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A segmental map of architectonic subdivisions in the diencephalon of the frog Rana perezi: acetylcholinesterase-histochemical observations.

The work examines frog diencephalic subdivisions from a segmental viewpoint and adds a number of details to the atlas of the bullfrog diencephalon reported by Neary and Northcutt [1983]. Acetylcholinesterase histochemistry was performed on brains of Rana perezi, sectioned either sagittally or in a plane roughly parallel to the optic tract to optimize detection of segmented landmarks. This material provided a very detailed picture of individual neurons, neuropils and some fiber tracts expressing the enzyme in diverse patterns characteristic for each diencephalic region. The main diencephalic areas previously recognized in the bullfrog appeared subdivided into smaller AChE-chemoarchitectonic units. Modified subdivisions are proposed for several entities: preoptic, suprachiasmatic, entopeduncular, ventral thalamic, anterior thalamic, pretectal, hypothalamic and tuberculum posterior regions. A number of cell groups are described for the first time in frogs. This mapping is expected to be useful for the interpretation of immunocytochemical and experimental hodologic results in the diencephalon of frogs and opens new possibilities for comparative analysis.

Acetylcholinesterase↗

Ontogeny of thyrotropin-releasing hormone gene expression in the rat diencephalon.

The development of thyrotropin-releasing hormone (TRH) gene expression in the rat diencephalon was studied using in situ hybridization histochemistry. The first neurons expressing the TRH gene were found on gestational day 14 (E14) in the lateral hypothalamus, shortly after completion of their last cell division. On E15 and E16, additional labeled cells appeared medially in the developing dorsomedial and paraventricular nuclei, respectively, followed on E17 by cells in the preoptic area. The number of labeled cells in the hypothalamus continued to increase during the last part of gestation. At birth, TRH mRNA neurons were present in all the locations seen in the adult hypothalamus. During the first week of life, the labeling intensity and number of neurons containing TRH mRNA continued to increase at the locations described above. TRH mRNA was not detected in the reticular thalamic nucleus until the 7th postnatal day when some labeled cells appeared in its dorsocaudal portion. Over the next 10 days, the number of labeled cells and the intensity of labeling in the thalamic reticular nucleus progressively increased. During the same period of time, only small changes in the number and intensity of labeled cells in the hypothalamus were seen. On the 21st postnatal day, after a decrease in labeling in the lateral hypothalamus had been noted, final adult patterns of expression were present. With the very sensitive and anatomically specific method of in situ hybridization histochemistry, the ontogeny of TRH gene expression in the rat diencephalon has been elucidated.

Age Factors↗

Glucocorticoid regulation of rat diencephalon angiotensinogen production.

To investigate whether glucocorticoids can stimulate rat brain angiotensinogen production directly, we have studied the effect of dexamethasone on angiotensinogen secretion and angiotensinogen mRNA concentration in primary astroglial cultures from rat diencephalon. Dexamethasone stimulated angiotensinogen secretion by astroglial cells in a dose-related fashion. The half-maximally effective concentration was 11 nM, and the effect was blocked by RU 486, an antagonist of type II glucocorticoid receptors. This was similar to what was observed in rat hepatoma H4IIEC cells, where the half-maximally effective concentration of dexamethasone on angiotensinogen secretion was 10 nM. At maximal concentrations, dexamethasone increased angiotensinogen secretion and angiotensinogen mRNA concentration 2-fold in astroglial cells. In the hepatoma cells, however, the increase in angiotensinogen secretion was 5-fold. The in vivo diencephalon angiotensinogen mRNA concentration was decreased after adrenalectomy. Dexamethasone restored those levels to normal and induced a modest increase when the animals were killed 6 h after drug administration. In contrast, dexamethasone induced a robust increase in liver angiotensinogen mRNA concentration in the same animals. These results indicate that glucocorticoids increase angiotensinogen production through a direct receptor-mediated mechanism in both liver and brain. However, the angiotensinogen gene appears much more responsive to the action of glucocorticoids in liver than in brain.

Adrenalectomy↗

Topography and associations of leu-enkephalin and luteinizing hormone-releasing hormone neuronal systems in the human diencephalon.

Although several studies indicated that leu-enkephalin controls gonadal function, the morphological substrate of this modulation is unknown. To reveal potential interaction sites between leu-enkephalin and LH-releasing hormone (LHRH) in the hypothalamus, the distribution and connections of leu-enkephalin-immunoreactive (IR) and LHRH-IR systems were examined in the human diencephalon using double-label immunohistochemistry. First the leu-enkephalin-IR and LHRH-IR neural elements were mapped, then the maps of the two different neurotransmitter systems were superimposed unveiling the overlapping areas. The putative juxtapositions between leu-enkephalin-IR and LHRH-IR structures were revealed with double label immunocytochemistry. Close contacts were detected in the medial preoptic area and in the infundibulum/median eminence. In these areas, diaminobenzidine-silver-intensified, black leu-enkephalin-IR fibers abutted fusiform, brown, diaminobenzidine-labeled LHRH neurons often forming multiple contacts. Examination of semithin sections of these close associations with the aid of oil immersion revealed no cleft between the contacting LHRH-IR and leu-enkephalin-IR elements. Our findings indicate that the juxtapositions between LHRH-IR and leu enkephalin-IR neurons may be functional synapses forming the morphological substrate of the leu-enkephalin-modulated LHRH secretion in the human diencephalon. Moreover, the wide distribution of leu-enkephalin-IR elements suggests leu-enkephalin control of other diencephalic functions as well.

Adult↗

Catecholaminergic axons innervate LH-releasing hormone immunoreactive neurons of the human diencephalon.

Catecholamines have been shown to modulate gonadal functions via interactions with hypothalamic LH-releasing hormone (LHRH)-synthesizing neurons. To reveal the morphological background of this phenomenon, the distribution of LHRH neurons and tyrosine hydroxylase (TH)-immunoreactive (IR), catecholaminergic structures were mapped in the human diencephalon. First, the location of LHRH and TH-IR neuronal elements was analyzed, and then the relationship between the two different systems was examined. The LHRH-IR cell bodies were mainly present in the medial preoptic and infundibular areas. The TH-IR perikarya were located in the periventricular, paraventricular, and supraoptic hypothalamic nuclei and also in the median eminence. The TH-IR fibers were numerous in septal, infundibular, periventricular, and lateral hypothalamic regions. The brown, diaminobenzidine-labeled LHRH-containing perikarya were found to receive black, silver-intensified, TH-positive axon terminals in the infundibular and medial preoptic areas. However, in the preoptic and caudal parts of the diencephalon, only a few juxtapositions were noted. The present results indicate that hormone released from diencephalic LHRH-IR neurons in humans may be influenced by the central catecholaminergic system via direct synaptic mechanisms.

Adult↗

The parapineal mediates left-right asymmetry in the zebrafish diencephalon.

The dorsal diencephalon (or epithalamus) of larval zebrafish displays distinct left-right asymmetries. The pineal complex consists of the pineal organ anlage and an unpaired, left-sided accessory organ - the parapineal. The neighboring brain nuclei, the left and right dorsal habenulae, show consistent differences in their size, density of neuropil and gene expression. Mutational analyses demonstrate a correlation between the left-right position of the parapineal and the laterality of the habenular nuclei. We show that selective ablation of the parapineal organ results in the loss of habenular asymmetry. The left-sided parapineal therefore influences the left-right identity of adjacent brain nuclei, indicating that laterality of the dorsal diencephalon arises in a step-wise fashion.

Animals↗

Msx1 is required for dorsal diencephalon patterning.

The dorsal midline of the neural tube has recently emerged as a major signaling center for dorsoventral patterning. Msx genes are expressed at the dorsal midline, although their function at this site remains unknown. Using Msx1(nlacZ) mutant mice, we show that the normal expression domain of Msx1 is interrupted in the pretectum of mutant embryos. Morphological and gene expression data further indicate that a functional midline is not maintained along the whole prosomere 1 in Msx1 mutant mice. This results in the downregulation of genes expressed laterally to the midline in prosomere 1, confirming the importance of the midline as a signaling center. Wnt1 is essential for dorsoventral patterning of the neural tube. In the Msx1 mutant, Wnt1 is downregulated before the midline disappears, suggesting that its expression depends on Msx1. Furthermore, electroporation in the chick embryo demonstrates that Msx1 can induce Wnt1 expression in the diencephalon neuroepithelium and in the lateral ectoderm. In double Msx1/Msx2 mutants, Wnt1 expression is completely abolished at the dorsal midline of the diencephalon and rostral mesencephalon. This indicates that Msx genes may regulate Wnt1 expression at the dorsal midline of the neural tube. Based on these results, we propose a model in which Msx genes are intermediary between Bmp and Wnt at this site.

Animals↗

Fgf3 signaling from the ventral diencephalon is required for early specification and subsequent survival of the zebrafish adenohypophysis.

The pituitary gland consists of two major parts: the neurohypophysis, which is of neural origin; and the adenohypophysis, which is of non-neural ectodermal origin. Development of the adenohypophysis is governed by signaling proteins from the infundibulum, a ventral structure of the diencephalon that gives rise to the neurohypophysis. In mouse, the fibroblast growth factors Fgf8, Fgf10 and Fgf18 are thought to affect multiple processes of pituitary development: morphogenesis and patterning of the adenohypophyseal anlage; and survival, proliferation and differential specification of adenohypophyseal progenitor cells. Here, we investigate the role of Fgf3 during pituitary development in the zebrafish, analyzing lia/fgf3 null mutants. We show that Fgf3 signaling from the ventral diencephalon is required in a non-cell autonomous fashion to induce the expression of lim3, pit1 and other pituitary-specific genes in the underlying adenohypophyseal progenitor cells. Despite the absence of such early specification steps, fgf3 mutants continue to form a distinct pituitary anlage of normal size and shape, until adenohypophyseal cells die by apoptosis. We further show that Sonic Hedgehog (Shh) cannot rescue pituitary development, although it is able to induce adenohypophyseal cells in ectopic placodal regions of fgf3 mutants, indicating that Fgf3 does not act via Shh, and that Shh can act independently of Fgf3. In sum, our data suggest that Fgf3 signaling primarily promotes the transcriptional activation of genes regulating early specification steps of adenohypophyseal progenitor cells. This early specification seems to be essential for the subsequent survival of pituitary cells, but not for pituitary morphogenesis or pituitary cell proliferation.

Amino Acid Sequence↗

Cell migration in the developing chick diencephalon.

We previously reported that retrovirally marked clones in the mature chick diencephalon were widely dispersed in the mediolateral, dorsoventral and rostrocaudal planes. The current study was undertaken to define the migration routes that led to the dispersion. Embryos were infected between stages 10 and 14 with a retroviral stock encoding alkaline phosphatase and a library of molecular tags. Embryos were harvested 2.5-5.5 days later and the brains were fixed and serially sectioned. Sibling relationships were determined following PCR amplification and sequencing of the molecular tag. On embryonic day 4, all clones were organized in radial columns spanning the neuroepithelium, which was composed primarily of a ventricular zone at this age. No tangential migration was seen in the ventricular zone. On embryonic day 5, most clones remained radial with many cells located in the ventricular zone; however, a few clones had cells migrating perpendicular to the radial column, in either a rostrocaudal or dorsoventral direction. The tangential migration began just beyond the basal limit of the ventricular zone. On embryonic days 6 and 7, many clones had cells migrating perpendicular to the radial column, which spanned from the ventricular to the pial surface. The migrating cells appeared to be aligned along axes that were perpendicular to the radial column. Using a combination of DiI tracing, immunohistochemistry and electron microscopy, we have determined that axonal tracts are present and are aligned with the migrating cells, suggesting that they support the non-radial cell migration. These data indicate that migration along pathways independent of radial glia occur outside of the ventricular zone in more than 50% of the clones in the chick diencephalon.

Animals↗

The winged helix gene, Mf3, is required for normal development of the diencephalon and midbrain, postnatal growth and the milk-ejection reflex.

The mouse Mf3 gene, also known as Fkh5 and HFH-e5.1, encodes a winged helix/forkhead transcription factor. In the early embryo, transcripts for Mf3 are restricted to the presomitic mesoderm and anterior neurectoderm and mesoderm. By 9.5 days post coitum, expression in the nervous system is predominantly in the diencephalon, midbrain and neural tube. After midgestation, the highest level of mRNA is in the mammillary bodies, the posterior-most part of the hypothalamus. Mice homozygous for a deletion of the mf3 locus on a [129 x Black Swiss] background display variable phenotypes consistent with a requirement for the gene at several stages of embryonic and postnatal development. Approximately six percent of the mf3-/- embryos show an open neural tube in the diencephalon and midbrain region, and another five percent show a severe reduction of the posterior body axis; both these classes of affected embryos die in utero. Surviving homozygotes have an apparently normal phenotype at birth. Postnatally, however, mf3-/- pups are severely growth retarded and approximately one third die before weaning. This growth defect is not a direct result of lack of circulating growth hormone or thyrotropin. Mice that survive to weaning are healthy, but they show an abnormal clasping of the hindfeet when suspended by the tail. Although much smaller than normal, the mice are fertile. However, mf3-/- females cannot eject their milk supply to feed their pups. This nursing defect can be corrected with interperitoneal injections of oxytocin. These results provide evidence that Mf3 is required for normal hypothalamus development and suggest that Mf3 may play a role in postnatal growth and lactation.

Animals↗

Retinal axon guidance by region-specific cues in diencephalon.

Retinal axons show region-specific patterning along the dorsal-ventral axis of diencephalon: retinal axons grow in a compact bundle over hypothalamus, dramatically splay out over thalamus, and circumvent epithalamus as they continue toward the dorsal midbrain. In vitro, retinal axons are repulsed by substrate-bound and soluble activities in hypothalamus and epithalamus, but invade thalamus. The repulsion is mimicked by a soluble floor plate activity. Tenascin and neurocan, extracellular matrix molecules that inhibit retinal axon growth in vitro, are enriched in hypothalamus and epithalamus. Within thalamus, a stimulatory activity is specifically upregulated in target nuclei at the time that retinal axons invade them. These findings suggest that region-specific, axon repulsive and stimulatory activities control retinal axon patterning in the embryonic diencephalon.

Animals↗

The midbrain-hindbrain boundary genetic cascade is activated ectopically in the diencephalon in response to the widespread expression of one of its components, the medaka gene Ol-eng2.

In vertebrates, the engrailed genes are expressed at early neurula stage in a narrow stripe encompassing the midbrain-hindbrain boundary (MHB), a region from which a peculiar structure, the isthmus, is formed. Knock-out experiments in mice demonstrated that these genes are essential for the development of this structure and of its derivatives. In contrast, little is known about the effect of an overexpression of engrailed genes in vertebrate development. Here we report the isolation of Ol-eng2, a medaka fish (Oryzias latipes) engrailed gene. We have monitored the effects of its widespread expression following mRNA injections in 1- and 2-cell medaka and Xenopus embryos. We found that the ectopic expression of Ol-eng2 predominantly results in an altered development of the anterior brain, including an inhibition of optic vesicle formation. No change in the patterns of mesencephalic and telencephalic markers were observed. In contrast, expressions of markers of the diencephalon were strongly repressed in injected embryos. Furthermore, the endogenous Ol-eng2, Pax2, Wnt1 and Fgf8, which are essential components of the MHB genetic cascade, were ectopically expressed in this region. Therefore, we propose that Ol-eng2 induces de novo formation of an isthmus-like structure, which correlates with the development of ectopic midbrain structures, including optic tectum. A competence of the diencephalon to change to a midbrain fate has been demonstrated in isthmic graft experiments. Our data demonstrate that this change can be mimicked by ectopic engrailed expression alone.

Amino Acid Sequence↗

Asymmetric nodal signaling in the zebrafish diencephalon positions the pineal organ.

The vertebrate brain develops from a bilaterally symmetric neural tube but later displays profound anatomical and functional asymmetries. Despite considerable progress in deciphering mechanisms of visceral organ laterality, the genetic pathways regulating brain asymmetries are unknown. In zebrafish, genes implicated in laterality of the viscera (cyclops/nodal, antivin/lefty and pitx2) are coexpressed on the left side of the embryonic dorsal diencephalon, within a region corresponding to the presumptive epiphysis or pineal organ. Asymmetric gene expression in the brain requires an intact midline and Nodal-related factors. RNA-mediated rescue of mutants defective in Nodal signaling corrects tissue patterning at gastrulation, but fails to restore left-sided gene expression in the diencephalon. Such embryos develop into viable adults with seemingly normal brain morphology. However, the pineal organ, which typically emanates at a left-to-medial site from the dorsal diencephalic roof, becomes displaced in position. Thus, a conserved signaling pathway regulating visceral laterality also underlies an anatomical asymmetry of the zebrafish forebrain.

Animals↗

Influence of liver injury on testosterone 5 alpha-reductase activity in the rat diencephalon.

Diencephalon testosterone 5 alpha-reductase activity and plasma testosterone level were measured in the rat with liver injury caused by i.p. administration of CCl4. Testosterone levels in plasma were decreased after CCl4 injection in both group I (0.1ml/150g B.W./once a day for 2 days) and group II (0.01ml/150g B.W./twice a week for three weeks). 5 alpha-Reductase activity in the diencephalon was decreased both on the 7th day after administration in group I and in group II, while being transiently increased on the 1st day after administration in group I. These results suggest that testosterone metabolism in the brain is inhibited during liver disorders.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗

N-methyl-D-aspartate receptor subunit NR2B is widely expressed throughout the rat diencephalon: an immunohistochemical study.

Glutamate (Glu), a major excitatory neurotransmitter within the hypothalamus and thalamus, acts upon many receptors, including the N-methyl-D-aspartate (NMDA) subtype. Abundant evidence suggests that variations in the subunit composition of NMDA receptors (NMDA-Rs) contribute to differences in Glu's immediate electrophysiological effects as well as to the patterns of signal transduction cascades it triggers to mediate long-term changes in neuronal function. We have previously shown that hypothalamic NMDA-Rs containing the NR2B subunit may be involved in the control of eating as well as in the mediation of physiological responses to osmotic stimuli. To broaden our understanding of diencephalic NMDA-R participation in other functions, we localized the NR2B subunit in the diencephalon of the adult male rat using immunoperoxidase, immunogold, and immunofluorescence techniques and an affinity-purified polyclonal antibody specific for the NR2B subunit of the NMDA-R. In addition, we used a monoclonal NR2B antibody with immunoperoxidase detection to confirm the NR2B distribution seen with the polyclonal antibody. In the hypothalamus, the highest levels of NR2B immunoreactivity (-ir) were found in the magnocellular neurosecretory system, including the paraventricular and supraoptic nuclei. A new finding was that intense NR2B-ir was present within perivascular "accessory" magnocellular groups of this system, including the nucleus circularis, anterior fornical nucleus, and scattered clusters of lateral hypothalamic cells apposed to blood vessels. Robust NR2B-ir was also present within the arcuate nucleus, the median eminence, and the tuberal nucleus, and light immunostaining was found in all other hypothalamic nuclei examined. In the thalamus, the highest NR2B-ir was observed in the medial habenula and the anterodorsal, paraventricular, rhomboid, reticular, and dorsal lateral geniculate nuclei. As in the hypothalamus, all thalamic nuclei examined displayed at least light immunostaining for this subunit. Control sections, including those incubated with the polyclonal NR2B antibody preadsorbed with its fusion protein, were virtually devoid of immunostaining. This demonstration that the NR2B subunit of the NMDA-R is widely distributed in the diencephalon, implicates it in a wide variety of functions, and provides a useful anatomical framework for establishing a comprehensive map of Glu receptor populations within this major subdivision of the brain.

Animals↗

"The diencephalon of Ptilocercus lowii (pen-tailed tree-shrew)".

The pen-tailed tree-shrew (Ptilocercus lowii) has been regarded by Le Gros Clark (1926), and Martin (1968) to possess more primitive morphological and to a certain extent, neuro-anatomical characteristics than the other tree-shrew species belonging to the sub-family Tupaiinae. Investigations have been carried out on the diencephalon of Ptilocercus lowii which has not been completely done by Le Gros Clark and other workers since 1926, to find out whether the diencephalon has actually undegone any phylogenetic changes that should be more advanced than those of the Insectivora or remain more primitive than that of the Tupaiinae. The diencephalic structure that show the most significant phylogenetic features which differe Ptilocerecus from Tupaia are observed in the anterior, dorsolateral and ventrolateral thalamic groups, and the geniculate bodies. The nucleus anteroventralis is, by comparison, much smaller and poorly differentiated from the nucleus anteromedialis. The nucleus anterodorsalis is also comparably large and does not reach the dorsal surface of the thalamus as it does in the primates. The midline nuclei do not show any significant differences, except the notably larger size of nucleus parataenialis in Ptilocercus. The nucleus mediodoralis is small and indifferentiated although it does show some incipient signs of cellular differentiation. The nucleus centralis lateralis is well developed; its inferior (ventral) part is larger than its superior part which is the better developed of the two parts in the tupaiids and primates. The nucleus centrum medianum appears to be very small and forms only a lateral extension of the nucleus parafascicularis. The ventrolateral thalamic group basically consists of nuclei ventrales anterior, lateralis and posterior without intermediate or transitional zones as found in Tupaia and Primates. The nucleus pretectalis is the largest and the best developed of all the elements of the posterior thalamic nuclear group. The lateral geniculate nucleus is not differentiated into laminae like that in Tupaia and Primates; it is merely a homogeneous structure that appears to be smaller in size that the pregeniculate and medial geniculate nuclei. The medial geniculate nucleus is large in proportional size of the whole thalamus and appears to be well differentiated cellularly into several small parts. No remarkable changes are noted in the epithalamus, subthalamus and hypothalamus. However, the nucleus ventromedialis appears to be the most outstanding structure in the infundibular region of the hypothalamus. The mammillary region is of a simpler construction in Ptilocercus than in Tupaia; it does not protrude from the ventral surface of the hypothalamus. In the light of these findings, the phyletic status of Ptilocercus in the family Tupaiidae is discussed.

Animals↗

[Angiomas of blood vessels supplying the basal ganglia and the diencephalon].

The author discusses the problem of surgical treatment of intracranial angiomas situated in basal ganglia and diencephalon. Vascular malformations in this area were found in 7.5% of cases in a group of 80 patients with intracranial angiomas. In all 6 cases the onset of the disease was sudden with meningocerebral haemorrhage, prolonged coma and hemiplegia. The malformations had usually the features of arteriovenous angioma. The afferent vessels come usually from the medial short and long vessels branching off from the anterior and middle cerebral arteries, the choroid arteries and the posterior communicating artery. The author isolated two types of malformations differing in their situation, shape and range of vascularization. In the "subventricular" type situated within the nucleus caudatus and lenticularis, internal capsule and thalamus the malformation can be exposed well from the approach through the lateral ventricle. The angiomas situated nearer to the base of hemisphere (the parabasal type), in the diencephalon, in the area of the olfactory triangle, substantia perforata anterior and even crus cerebri can be exposed best using the subfrontal approach. The author believes that in many cases of these malformations regarded usually as inoperable, radical operation can be done with selective removal of angioma by means of microsurgery. This procedure was applied in 2 cases (Fig. 2 and 3).

Adolescent↗

Immunohistochemical studies on the localization and distribution of monoamine neuron systems in the rat brain. I. Tyrosine hydroxylase in the mes- and diencephalon.

The localization and distribution of tyrosine hydroxylase (TH), the first enzyme in the catecholamine synthesis, in the mes- and diencephalon has been studied with the indirect immunofluorescence technique of Coons and collaborators. Principally, TH was present in neuron systems with a distribution similar to known dopamine, noradrenaline and adrenaline systems. The present data, taken together with published and some unpublished results, indicate that all parts of most central dopamine neurons, i.e. cell body, dendrites, axon and nerve terminals, appear strongly fluorescent. The adrenaline neurons also appeared strongly fluorescent, except for their axons, which only exhibited a weak fluorescence. Only cell bodies of noradrenaline neurons were strongly fluorescent, whereas the nerve terminals and axons showed a weak or moderate fluorescence intensity. The fine noradrenaline nerve terminals in some areas, such as the thalamus, were invisible or, under favourable conditions, weakly fluorescent. Therefore, in the present study we are mainly dealing with the dopamine neurons of the upper brain stem. Our results demonstrate a widespread occurrence of TH-positive neuron systems in the mes- and diencephalon. The different mesencephalic dopamine systems and their ascending projections were visualized. Numerous TH-positive cell bodies were present along the ventricle system extending from the aqueductus cerebri to the most cranial periventricular parts of the third ventricle. The caudal part of these neurons, consisting of very small cell bodies, belong to the dorsal periventricular system described by Lindvall and Björklund. Several TH-positive cell bodies were also observed in the inferior collicle of young animals. In the superficial layers of the inferior collicles TH positive nerve terminals were seen. At the hypothalamic level the A11 to A14 cell groups as well as some additonal cell bodies and extensive nerve terminal plexuses appeared strongly fluorescent. The differences in the intensity of the TH-related immunofluorescence between various brain regions and between various neuron systems may well reflect differences in enzyme levels between the various catacholamine systems rather than be due to the existence of different types of TH.

Adrenergic Fibers↗