads to adaptations of synaptic strength in the hippocampus and the neocortex that may mediate some of the acute and long-term behavioral effects of these agents.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1997

Zinc transport in the rat olfactory system.

To study zinc (Zn) mobility in the rat olfactory tract, brain distribution of 65Zn after injection into the olfactory bulb or amygdaloid nuclei was analyzed by autoradiography. Twenty-four hours after 65Zn injection into the olfactory bulb, 65Zn was distributed in the ipsilateral piriform cortex, amygdaloid nuclei and the anterior commissure. Moreover, in the case of injection of a higher level of 65Zn into the olfactory bulb, 65Zn was distributed in the ipsilateral entorhinal cortex in addition to the above regions. Twenty-four hours after 65Zn injection into the amygdaloid nuclei, 65Zn was distributed in the ipsilateral piriform and entorhinal cortex. These results suggest that Zn is intraneuronally transported along the olfactory tract. Zn may be taken up by the piriform neurons after release from the secondary olfactory neuron terminals and transported to the entorhinal area.

Amygdala↗

PubMed2026

Biophysical mechanisms underlying the generation and maintenance of rule-learning engram.

Training rodents in a particularly difficult olfactory-discrimination task results with acquisition of high-skill to perform the task superbly, termed 'rule-learning'. We show that rule-learning occurs abruptly, in a "light-bulb moment". Using whole-cell patch-clamp recordings from the piriform cortex (PC) of Fos2A-iCreER/TRAP2 mice, we target activated-neurons, expressing immediate early genes (IEG). We notice, from the onset of training, IEG-positive neurons from trained animals display enhanced intrinsic excitability. Subsequently, synaptic excitation and inhibition are enhanced in these neurons, in a coordinated, cell-wide process. Additionally, in parallel, we detect the density of IEG-expressing neurons sharply declines. Double labeling with TRAP and c-Fos reveal that nearly two-thirds of the rule-memory cell ensemble neurons are activated from the beginning of training. Silencing TRAP-expressing neurons using inhibitory DREADD leads to a complete loss of rule memory. Hence, we propose that rule learning occurs at a discrete moment and is developed through a gradual process that stabilizes the memory of the rule.

Animals↗

PubMed1997

Intracellular recording of magnocellular preoptic neuron responses to olfactory brain.

The magnocellular preoptic nucleus of the rat supplies centrifugal input to the olfactory bulb as well as projecting to other olfactory-related areas. The extent to which the piriform and entorhinal cortices can influence the activity of magnocellular preoptic neurons and hence that of the olfactory bulb were examined using intracellular in vivo recording. Stable recordings were obtained in 58 neurons impaled in the magnocellular preoptic nucleus. Antidromic responses occurred on stimulating olfactory bulb (15), piriform cortex (14), or entorhinal area (eight). Monosynaptic excitation was evoked by piriform (27 of 37 tested) and entorhinal cortex (15 of 32 tested) stimulation with polysynaptic inhibition occurring in seven and five neurons, respectively. Polysynaptic as well as antidromic excitation by olfactory bulb stimulation occurred in four; a further 28 tested responded polysynaptically. No response to olfactory bulb stimulation was monosynaptic. In stable impalements, 29 neurons discharged spontaneously in the absence of applied current. Lucifer Yellow and Neurobiotin were used to label 16 cells. All but one had smooth dendrites with soma diameters ranging from 8 to 24 microm. These results provide a framework in which magnocellular preoptic neurons can influence olfactory processing by direct action on the olfactory bulb, which action can be boosted by positive feedback from the bulb through the olfactory piriform and entorhinal cortices.

Animals↗

PubMed1995

Distribution of six transplasma membrane NADH-dehydrogenases in rat brain tissue.

Transplasma membrane redox plays a significant role in cellular activation and growth. Six isoenzymes could be prepared from purified rat brain synaptic plasma membrane. Polyclonal antibodies have been prepared against six transplasma membrane oxydoreductases (PMO-I to PMO-VI) and the tissue distribution of the various iso-enzymes have been investigated in adult rat brains by means of immunohistochemistry. PMO-I is densely observed in layers I, IV and V of the parietal cortex, in CA1 of the hippocampus (except for the molecular layer), in the caudate putamen, in the dorsal, granular and ventral parts of the auditory nuclei, in some loci of the vestibular nuclei as well as in the deep cerebellar nucleus and in the granular layer of the cerebellar cortex. PMO-II is mainly located in the polymorphic layer of the dentate gyrus and in the deep cerebellar nucleus and in the granular layer of the cerebellar cortex. PMO-III is abundant in the piriform cortex, in the pyramidal layers of both CA1 and CA2, in the diagonal band of the basal ganglia, in the supraoptic nucleus and in various loci of the magnetocellular paraventricular nucleus of the hippothalamus as well as in the vestibular nuclei from the brain stem. In addition PMO-III is also densely present in motor nuclei (oculomotor, facial, hypoglossal and ambiguus nuclei), in the reticular formation and in the deep cerebellar nucleus as well as in the Purkinje layer of the cerebellar cortex. PMO-IV has a similar location but is less abundant in the vestibular nuclei of the sensory brain stem and in the motor nucleus. PMO-V in contrast is poorly present in most brain areas compared to the other iso-enzymes, apart of the Purkinje layer of the cerebellar cortex. Finally PMO-VI is mainly present in the oriens layer and in the stratum radiatum of the hippocampus formation, in the supraoptic and lateral magnocellular nucleus of the hypothalamus, in the mesencephalic trigeminal nucleus, in the ventral auditory nucleus and in the facial nucleus of the brain stem as well as in red nucleus of the reticular formation and in the Purkinje layer of the cerebellar cortex. These data show that the iso-enzymes are located in specific brain nuclei. The significance of the results in respect to the yet very poorly defined function of PMO's is discussed.

Animals↗

PubMed1993

Prominent expression of the actin-sequestering peptide Fx gene in the hippocampal region of rat brain.

We have analyzed by in situ hybridization the distribution of Fx (an actin-sequestering peptide) mRNA in the brain of young and old rats. The strongest Fx mRNA-specific hybridization signal was located in the hippocampo-entorhinal cortex; this mRNA was also found in the piriform cortex, amygdala, lateral septum and neocortex. Northern blot analysis confirmed the prominent expression of the Fx transcript in the hippocampus and showed a notably lower amount of this mRNA in the hippocampus of old rats suggesting an influence of aging on the expression of this gene. The possible implication of Fx in synaptic plasticity and in long-term potentiation is discussed.

Aging↗

PubMed1997

Region-specific developmental patterns of atrial natriuretic factor- and nitric oxide-activated guanylyl cyclases in the postnatal frontal rat brain.

In the rat central nervous system, cyclic GMP can be produced by two isoforms of guanylyl cyclase: a cytosolic isoform, which is activated by nitric oxide, and a membrane-bound isoform, activated by atrial natriuretic factor. We studied the development of guanylyl cyclase activity upon maturation of the rat forebrain from postnatal days 4 to 24, using a combined immunocytochemical and biochemical approach. Atrial natriuretic factor-activated particulate guanylyl cyclase activity was found to decrease in the frontal cortex, in the lateral septum and in the piriform cortex upon maturation. A transient expression of atrial natriuretic factor-sensitive guanylyl cyclase activity was observed at postnatal day 8 in the caudate putamen complex, whereas an increase was observed in the lateral olfactory tract from postnatal days 8 to 24. Biochemical and immunocytochemical studies using the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester, or the inhibitor of soluble guanylyl cyclase 1H-[1,2,4]oxadiazolo[4,3-a]quinaloxin-1-one, indicated high levels of endogenous nitric oxide release at postnatal days 4 and 8. This activity decreased strongly in all brain areas examined. From postnatal day 8 onwards, atrial natriuretic factor-responsive cyclic GMP-immunoreactive cells could be characterized as astrocytes, with the exception of those in the the lateral olfactory tract, where the myelinated fibers became cyclic GMP producing. Furthermore, our results on activation of both guanylyl cyclases at postnatal day 8 leads to the suggestion that both isoforms might be found in the same cells. This study shows that there are pronounced differences between various frontal brain areas in the development of the responsiveness of both the particulate and soluble isoforms of guanylyl cyclase, and lends further support to the hypothesis that natriuretic peptides have a role in neuronal growth and plasticity of the rat brain.

1-Methyl-3-isobutylxanthine↗