Anterior Hypothalamic Nucleus Research Articles

Autoradiographic distribution of 125I-galanin binding sites in the rat central nervous system

Galanin (GAL) binding sites in coronal sections of the rat brain were demonstrated using autoradiographic methods. Scatchard analysis of 125I-GAL binding to slide-mounted tissue sections revealed saturable binding to a single class of receptors with a Kd of approximately 0.2 nM. 125I-GAL binding sites were demonstrated throughout the rat central nervous system. Dense binding was observed in the following areas: prefrontal cortex, the anterior nuclei of the olfactory bulb, several nuclei of the amygdaloid complex, the dorsal septal area, dorsal bed nucleus of the stria terminalis, the ventral pallidum, the internal medullary laminae of the thalamus, medial pretectal nucleus, nucleus of the medial optic tract, borderline area of the caudal spinal trigeminal nucleus adjacent to the spinal trigeminal tract, the substantia gelatinosa and the superficial layers of the dorsal spinal cord. Moderate binding was observed in the piriform, periamygdaloid, entorhinal, insular cortex and the subiculum, the nucleus accumbens, medial forebrain bundle, anterior hypothalamic, ventromedial, dorsal premamillary, lateral and periventricular thalamic nuclei, the subzona incerta, Forel's field H 1 and H 2, periventricular gray matter, medial and superficial gray strata of the superior colliculus, dorsal parts of the central gray, peripeduncular area, the interpeduncular nucleus, substantia nigra zona compacta, ventral tegmental area, the dorsal and ventral parabrachial and parvocellular reticular nuclei. The preponderance of GAL-binding in somatosensory as well as in limbic areas suggests a possible involvement of GAL in a variety of brain functions.

Concentrations of gaba and glycine in discrete brain nuclei: Stress-induced changes in the levels of inhibitory amino acids

Concentrations of γ-aminobutyric acid (GABA), glycine and serine have been measured in 44 microdissected areas of the brain of the rat. All three amino acids were ubiquitously present and distributed unevenly in the brain. Very high levels of GABA were found in the anterior hypothalamic and medial preoptic nuclei and the substantia nigra; high levels were found in the interpeduncular and red nuclei in the mesencephalon and in several hypothalamic nuclei. Glycine was distributed fairly uniformly with large concentrations in certain lower brainstem nuclei. In these areas, the concentrations of glycine exceeded those of serine, while the serine-glycine ratio was 4.5:1 in the caudate nucleus, 4:1 in the cerebellum and 2.5:1 in the cerebral cortical areas. Acute stress induced with formalin (pain) resulted in a significant depletion of levels of GABA in the hypothalamus and the lower brainstem but not in the cortical areas. In the same animals, concentrations of glycine doubled in the cerebral cortex and remained unchanged elsewhere in the brain. Increased motor and behavioral activity after the acute administration of a large dose of amphetamine were associated with a 2–5-fold increase in the levels of glycine in brain, and markedly elevated the concentrations of GABA in the major biogenic amine-containing cell groups only (substantia nigra, locus coeruleus and dorsal raphe).

Distribution of immunoreactive melanin-concentrating hormone in the central nervous system of the rat

The distribution of melanin-concentrating hormone-like immunoreactivity (MCH-LI) in 41 microdissected brain and spinal cord regions was determined using radioimmunoassay with antibodies to salmon MCH. The highest concetration of MCH-LI was detected just ventral to the zona incerta (subzona incerta) (2923.2 fmol/mg protein). Very high concentrations of MCH-LI (1000f mol/mg protein) were detected also in the nucleus of the diagonal band, medial forebrain bundle, posterior hypothalamic nucleus and medial mammillary nucleus. High concentrations of the peptide (between 500–1000 fmol/mg protein) were measured in 11 brain regions, including bed nucleus of stria terminalis, paraventricular nucleus, anterior hypothalamic nucleus, median eminence, parabrachial nucleus. Moderate concentrations of MCH-LI (between 250–500 fmol/mg protein) were measured in 16 brain regions, such as frontal cortex, central amygdaloid nucleus, medial septum, periventricular nucleus (preoptic) and nucleus of the solitary tract. Low concentrations of MCH-LI (<250 fmol/mg protein) were measured in 9 brain regions such as cortical areas, hippocampus, caudate nucleus and substantia nigra. Cervical spinal cord and neurointermediate lobe of the pituitary gland contain low concentrations of the peptide.

Effects of clonidine on the stimulation-evoked release of 3H-noradrenaline from superfused rat brain slices as a function of the biophase concentration. Temperature dependent widening of extracellular space.

The influence of clonidine on the stimulation-evoked overflow of tritium was studied in brain slices preincubated with 3H-noradrenaline. The slices were prepared from parietal cortex (Cx), nucleus anterior hypothalami (nah) and nucleus tractus solitarii (nts). After preincubation, the tissues were superfused at 23 degrees C or 37 degrees C with a medium containing the noradrenaline uptake inhibitor desipramine. Electrical field stimulation was applied using stimulation frequencies of 0.3-10 Hz. At 23 degrees C/0.3 Hz, clonidine concentration-dependently inhibited the evoked overflow of tritium in all three brain regions. In contrast, at 23 degrees C/3 Hz the inhibitory effect of the drug in the Cx was abolished and a facilitation was observed in the nah and nts. When tested at increasing frequencies of stimulation in the nts at 23 degrees C, clonidine exerted a dual action, characterized by a reduction of electrically evoked responses at frequencies below 1 Hz and a facilitation at frequencies above 1 Hz. At 37 degrees C, clonidine concentration-dependently decreased the evoked overflow in all brain regions studied, this effect being more pronounced at 0.3 Hz than at 3 Hz. The apparent lack of an effect of clonidine on the stimulation-evoked overflow of tritium in the Cx at 23 degrees C/3 Hz was turned to a facilitation when noradrenaline (0.01 mumol/l) was included in the superfusion medium. Conversely, an inhibitory effect of clonidine was seen when the uptake blocker desipramine (as well as noradrenaline) was omitted from the superfusion medium.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypothalamic and ventral thalamic projections to the superior colliculus in the cat.

The present report describes the organization of collicular afferents that arise within either the hypothalamus or the ventral thalamus. Following the placement of large injections of WGA-HRP into the superior colliculus of the cat, retrogradely labeled neurons are located within the reticular nucleus of the thalamus, the zona incerta, the fields of Forel, and throughout the hypothalamus. Although the dorsal hypothalamic area contains the largest number of labeled hypothalamic neurons, labeled cells are also found within the periventricular, paraventricular, dorsomedial, ventromedial, posterior, lateral, and anterior hypothalamic nuclei. A strikingly similar pattern of distribution of labeled neurons is also observed following placement of small injections of WGA-HRP that are restricted within the stratum griseum intermedium (SGI). In contrast, hypothalamic and ventral thalamic labeling is not seen after placement of injections within the stratum griseum superficiale. Following the placement of injections of tritiated anterograde tracers within the dorsal hypothalamic area, transported label is organized in two bands of clusters over the SGI. When injections of tritiated tracers are placed within the zona incerta, terminal label is also located over the SGI; however, the distribution of silver grains does not appear as clusters or distinct puffs. On the basis of the comparison of the cellular types that give rise to these projections and the differences in terminal distribution, we suggest that the hypothalamic and ventral thalamic projections to the superior colliculus are totally separate and unrelated pathways. The functional implications of the hypothalamotectal pathway are also discussed.

Estrogen induction of progestin receptors in microdissected hypothalamic and limbic nuclei of female guinea pigs.

Estrogen induction of cytosolic progestin receptors (CPRs) in the hypothalamus-preoptic area of the female guinea pig is correlated with facilitation of female sexual behavior and gonadotropin secretion by progesterone. The present study validated a CPR microassay and determined where, within microdissected areas of the hypothalamus-preoptic area of the female guinea pig, induction of CPRs by estradiol occurs. Ovariectomized adult guinea pigs were given 20 micrograms estradiol benzoate (EB) or oil vehicle for 3 successive days. CPRs were measured using the synthetic progestin [3H]-R5020. The highest basal (no estrogen treatment) level of CPRs was seen in the arcuate-median eminence (34.1 +/- 3.7 fmol/mg). With EB treatment, the highest level of CPRs was again in the arcuate-median eminence (178.0 +/- 12.0 fmol/mg). EB-treated females also had high CPR levels in the periventricular area (88.5 +/- 10.8 fmol/mg) and the medial preoptic area (86.3 +/- 9.3 fmol/mg). Moderate levels were seen in the ventromedial nucleus of the hypothalamus (32.7 +/- 3.0 fmol/mg) and in the anterior hypothalamic nucleus (13.0 +/- 2.1 fmol/mg), but these were not significantly different from the low levels in the medial amygdala (4.5 +/- 1.2 fmol/mg) and in the dorsomedial nucleus of the hypothalamus (5.4 +/- 1.1 fmol/mg) of EB-treated females. However, EB caused a significant induction over baseline levels not only in the arcuate-median eminence, periventricular area, and medial preoptic area, but also in the ventromedial nucleus of the hypothalamus and the anterior hypothalamic nucleus. EB did not increase CPRs in the medial amygdala or the dorsomedial nucleus of the hypothalamus.

Catechol estrogen formation by the CNS: regional distribution of estrogen-2/4-hydroxylase activity in rat brain.

Estrogen-2/4-hydroxylase (E-2/4-H) activity was measured by a direct product isolation assay in punch biopsy specimens obtained from nine nuclear regions from forebrain of adult male rats. Tritiated catechol estrogens were isolated from incubations of tissues with [6,7-3H]estradiol from all regions studied. The amount of 4-hydroxyestradiol (4-OH-E2) formed equaled or exceeded that of 2-hydroxyestradiol (2-OH-E2). There were significant regional differences in the amounts of catechol estrogen produced. The difference was nearly 8-fold between the arcuate-median eminence (ARC-ME) and the medial preoptic nucleus (POM), regions with the highest and lowest specific activities, respectively (37.7 +/- 6.2 vs. 5.1 +/- 0.7 pmol/mg protein/10 min 2-OH-E2, mean + SEM, n = 6). The supraoptic nucleus was the site of second highest concentrations of E-2/4-H activity (20.3 pmol 2-OH-E2/mg protein/10 min). Estrogen-2/4-H activity in the paraventricular (PVN) and periventricular (PERI) nuclear regions, though only about half that in the SON, was significantly greater than in the remaining brain areas (nucleus interstitialis striae terminalis, caudate, anterior hypothalamic and medial preoptic nuclei and cortex. The ARC-ME, the region with the highest E-2/4-H activity is where the dopaminergic neurones and terminals from the Gn-RH neurons are concentrated. The functions regulated by these two classes of neurones, the secretion of prolactin and gonadotrophins, respectively, have been the subject of most of the previous studies aimed at establishing the role of catechol estrogen formation in the hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)

Studies on neuropeptide Y-catecholamine interactions in the hypothalamus and in the forebrain of the male rat. Relationship to neuroendocrine function

Neuropeptide Y-catecholamine interactions have been analyzed within the hypothalamus and in the forebrain of male rats by means of immunocytochemistry in combination with morphometry, quantitative histofluorimetry on catecholamine fluorescence in discrete catecholamine nerve terminal systems, biochemical analysis of catecholamines as well as by studies on serum levels of adenohypophyseal hormones vasopressin, adrenocortical hormones and angiotensin II using radioimmunoassay determinations. (1) Morphologic and morphometrical evidence indicates the existence of separate populations of neuropeptide Y and tyrosine hydroxylase immunoreactive nerve cell bodies in the parvo- and magnocellular components of the arcuate nucleus respectively. In addition, a significant codistribution of NPY immunoreactive nerve terminals and tyrosine hydroxylase immunoreactive nerve cell bodies were demonstrated in the ventrolateral part of the magnocellular component of the arcuate nucleus. (2) Immunocytochemical studies on the distribution of tyrosine hydroxylase, phenyl ethanolamine- N-methyltransferase and neuropeptide Y immunoreactive nerve terminal networks in the peri- and paraventricular hypothalamic nucleus indicated that these types of immunoreactive nerve terminals densely innervate the medial and anterior parvocellular part of the paraventricular hypothalamic nucleus and anterior periventricular hypothalamic nucleus. From studies on the pattern of terminal distribution results have been obtained compatible with the view that neuropeptide Y or a neuropeptide Y related peptide can be a comodulator in noradrenaline and adrenaline nerve terminal networks of these regions. (3) Acute intraventricular injections of neuropeptide Y (1.25 nmol) do not change dopamine and noradrenaline levels in any hypothalamic and telencephalic dopamine and noradrenaline nerve terminal system analyzed with the exception of the anteromedial frontal cortex, in which area a significant increase in the dopamine levels was observed as revealed biochemically. (4) By means of the tyrosine hydroxylase inhibition method it was possible to show that acute intraventricular injection of NPY (1.25 nmol) increased dopamine utilization in the medial and lateral palisade zone of the median eminence and in the anteromedial frontal cortex and reduced noradrenaline utilization in the parvocellular part of the paraventricular hypothalamic nucleus, while dopamine utilization was not influenced in the nucleus caudatus putamen, nucleus accumbens or in the tuberculum olfactorium. (5) In the intraventricular experiments reported above neuropeptide Y (1.25 nmol, 1 h) reduced the serum levels of thyreotropin stimulating hormone, prolactin and luteinizing hormone and increased serum corticosterone, adrenocorticotrophin, vasopressin, angiotensin II and aldosterone levels. The presence of the tyrosine hydroxylase inhibitor by itself, increased corticosterone, adrenocorticotrophin and aldosterone serum levels and reduced serum luteinizing hormone levels. Neuropeptide Y together with the tyrosine hydroxylase inhibitor further enhanced the adrenocorticotrophin, angiotensin II and aldosterone serum levels seen with the inhibitor, but could no longer produce its excitatory and inhibitory effects on serum corticosterone and luteinizing hormone levels, respectively. Vasopressin serum levels were increased to the same extent in the absence or presence of tyrosine hydroxylase inhibition. The present morphological, neurochemical and functional studies indicate that neuropeptide Y given intraventricularly inhibit the secretion of prolactin, luteinizing and thyreotropin stimulating hormones probably by activation mainly of neuropeptide Y receptors located in the somadendritic region of the arcuate DA cell bodies, leading to increased activity in inhibitory tubero-infundibular dopamine neurons. In addition, it is suggested that the ability of neuropeptide Y to increase adrenocorticotrophin and corticosterone secretion is at least in part related to its ability to reduce noradrenaline turnover in the parvocellular part of the paraventricular hypothalamic nucleus, rich in corticotrophin releasing factor immunoreactive nerve cell bodies. It is speculated that neuropeptide Y as a comodulator in the noradrenaline nerve terminals in this area may enhance the excitatory actions of noradrenaline on the corticotrophin releasing factor immunoreactive nerve cells. Such an action will lead to increases of corticotrophin releasing factor neuronal activity and of adrenocorticotrophin hormone secretion producing a feedback response, which may reduce noradrenaline turnover exclusively in this nucleus as was observed in the present experiments. The increase in aldosterone may be induced by the increased adrenocorticotrophin serum levels but the increase in vasopressin secretion and in angiotensin II serum levels may be secondary to the hypotensive activity of neuropeptide Y. Finally, it is suggested that neuropeptide Y mechanisms can increase dopamine synthesis and release in the anteromedial frontal cortex. Thus, neuropeptide Y mechanisms may participate in the control of cortical functions at least partly by regulating the cortical dopamine neurotransmission.

Lateral hypothalamic lesions and fenfluramine increase thermogenesis in brown adipose tissue

The effects of treatment with fenfluramine or electrolytic lesions in the lateral hypothalamus (LH) on binding of guanosine 5-diphosphate (GDP) by mitochondria from brown adipose tissue have been compared in 4 experiments. In 2 experiments the lesions were lateral to the anterior hypothalamic nucleus and in the other two they were lateral to the ventromedial hypothalamic nucleus. Binding of GDP to mitochondria was significantly increased 18 hours after an electrolytic lesion in either LH site. d,1-Fenfluramine, 20 mg/kg, also increased GDP binding in both acute experiments. In the other 2 experiments GDP binding was measured 11 days after the LH lesion or after 11 daily injections of fenfluramine. When the chronic lesions were lateral to the VMN, there was a transient drop in food intake and body weight. With more anterior lesions, body weight remained significantly lower than in sham-operated rats although food intake returned slowly to control levels. Fenfluramine-treated rats had lower body weights in both chronic experiments even after food intake returned to normal. GDP-binding to mitochondria from interscapular brown adipose tissue was elevated in both of the chronically-treated fenfluramine groups but was only increased in the LH-lesioned rats whose body weight remained below normal.

Distribution of immunoreactive metorphamide (adrenorphin) in discrete regions of the rat brain: Comparison with met-enkephalin-Arg 6-Gly 7-Leu 8

The distribution of immunoreactive (ir)-metorphamide (adrenorphin) in 101 microdissected rat brain and spinal cord regions was determined using a highly specific radioimmunoassay. The highest concentration of metorphamide in brain was found in globus pallidus (280.1 fmol/mg protein). High concentrations of ir-metorphamide (>120 fmol/mg protein) were found in 9 nuclei, including central amygdaloid nucleus, lateral preoptic area, anterior hypothalamic nucleus, hypothalamic paraventricular nucleus, interpeduncular nucleus, periaqueductal grey matter and nucleus of the solitary tract. Moderate concentrations of the peptide (between 60 and 120 fmol/mg protein) were found in 47 brain nuclei such as nucleus accumbens, bed nucleus of stria terminalis, several septal and amygdaloid nuclei, most of the hypothalamic nuclei, ventral tegmental area, red nucleus, raphe nuclei, lateral reticular nucleus, area postrema and others. Low concentrations or ir-metorphamide (<60 fmol/mg protein) were measured in 41 nuclei, e.g., cortical structures, hippocampus, caudate nucleus, thalamic nuclei, supraoptic nucleus, substantia nigra, vestibular nuclei, cerebellum (nuclei and cortex). The olfactory bulb has the lowest metorphamide concentration (5.8 fmol/mg protein). Spinal cord segments exhibit very low peptide concentrations.

Mapping of glucocorticoid receptor immunoreactive neurons in the rat tel- and diencephalon using a monoclonal antibody against rat liver glucocorticoid receptor.

By means of a monoclonal antibody against the rat liver glucocorticoid receptor (GR) in combination with the indirect immunoperoxidase technique it has been possible to demonstrate GR-immunoreactive nerve and glial cell nuclei all over the tel- and diencephalon of the male rat. Strongly GR-immunoreactive nerve cell nuclei were only present in the parvocellular part of the paraventricular hypothalamic nucleus, in the anterior periventricular hypothalamic nucleus, in the ventral part of the mediobasal hypothalamus, and in the CA1 and CA2 subregion of the hippocampal formation. Within the paraventricular hypothalamic nucleus a substantial overlap exists between the GR-immunoreactive area and the CRF-immunoreactive area. Medium to high densities of moderately GR-immunoreactive nerve cell nuclei were present all over the cortical hemispheres. Medium densities of moderately GR-immunoreactive nerve cells were demonstrated in many thalamic nuclei and in the central amygdaloid nucleus. After adrenalectomy the GR immunoreactivity was predominantly located in the pericaryon. Upon acute corticosterone treatment of adrenalectomized male rats, the GR immunoreactivity was again mainly demonstrated in the nerve cell nuclei indicating that corticosterone can translocate GR from the cytoplasm to the cell nuclei. It is suggested that the hypothalamic GR may be involved in the regulation of especially CRF secretion but also in the secretion of other anterior pituitary hormones such as TRH and somatostatin.

Long-term reorganization of afferents to the mediobasal hypothalamus following retrochiasmatic knife cuts. A study using horseradish peroxidase

Retrochiasmatic knife cuts produce a series of dynamic changes across time in the luteinizing hormone-releasing hormone and catecholamine content of the mediobasal hypothalamus (MBH). We have examined the sources of afferents projecting to the mediobasal hypothalamus of female rats at 7, 60 and 90 days following retrochiasmatic frontal cut (FC) surgery using the intra-axonal retrograde transport of horseradish peroxidase (HRP) in order to better define the functional plasticity demonstrated by the MBH at these time periods after damage. Age-matched, previously unoperated, female rats served as controls. Small HRP injections placed in the ventromedial nucleus (VMN) in control animals labelled neurons within the VMN, dorsomedial nucleus (DMN) and lateral hypothalamic area (LHA). Larger injections also labelled neurons in the anterior hypothalamic area (AHA), preoptic area (POA), septal nuclei, periventricular nuclei (PVN), supraoptic nucleus (SON), zona incerta (ZI) and suprachiasmatic nucleus (Schn). Seven days after surgery, no labelled neurons could be detected rostral to the knife cut when the injection site was confined to the boundary of the glial scar. At 60 days, labelled soma were observed in LPOA, POA, AHA, PVN, SON and ZI. At 90 days only the SON contained labelled neurons rostral to the knife cut. These results suggest a dynamically changing pattern of innervation to the MBH following damage.

The effects of calcitonin on central neurons in the rat

The effects of salmon calcitonin on central neurons were studied in anesthetized rats. Calcitonin applied iontophoretically consistently inhibited spontaneous activity in half of the neurons tested in the anterior hypothalamic nucleus and subthalamus but had virtually no effect on cortical and thalamic neurons. Calcitonin also inhibited glutamate-evoked activity in the neurons tested. Calcitonin administered into the brain ventricular system led to a marked decrease in spontaneous discharge of hypothalamic cells in the majority of cells tested. The onset of this response began within 20 and 30 min of calcitonin application.

The calcitonin gene-related peptide-containing fiber projection from the hypothalamus to the lateral septal area including its fine structures

The afferent source of calcitonin gene-related peptide-like immunoreactive (CGRPI) fibers in the lateral septal area of the rat was sought by using indirect immunofluorescence technique. These fibers decreased markedly on the operated side after the destruction of the area between the anterior hypothalamic nucleus and the lateral hypothalamus where a number of CGRPI cells. We also examined the fine structure of CGRPI fibers in the lateral septal area. Many CGRPI fibers forming axosomatic synapses were identified. These facts strongly suggest that CGRPI cells in the area between the anterior hypothalamic nucleus and the lateral hypothalamus project ipsilaterally to the lateral septal area and directly influence the soma there.

Water deprivation increases anterior hypothalamic norepinephrine metabolism in the rat

Rats were limited to 10 min of access to water per day. After 1 week, concentrations and rate of metabolism of dopamine, norepinephrine and epinephrine were determined in hypothalamic and limbic areas associated with regulation of water homeostatis. Chronic water deprivation caused hypovolemia, hypotension and ingestion of a large volume of water when water became available. Norepinephrine metabolism was consistently increased in samples containing the anterior hypothalamic nucleus, but no other catecholamine in any other brain area was significantly affected by the deprivation schedule. We conclude that the anterior hypothalamic nucleus is involved in the response to chronic disruption of water balance in the rat.

Intrahypothalamic 5,7-dihydroxytryptamine: Temporal analysis of effects on 5-hydroxytryptamine content in brain nuclei and on facilitated lordosis behavior

The long-term relationship between serotonin (5-HT) levels in discrete hypothalamic nuclei and female rat sexual behavior, the lordosis response, was examined following intrahypothalamic injection of 5,7-dihydroxytryptamine (5,7-DHT). One week following 5,7-DHT injection, 5-HT levels in the ventromedial hypothalamic nucleus, dorsomedial nucleus, anterior hypothalamic nucleus and the medial preoptic nucleus were approximately 90% depleted as compared to sham animals. Other hypothalamic and preoptic areas including the arcuate-median eminence, vertical nucleus of diagonal band and lateral septal nucleus showed smaller reductions in 5-HT, from 40 to 70% of sham values. At this time estrogen-dependent lordosis behavior in the lesioned group was facilitated. Behavioral facilitation was greatest at 4 weeks post lesion when depletion of 5-HT in the VMN was maximal. 5-HT levels increased at 57 days after 5,7-DHT treatment in most areas, and by 71 days post lesion, no significant differences in 5-HT levels were found between sham and 5,7-DHT-treated groups. Concomitant with the increases in 5-HT, facilitated lordosis behavior gradually decreased. Loss of behavioral facilitation appeared to be most closely related to increases in content of 5-HT in the ventromedial nucleus. These results further support the hypothesis that 5-HT endings in the hypothalamus exert tonic inhibitory regulation over hormone-dependent lordosis in the female rat. They also indicate that regenerating 5-HT fibers in the hypothalamus can reinstate a normal pattern of hormone-dependent behavioral function.

Calcitonin gene-related peptide: Detailed immunohistochemical distribution in the central nervous system

With the use of an antiserum generated in rabbits against synthetic human calcitonin gene-related peptide (CGRP) the distribution of CGRP-like immunoreactive cell bodies and nerve fibers was studied in the rat central nervous system. A detailed stereotaxic atlas of CGRP-like neurons was prepared. CGRP-like immunoreactivity was widely distributed in the rat central nervous system. CGRP positive cell bodies were observed in the preoptic area and hypothalamus (medial preoptic, periventricular, anterior hypothalamic nuclei, perifornical area, medial forebrain bundle), premamillary nucleus, amygdala medialis, hippocampus and dentate gyrus, central gray and the ventromedial nucleus of the thalamus. In the midbrain a large cluster of cells was contained in the peripeduncular area ventral to the medial geniculate body. In the hindbrain cholinergic motor nuclei (III, IV, V, VI, VII XII) contained CGRP-immunoreactivity. Cell bodies were also observed in the ventral tegmental nucleus, the parabrachial nuclei, superior olive and nucleus ambiguus. The ventral horn cells of the spinal cord, the trigeminal and dorsal root ganglia also contained CGRP-immunoreactivity. Dense accumulations of fibers were observed in the amydala centralis, caudal portion of the caudate putamen, sensory trigeminal area, substantia gelatinosa, dorsal horn of the spinal cord (laminae I and II). Other areas containing CGRP-immunoreactive fibers are the septal area, nucleus of the stria terminalis, preoptic and hypothalamic nuclei (e.g., medial preoptic, periventricular, dorsomedial, median eminence), medial forebrain bundle, central gray, medial geniculate body, peripeduncular area, interpeduncular nucleus, cochlear nucleus, parabrachial nuclei, superior olive, nucleus tractus solitarii, and in the confines of clusters of cell bodies. Some fibers were also noted in the anterior and posterior pituitary and the sensory ganglia. As with other newly described brain neuropeptides it can only be conjectured that CGRP has a neuroregulatory action on a variety of functions throughout the brain and spinal cord.

Localization of chick retinal visinin-like immunoreactivity in the rat forebrain and diencephalon

The present study is an examination, using an indirect immunofluorescence method, of the distribution of visinin, a 24,000 dalton peptide, in the rat forebrain and diencephalon. Immunoreactive structures were localized in the neuronal elements showing an uneven distribution. Immunoreactive neurons were found in the olfactory bulb, anterior olfactory nucleus, cerebral cortex, amygdaloid complex, ventral portion of the nucleus caudatus putamen, septal area, nucleus accumbens, nucleus paratenialis, nucleus rhomboideus, nucleus reuniens, nucleus paraventricularis hypothalami, nucleus supraopticus, nucleus anterior hypothalami, preoptic area, hypothalamic periventricular nucleus, nucleus mammillaris medialis, medial habenular nucleus, zona incerta. nucleus lateralis thalami, nucleus tractus optici and gyrus dentatus. Immunoreactive fibers were observed in the above areas, particularly near the labelled cells, forming fiber plexuses of varying density. In addition, dense plexuses were also seen in the globus pallidus, anteroventral nucleus of the thalamus, substantia nigra and hippocampus. In the former three structures, no labelled cells were present and in the latter, a few scattered neurons were found, indicating that these fibers originate from extrinsic sources.

Direct projections of the hypothalamic nuclei to the thalamic mediodorsal nucleus in the cat

Direct projections of the hypothalamic nuclei to the thalamic mediodorsal nucleus (MD) were studied using retrograde and anterograde transport of horseradish peroxidase (HRP) and wheat germ agglutinin (WGA)—HRP. HRP and WGA—HRP were injected into the MD, thalamic paraventricular, lateral habenular and hypothalamic nuclei. The results indicate that the MD, particularly its medial part, receives a moderate amount of hypothalamic afferents, and that most of these afferents originate in the medial part of the lateral hypothalamic nucleus at anterior levels, while a limited number are derived from the dorsal, dorsomedial, ventromedial and anterior hypothalamic and lateral preoptic nuclei.

An enkephalinergic projection from the hypothalamic paraventricular nucleus to the hypothalamic ventromedial nucleus of the rat: An experimental immunohistochemical study

The distribution and origins of enkephalin-like immunoreactive (ENK-IR) fibers in the nucleus ventromedialis hypothalami (vm) of the rat were examined using immunohistochemistry. A dense plexus was evenly distributed in the vm with no regional differences. A group of ENK-IR neurons was concentrated in the ventrolateral portion of the vm. The destruction of the hypothalamic paraventricular nucleus (pv) which contained numerous ENK-IR neurons, resulted in a marked decrease in ENK-IR fibers in the vm on the operated side. In addition, the destruction of the magnocellular portion of the pv, while leaving most of parvocellular portion intact, failed to substantially decrease the ENK-IR fibers in the vm, suggesting that these fibers originate from ENK-IR neurons located in the parvocellular portion of the pv. The present study further showed that the axons of these neurons first proceeded laterally to the perifornical area, next ran ventrolaterally to the ventrolateral portion of the anterior hypothalamic nucleus and finally turned medially to the vm.