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PubMed2002

Exposure to short-lasting impulse noise causes neuronal c-Jun expression and induction of apoptosis in the adult rat brain.

Exposure to impulse noise, above a certain intensity, is harmful to auditory function. Effects of impulse noise on the central nervous system (CNS) are largely unexplored, and there is little information on critical threshold values and time factors. We have recently shown that neurofilament proteins are affected in the cerebral cortex and the hippocampus. Now we show that impulse noise induces expression of the immediate early gene c-Jun products, proposed to play a role in the initiation of neuronal death, and apoptosis as revealed by TUNEL staining. Rat brains were investigated immunohistochemically 2 h to 21 days after exposure to impulse noise of 198 dB or 202 dB. c-Jun was expressed in neuronal perikarya in layers II-VI of the temporal cortex, the cingulate and the piriform cortices at 2 h to 21 days after both exposure levels. Granule neurons of the dentate gyrus and the CA1-3 in the hippocampus pyramidal neurons were similarly affected. The elevated expression of c-Jun products remained high at all postexposure times. TUNEL staining was positive among the same nerve cell populations 6 h after exposure and persisted even at 7 days at both exposure levels.

Animals↗

PubMed1990

Corticotropin-releasing factor receptors in the rabbit brain visualized by in vitro autoradiography.

Corticotropin-releasing factor (CRF) binding sites were visualized in the rabbit brain by in vitro autoradiography using the radioligand 125I-[Tyr0]ovine CRF. The radioligand binding to sections of rabbit cingulate cortex were competed for by ovine and rat CRF with inhibitory constants (Ki) of 26 and 37 nM, respectively, whereas sauvagine and alpha-helical CRF9-41 were approximately 10-fold less potent. In the rabbit brain, the highest densities of binding sites for CRF are found in the pineal gland and the choroid plexus. The cerebral cortex is labelled throughout, with the highest concentration of binding sites in the piriform and primary olfactory divisions. In the cerebellar cortex, the granular layer is more intensely labelled than the molecular layer. The distribution of CRF binding sites in the hippocampus follows a laminar pattern; the molecular layer of the dentate gyrus is intensely labelled, the oriens, radiatum and lacunosum moleculare layers of Ammon's horn contain moderate densities of binding and no binding is observed in the granular layer of the dentate gyrus and the pyramidal cell layer. The ventral subnucleus of the lateral septum, the zonal and superficial layers of the superior colliculus contain high densities of receptors. A moderate concentration of binding sites is observed in the caudate nucleus, putamen, bed nucleus of the stria terminalis, paraventricular, anterodorsal and anteroventral thalamic nuclei and the medial nucleus of the mammillary body.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2001

Effects of protracted nicotine exposure and withdrawal on the expression and phosphorylation of the CREB gene transcription factor in rat brain.

Addiction to nicotine may result in molecular adaptations in the neurocircuitry of specific brain structures via changes in the cyclic AMP-responsive element binding protein (CREB)-dependent gene transcription program. We therefore investigated the effects of chronic nicotine exposure and its withdrawal on CREB and phosphorylated CREB (p-CREB) protein levels in the rat brain. We report here that chronic nicotine exposure (1-h withdrawal) had no effect on the expression of CREB and p-CREB in the rat cortex and amygdala. On the other hand, decreases in the expression of CREB protein and phosphorylation of CREB occur in the cingulate gyrus, and in the parietal and the piriform but not in the frontal cortex during nicotine withdrawal (18 h) after nicotine exposure. It was also observed that CREB and p-CREB protein levels were significantly decreased in the medial and basolateral, but not in the central amygdala during nicotine withdrawal (18 h) after chronic nicotine exposure. Furthermore, it was found that nicotine withdrawal (18 h) after chronic nicotine exposure leads to decreased CRE-DNA binding without modulating cAMP-dependent protein kinase A activity in the cortex and the amygdala of rats. In addition, chronic nicotine treatment produced anxiolytic effects whereas nicotine withdrawal (18 h) produced anxiety in rats as measured by the elevated plus-maze test. These results provide the first evidence that decreased CREB activity and/or expression in specific cortical and amygdaloid brain structures may be involved in the underlying molecular mechanisms of nicotine dependence.

Amygdala↗

PubMed1989

Differential projection from the motor and limbic cortical regions to the mediodorsal thalamic nucleus in the dog.

The cortical afferents to the mediodorsal thalamic nucleus in the dog were studied by using horseradish peroxidase. Small injections allowed to establish two specific projection zones connected separately with the lateral and medial segments of the nucleus. The lateral segment received the major projection from the dorsal half of the hemisphere. It included premotor and part of the motor cortices in the anterior sigmoid gyrus and precruciate areas as well as the presylvian cortex. The medial segment of the nucleus was innervated by the limbic areas of the ventral half of the hemisphere. These areas included the medioventrally located genual, subcallosal and piriform cortices, as well as the cortex of the ventral bank of the anterior rhinal sulcus and the caudal part of the orbital gyrus. The cortical fields situated between these two main cortical zones, both on the lateral and medial surfaces (rhinal and sylvian sulci and anterior cingular gyrus, respectively) sent projections to both medial and lateral segments of the nucleus. These results indicate that in the mediodorsal thalamic nucleus may take place the integration of information from two functionally defined systems, the motor and limbic ones.

Animals↗

PubMed1998

Effects of prolactin on expression of the mRNAs encoding the immediate early genes zif/268 (NGF1-A), nur/77 (NGF1-B), c-fos and c-jun in the hypothalamus.

Prolactin (PRL) exerts a short-loop negative feedback effect on hypothalamic neurons which control its secretion from the anterior pituitary gland. The purpose of this study was to identify the location of hypothalamic neurons which respond to acute PRL exposure. Increasing evidence indicates that excitation of neurons often results in the rapid transcription of immediate early genes (IEGs). In the present study, quantitative in situ hybridization histochemistry (ISHH) was used to visualize the induction of mRNAs for four different IEGs: zif/268 (NGF1-A), nur/77 (NGF1-B), c-fos and c-jun. Three groups of male rats were compared: unmanipulated controls, rats injected s.c. with 2.4 mg ovine PRL (oPRL) suspended in polyvinylpyrrolidone (PVP), and PVP-injected controls. Animals were decapitated 0, 0.5, 1, 2, 3 or 4 h following injection. In all rats, the four probes labeled cells within the cortex, particularly the cingulate and piriform cortices, the hippocampus and the striatum. In the arcuate nucleus, there was a modest increase in the average number of cells/animal which expressed zif/268 mRNA following the injection of PVP and oPRL at all times studied. The average area of grains/cell representing zif/268 message also increased following the injection stimulus. The number of neurons expressing nur/77 mRNA was greater in PRL-treated rats compared with PVP-treated controls 0.5 and 1 h following injection. Nur/77-labeled neurons were co-extensive with the tuberoinfundibular dopaminergic (TIDA) neurons. The data suggest that cells located within the arcuate nucleus are involved in mediating PRL autofeedback on the brain.

Animals↗

PubMed1989

Dopamine D2 receptors labeled with [3H]raclopride in rat and rabbit brains. Equilibrium binding, kinetics, distribution and selectivity.

The binding properties of the substituted benzamide raclopride to dopamine D2 receptors were studied with membrane preparations from rat and rabbit neostriatum. An analysis of the association kinetics suggested a single binding site but the data from the dissociation experiments were better described by a two-site model. Examination of saturation curves at equilibrium revealed a single class of binding sites in the neostriatum from both species (rat: maximum binding capacity (Bmax) = 247 fmol/mg of protein; rabbit: Bmax = 337 fmol/mg of protein). In cortical regions known to possess a distinct dopaminergic innervation (piriform-entorhinal areas and cingulate cortex) the Bmax values ranged between 9 and 22 fmol/mg of protein. [3H]Raclopride binding sites (less than 12 fmol/mg of protein) were also detectable in the dorsal and ventral hippocampus as well as in the somatosensory and visual cortices. The selectivity in the neostriatum was examined by competition experiments with dopaminergic drugs. The rank of potency of agonists and antagonists to displace [3H]raclopride binding revealed its selectivity for the dopamine D2 receptor and was essentially the same for both species. Antagonist competition curves could be fitted to a single site but inhibition by agonists was better described assuming a two-site model. The stereospecificity of binding was demonstrated by the use of the enantiomer pairs. These results validate the utilization of the novel benzamide [3H]raclopride as a selective marker of dopamine D2 receptors.

Animals↗

PubMed1988

[Localization of alcohol and aldehyde dehydrogenases in the human spinal cord and brain].

Location of aldehyde dehydrogenase (AldDG) and alcohol dehydrogenase (ADG) has been studied in 38 nuclei of the human brain. Neurons with a high AldDG activity predominate in the nucleus of the descending root of the trigeminal nerve, motor nuclei of the craniocerebral nerves (trigeminal, facial, abducent, blocking, sublingual, supraspinal), motor nuclei of the anterior horns of the spinal cord, lateral vestibular nucleus, posterior nucleus of the vagus nerve, pedunculopontine nucleus, superior salivary nucleus, and in the nucleus of Westphal-Edinger-Jacobovich. Neurons with a moderate AldDG activity predominate in the superior olivary complex, nucleus of the lateral loop, parabrachial (pigmented) mesencephalic nucleus and reticular lateral nucleus. A low enzymatic activity is specific for neurons of the pons proper, inferior vestibular nucleus, trapezoid body of the inferior olivary complex, dentate nucleus of the cerebellum, reticular nucleus of the tegmen of Bekhterev's pons and posterior nucleus of Gudden's suture. A high ADG activity is revealed in piriform neurons of the cerebellar cortex. Functional importance of ADG and AldDG activity in the brain is discussed.

Adult↗

PubMed1997

Transient developmental expression of CD15 in the motor and auditory cortex of the mouse.

The distribution of the glycoprotein CD15 (FAL, SSEA-1, Le(x)) in the developing cortex of the mouse has been examined by immunohistochemistry of paraffin sections. The pattern of CD15 immunoreactivity was observed to occur in 4 stages. In the first stage, the presumptive subplate region in the lateral and rostral parts of the developing isocortex was transiently labelled at E12. In the second stage, between E13 and E17, very faint label was found only in the ventricular germinal zone, possibly within radial glial fibres. The third stage began at E18, when transient labelling of several discrete cortical areas was apparent; the motor cortex (from E18 to P3), an area in the temporal lobe (presumptive primary auditory cortex; from E18 to P5.5) and the piriform and entorhinal cortices (from E18 to P3). The final stage began at P2, when a mosaic camouflage pattern of labelling started to appear throughout the developing cortex, particularly in layer I. The distribution of the transient label in the motor cortex during the perinatal period suggests that it may be associated with early events in corticospinal or other projection neuron maturation (apical dendrite growth and differentiation). The labelling in the presumptive auditory cortex (Te1) may also be involved in the differentiation of neurons in the upper cortical plate.

Aging↗

PubMed2000

Blast exposure causes redistribution of phosphorylated neurofilament subunits in neurons of the adult rat brain.

There is little information on threshold levels and critical time factors for blast exposures, although brain damage after a blast has been established both clinically and experimentally. Moreover, the cellular pathophysiology of the brain response is poorly characterized. This study employs a rat model for blast exposure to investigate effects on the neuronal cytoskeleton. Exposure in the range of 154 kPa/198 dB or 240 kPa/202 dB has previously been shown neither to cause visual damage to the brain, nor to affect the neuronal populations, as revealed with routine histology. Here, the brains were investigated immunohistochemically from 2 h to 21 days after blast exposure. A monoclonal antibody was used which detects only the phosphorylated epitope of the heavy subunit of the neurofilament proteins (p-NFH). This epitope is normally restricted to axons, that is, not demonstrable in the perikarya. Eighteen hours after exposure in the 240-kPa/202-dB range, p-NFH immunoreactivity accumulated in neuronal perikarya in layers II-IV of the temporal cortex and of the cingulate and the piriform cortices, the dentate gyrus and the CA1 region of the hippocampus. At the same time, the p-NFH immunoreactivity disappeared from the axons and dendrites of cerebral cortex neurons. The most pronounced immunostaining of neuronal perikarya was found in the hemisphere, which faced the blast source. The perikaryal accumulation of p-NFH was present also at 7 days but the neuronal perikarya had become negative at 21 days, at which time the axons again displayed p-NFH immunoreactivity. Exposure in the range of 154 kPa/198 dB caused similar, although less marked accumulation of p-NFH immunoreactivity in the neuronal perikarya. The findings are interpreted to show a dephosphorylation of NFHs in axons and dendrites and a piling up of p-NFHs in the perikarya due to disturbed axonal transport.

Animals↗

PubMed1981

Olfactory bulb projections to the parahippocampal area of the rat.

Recent evidence suggests that the main olfactory bulb projects caudally beyond the prepiriform cortex and the cortical amygdaloid nuclei to the region of the piriform lobe called the parahippocampal area. Included within this area is the entorhinal cortex, which is composed of six major subdivisions. Since questions remain as to which of these subdivisions receives centripetal fibers from the bulb, we reexamined these projections using autoradiography and HRP histochemistry and correlated the sites of termination with the cytoarchitecture of the entorhinal cortex. The results indicate that olfactory bulb axons reach all parts of the parahippocampal area, including the cortex which forms the medial and lateral banks of the amygdaloid sulcus (area TR), and both subdivisions of the laterally located entorhinal cortex (28L' and 28L). Also, label is observed over the more medially located fields of the entorhinal cortex, including the cortex posterior to the cortical amygdaloid nucleus (28M'), as well as the ventrolateral parts of medial entorhinal cortex (28M). In addition, evidence of label occurs over the full extent of the transition zone (28i) which separates areas 28L and 28M. These results suggest that the olfactory bulb has a more extensive projection to the parahippocampal area in the rat than previously thought, and may provide at least some input to all of the parahippocampal areas which project to the hippocampal formation.

Animals↗

PubMed1994

Ultrastructural features of the isolated guinea-pig brain maintained in vitro by arterial perfusion.

The morphological features of cerebral tissue in the isolated guinea-pig brain maintained in vitro by arterial perfusion are described. Light and electron microscopic analysis of the thalamus, the somatosensory cortex and the limbic cortices (hippocampus, piriform and entorhinal cortices) was performed after different periods of incubation in vitro (1, 7 and 12 h), in parallel with an electrophysiological study. The morphological analysis showed that neuronal elements retained their normal appearance at both cellular and subcellular level in the examined brain regions up to an incubation period of 12 h. Immunoreactivity for GABA was also preserved for up to 12 h of in vitro perfusion. Vasogenic edema and perivascular extracellular swelling appeared after 7 h, together with signs of progressive astrocytic deterioration. These findings show that normal electrophysiological recordings correlate with good anatomical preservation of the isolated guinea-pig brain preparation after prolonged times of arterial in vitro perfusion.

Animals↗

PubMed2000

Convulsive effects of thiophene, a heterocyclic hydrocarbon: behavioral, electrographic and c-Fos immunocytochemical studies.

The behavioral, electrographic and histopathological changes induced by the heterocyclic hydrocarbon thiophene were investigated in rats following intramuscular injection of 0.3 mL thiophene for 5 days. Generalized convulsions were noted in 29 out of 34 animals (85%) between 1 and 28 h after the final dose. Electroencephalography revealed that the discharges in the hippocampus and forebrain occurred simultaneously, although epileptic activity emerged more strongly from the hippocampus than from any other region. Neuron damage was detected histologically in the temporal and parietal neocortex, piriform gyrus, amygdaloid nucleus and cerebellar cortex, but not in the hippocampus. In contrast, c-Fos was induced widely in the cerebral cortex and hippocampus, and was most marked in the dentate gyrus. These findings suggest that the hippocampus plays a crucial role in seizure onset following thiophene injection.

Animals↗

PubMed1985

The afferent connections of the substantia innominata in the monkey, Macaca fascicularis.

The afferent connections of the substantia innominata and the magnocellular nuclei within it (the nucleus of the horizontal limb of the diagonal band, NHDB, and the nucleus basalis of Meynert, NBM) have been studied with anterograde and retrograde axonal tracing techniques. Prominent inputs arise in the amygdaloid complex, restricted areas of the cerebral cortex, parts of the thalamus and hypothalamus, and nuclei of the lower brainstem. Autoradiographic tracing experiments indicate that the amygdaloid fibers are distributed throughout the NHDB and the NBM, and to a lesser extent to the ventral pallidum. Relatively few fibers innervate the more medially located nucleus of the vertical limb of the diagonal band (NVDB) and the medial septal nucleus. Visualization of the amygdalofugal fibers with the tracer PHA-L (Phaseolus vulgaris leuco-agglutinin) shows that they have varicosities resembling boutons en passant along their length in the substantia innominata. Retrograde tracing experiments using WGA-HRP indicate that the cells of origin of the projection from the amygdala are concentrated in the parvicellular basal nucleus, the caudal part of the magnocellular basal nucleus, the magnocellular accessory basal nucleus, and the central nucleus. Relatively few fibers to the substantia innominata arise in the rostrodorsal part of the magnocellular basal nucleus, or in the lateral or parvicellular accessory basal nuclei. Cortical cells projecting to the substantia innominata were retrogradely labeled in the orbitofrontal cortex (including areas 11-14 and 25), the rostral insula (especially the agranular area), the rostroventral temporal cortex (including areas 35, 36, and parts of TG and TE), and the piriform and entorhinal cortices. The projections from the orbital and rostral temporal cortex were confirmed with anterograde tracers. Projections to the substantia innominata were not found from the more lateral, dorsal or caudal parts of the cerebral cortex, although fibers from temporal area TA may pass through the dendritic field of the most caudal cells of the NBM. Diencephalic cells projecting to the substantia innominata are distributed diffusely throughout the preoptic area and hypothalamus, with higher concentration in the lateral preoptic area and in the pre-, supra-, and tubero-mammillary nuclei. Cells are also found in the midline thalamic nuclei and in the region between the peripeduncular and subparafascicular nuclei.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗

PubMed2001

Topology of ionotropic glutamate receptors in brains of heterozygous and homozygous weaver mutant mice.

In weaver mice, mutation of a G-protein inwardly rectifying K(+) channel leads to a cerebellar developmental anomaly characterized by granule and Purkinje cell loss and, in addition, degeneration of dopaminergic neurons. To evaluate other deficits, ionotropic glutamate receptors sensitive to N-methyl-D-aspartate (NMDA), amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), and kainic acid (KA) were examined by autoradiography with [(3)H]MK-801, [(3)H]AMPA, and [(3)H]KA. These surveys were carried out in selected areas of cerebral cortex, hippocampus and related limbic regions, basal ganglia, thalamus, hypothalamus, brainstem, and cerebellum from heterozygous (wv/+) and homozygous (wv/wv) weaver mutants, and compared to wild-type (+/+) mice. In wv/+ and wv/wv mutants, NMDA receptor levels were lower in cortical areas, septum, hippocampus, subiculum, neostriatum, nucleus accumbens, superior colliculus, and in the cerebellar granular layer. Densities of KA receptors were lower in cortical areas, hippocampus, limbic system structures, neostriatum, nucleus accumbens, thalamus and hypothalamus, superior and inferior colliculi, and cerebellar cortex of wv/wv mutants. Levels of AMPA receptors in the weaver were higher than in +/+ mice, particularly in somatosensory and piriform cortices and periaqueductal gray of wv/+, and in somatosensory cortex, CA1 field of Ammon's horn and cerebellar granular layer of wv/wv. Abnormal developmental signals, aberrant cellular responses, or a distorted balance between neurotransmitter interactions may underlie such widespread and reciprocal glutamate receptor alterations, while in the case of cerebellar cortex, NMDA receptors are lacking due to a massive disappearance of cerebellar granule cells and some loss of Purkinje neurons.

Animals↗

PubMed1982

Convergence of autonomic and limbic connections in the insular cortex of the rat.

The connections of the insular cortex in the rat were studied by using the anterograde and retrograde transport of wheat germ agglutinin-conjugated-horseradish peroxidase. Both anterograde and retrograde transport were seen in the ipsilateral lateral frontal, infralimbic, piriform, and perirhinal cortical areas and in the contralateral insular cortex. In the thalamus, both types of labeling were seen in the mediodorsal and ventroposteromedial parvocellular nuclei; primarily retrograde labeling was seen in the centromedial and paracentral nuclei. In the basal forebrain, anterograde labeling was seen in the lateral part of the bed nucleus of the stria terminalis and in the central nucleus of the amygdala, while retrogradely labeled neurons were found in the magnocellular basal nucleus and in the lateral and the basolateral amygdaloid nuclei. Both types of labeling were seen in the posterior lateral hypothalamic area; the tuberomammillary nucleus contained retrogradely labeled neurons bilaterally. In the midbrain, retrogradely labeled neurons were found in the ventral tegmental area and in the dorsal and superior central raphe nuclei. In the pons, both retrogradely and anterogradely transported label was seen bilaterally in the parabrachial nucleus, primarily in the ventromedial caudal part of the medial subnucleus. Retrogradely labeled neurons were found bilaterally in the locus coeruleus. Anterograde transport was followed into the medulla, bilaterally but more heavily in the contralateral side. Labeled axons appeared to terminate in a topographic pattern in the nucleus of the solitary tract. These results indicate that the insular cortex of the rat is an important part of the highly interconnected central autonomic system. Furthermore, the autonomic representation in the insular cortex may be organized in a viscerotopic manner. The insular cortex also has connections with the limbic system and with the lateral frontal cortical system. Although it is not yet clear whether these connections converge upon the same neurons within the insular cortex, earlier physiological data suggest that each of the diverse systems of connections of this area receives relayed vagal inputs. The insular cortex of the rat may contain a primary cortical visceral representation, and its connections may underlie autonomic integration with behavioral and emotional events.

Amygdala↗

PubMed1996

Neuronal degeneration in rat cerebrocortical and olfactory regions during subchronic "binge" intoxication with ethanol: possible explanation for olfactory deficits in alcoholics.

Severe, repetitive ("binge") ethanol intoxication in adult rats (intragastric delivery 3 times daily for 4 days in a modification of the Majchrowicz method) precipitates neuronal degeneration in selected cerebral cortical regions involved in memory and olfaction, confirming the results of Switzer and colleagues (Anat. Rec. 202: 186a, 1982). Neuronal damage was visualized with the de Olmos cupric silver technique for degenerating neurons and processes (argyrophilia), and was quantitated by total counts and densities of argyrophilic cells/fields. The specificity of the degeneration provides a neuropathological basis for the olfactory memory deficits in chronic alcoholics. In highly intoxicated rats, argyrophilia was most extensive among hippocampal dentate gyrus granule cells, pyramidal neurons in layer 3 of the entorhinal cortex, and olfactory nerve terminals in the olfactory bulb. Degenerating pyramidal neurons were also consistently seen in the insular cortex and olfactory cortical regions, such as the piriform and perirhinal cortices. There were few argyrophilic neurons in the CA regions of the hippocampus and none in the cerebellum--regions generally shown to have cell loss in long-term ethanol feeding models--but degenerating mossy fibers in the CA2 region were observed. Degeneration was maximal before the peak period of abstinence symptoms in this model, because argyrophilic densities were no greater 36 hr, compared with 8 hr after the last ethanol dose. High blood ethanol levels were required, because argyrophilia, absent from isocaloric controls, also was only evident in ethanol-intoxicated rats with mean blood ethanol levels for days 2 to 4 above 300 mg/dl; however, it increased substantially between 350 and 550 mg/dl. The resemblance of the argyrophilic distribution to the regional neuropathology that occurs in experimental seizures indicates that the ethanol-induced degeneration may have an excitotoxic basis. Progressive reductions in the seizure threshold (e.g., kindling phenomena that have been documented during binge ethanol intoxication) might be associated with excitotoxic hyperactivity during the repetitive nadirs between high blood and brain ethanol peaks. However, direct toxic actions of ethanol or its metabolites could also be involved. Overall, the model should be useful for studying mechanisms of ethanol-induced selective cortical and olfactory brain damage.

Alcoholic Intoxication↗

PubMed1994

The contralaterally projecting neurons of the isthmic nucleus in five anuran species: a retrograde tracing study with HRP and cobalt.

The morphology of projection neurons of the isthmic nucleus was studied in Rana esculenta, R. nigromaculata, Bufo marinus, B. bufo gargarizans, and Xenopus laevis from a comparative anatomical point of view. The main point of this work was to provide an anatomical basis for electrophysiological studies. Neurons projecting to the ipsilateral optic tectum were labeled by retrograde transport of horseradish peroxidase and cobaltous lysine complex injected into the optic tectum. Contralaterally projecting cells were filled by injecting the tracer substances into the crossed isthmotectal tract. Cells of the anterior nonrim cortex and the rostral part of the medulla project to the ipsilateral tectum. A band of cells in the middle of the medulla, a few cells in the caudal part of the medulla, and most of the neurons in the rim cortex project to the contralateral tectum. Five types of neurons were distinguished in the rim cortex of R. esculenta. Most of them have piriform perikarya and their dendrites arborize in the rim neuropil. In the medulla of the isthmic nucleus of R. esculenta, seven types of neurons were distinguished. Most of these neurons also exist in the other species. Medullary cells are piriform, fusiform, or multipolar, and are variable in size and in dendritic arborization. The isthmic neurons of the two Ranae and Bufo species are similar. The dominant cell types in Xenopus are multipolar with extensive dendritic arborization, which occupies more space in the nucleus than in the other species. Neurons with narrow dendritic trees may represent a system of fine resolution, and those neurons with extensive dendritic arborization may belong to a coarser system.

Animals↗

PubMed1995

Distribution of preproenkephalin messenger RNA in the basal ganglia and limbic-associated regions of the monkey telencephalon.

We studied the distribution of preproenkephalin messenger RNA in the monkey forebrain, using a free-floating method for in situ hybridization histochemistry. Autoradiographs reveal a high level of specific hybridization to preproenkephalin messenger RNA in the monkey striatum and forebrain regions. In the monkey striatum, the distribution of preproenkephalin messenger RNA is heterogeneous. There is variation in the general labeling pattern between regions of the striatum. For example, a particularly densely labeled area of preproenkephalin messenger RNA is observed in the ventral part of the caudal putamen. In addition, at the macroscopic level, there are patches of specific hybridization intermingled with areas containing less specific labeling. This forms a mosaic-like pattern. At the microscopic level, densely labeled individual cells are found among those with little or no specific labeling. Adjacent sections, processed for in situ hybridization and immunohistochemistry, show some correlation between the perikarya containing preproenkephalin messenger RNA and enkephalin-positive fibers in the striatum. Specific hybridization to preproenkephalin messenger RNA is evident throughout the cortical mantle, primarily concentrated in layers 2 and 3. Particularly high levels of preproenkephalin messenger RNA are found in specific limbic-associated cortices, including the piriform allocortex, the agranular area of the orbitofrontal cortex, the agranular insular cortex and the caudal field of the entorhinal cortex. Specific labeling is also present in the granular cell layer of the dentate gyrus and in the amygdaloid complex. This study reveals heterogeneous distribution of dense preproenkephalin messenger RNA in the basal ganglia and high levels of preproenkephalin messenger RNA in specific limbic-associated regions of the monkey telencephalon.

Animals↗