Serotonergic split brain and suicide.
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Biomedical subjects
Publications and source records attributed to M Palkovits.
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The presence of corticotropin-releasing factor (CRF) in the olivocerebellar system was demonstrated in rats by light- and electron-microscopic immunohistochemistry, as well as by in situ hybridization histochemistry. CRF-like immunoreactivity was present in each portion of the olivocerebellar system: In colchicine-treated rats, CRF-immunostained cells were found in each nuclei and subunit of the inferior olive. After surgical transection of the medullary portion of the olivocerebellar tract, CRF-immunostaining accumulated in inferior olive neurons contralateral to the lesion. In situ hybridization histochemistry indicated that CRF mRNA is transcribed in inferior olive neurons for translation to CRF precursor, whereas CRF mRNA was depleted contralateral to the lesion. CRF-immunopositive fibers of the olivocerebellar tract were demonstrated ipsilateral to the transection due to an accumulation in the proximal portion of transected axons. CRF-immunopositivity was demonstrated in climbing fibers in the molecular layer of the cerebellum at both light- and electron-microscopic levels. CRF-immunostained nerve terminals (climbing fiber varicosities) established synaptic contact with dendritic spines of the Purkinje cells. These three observations provide morphological evidence suggesting that CRF might serve as a neurotransmitter in the olivocerebellar system.
1. The influence of two angiotensin-converting enzyme inhibitors, captopril and enalapril, on the cAMP content of microdissected brain areas was examined in spontaneously hypertensive rats. Both drugs depleted systolic arterial blood pressure significantly. 2. Captopril and enalapril increased the level of cAMP in catecholaminergic cell groups in the lower brain-stem. Captopril was more effective in the substantia nigra, while enalapril treatment resulted in high cAMP levels in the ventrolateral medulla oblongata (A1 catecholaminergic cell group). 3. Both drugs, especially captopril, depleted cAMP content in the cingulate cortex. 4. No changes in cAMP levels were measured in the primary baroreceptor centre (nucleus of the solitary tract) following either captopril or enalapril treatment.
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In the rat median eminence immunoreactive galanin nerve fibers and terminals are present in high numbers in the external layer, and fibers in moderate numbers are seen in the internal layer. The possible sources of these galanin-containing fibers were studied by means of radioimmunoassay and immunohistochemistry in rats with different types of hypothalamic lesions. Galanin-like neurons were found both (1) in the magnocellular hypothalamo-neurohypophyseal system and (2) in the parvocellular hypothalamo-median eminence-anterior pituitary system. Cell bodies containing galanin-like immunoreactivity were localized in the supraoptic, magnocellular paraventricular and accessory magnocellular neurons with axons traversing the internal layer and terminating in the posterior pituitary. Surgical isolation of these neurons from the median eminence resulted in a marked depletion of immunoreactive galanin from the internal layer of the median eminence and the posterior pituitary. Due to the retrograde accumulation of axonally transported substances in cells proximal to the lesions, immunoreactive galanin-like cells became visible in the supraoptic and paraventricular nuclei ipsilateral to the knife cuts, and levels of galanin-like immunoreactivity increased in these nuclei 7 days after bilateral transections of the hypothalamo-hypophyseal tract. Immunoreactive galanin fibers in the external layer of the median eminence around the portal capillaries were found to be of paraventricular and arcuate nucleus origin. Bilateral paraventricular lesions caused marked (70%) reduction in levels of galanin-like immunoreactivity in the median eminence. The remaining 30% of the galanin immunoreactivity in the external layer may arise from the arcuate nucleus, which contains a great number of galanin-containing cell bodies.(ABSTRACT TRUNCATED AT 250 WORDS)
Atrial natriuretic peptide (ANF)-containing cells in the paraventricular nucleus are the major, if not the only source of ANF-containing nerve fibers and terminals in the median eminence. One week after bilateral lesioning of the paraventricular nucleus, immunoreactive ANF disappeared almost completely (87-92%) from the median eminence. The paraventriculo-median eminence ANF system appears to be distinct from the periventricular ANF system. Since adrenalectomy did not influence median eminence ANF levels in either sham-operated or paraventricular nucleus-lesioned animals, but depleted ANF levels in the preoptic and hypothalamic periventricular nuclei, it would appear that the latter system is intimately involved in the CNS control of fluid and electrolyte homeostasis.
The cell-groups of the human septum pellucidum are demonstrated in a series of 27 frontal sections. The basal part of the septum which contains mainly nerve cells extends 14-16 mm in the oro-caudal direction. Within this region two medial nuclei with 6 subdivisions and two lateral nuclei with 3 subdivisions were distinguished. The definition of oro-caudal coordinates and the topographical description of nuclei may be of help in localizing with sufficient accuracy clinico-pathological alterations of the septum.
Previous structure-activity and pharmacologic studies with duodenal ulcerogens cysteamine and propionitrile implicating catecholamines in the pathogenesis of duodenal ulceration have now been followed up by dose- and time-response biochemical investigations to assess the importance of monoamines in the development of duodenal ulcers. The concentrations of norepinephrine (noradrenaline), dopamine, serotonin and their metabolites were measured in total brain, brain regions, stomach, duodenum, pancreas and adrenals in the rat. Turnover of catecholamines was determined in rats pretreated with the inhibitor of tyrosine hydroxylase alpha-methyl-p-tyrosine. The duodenal ulcerogens caused a dose- and time-dependent depletion of norepinephrine in virtually all the tissues examined. The effect was maximal 4 or 7 hr after cysteamine or propionitrile, and norepinephrine levels returned to normal in 24 hr. Dopamine changes were selective and often biphasic, e.g., elevation in adrenals, biphasic in brain cortex, hippocampus and midbrain, but uniformly decreasing in glandular stomach and duodenum. In the median eminence dopamine levels decreased by 181 and 324% at 15 and 30 min, respectively, after cysteamine, but neither dopamine nor 3,4-dihydroxyphenylacetic acid was modified in the periventricular nucleus. Serotonin levels were relatively stable, revealing slight elevations or no changes in most of the tissues. The turnover of norepinephrine was accelerated by both chemicals in virtually all brain regions, but dopamine turnover was affected only in a few areas, e.g., in the corpus striatum and medulla oblongata cysteamine decreased dopamine turnover, whereas propionitrile first (at 1 hr) accelerated then (at 8 hr) significantly suppressed it.(ABSTRACT TRUNCATED AT 250 WORDS)
Immunoreactive substance P (SPi) was measured in the various hypothalamic structures and amygdala one week after placing a cut around the medial basal hypothalamus (MBH). SPi content decreased in the stalk-median eminence (SME), anterior and posterior parts of the arcuate nucleus (inside the isolated region) as well as in the paraventricular nucleus (outside the cut), while there was no change in the posteromedial amygdaloid nucleus. We suggest that there is a tuberoinfundibular neuronal system containing SPi with cell bodies in the MBH and terminals in the SME. In addition, nerve fibers containing SPi from outside the MBH may reach both the SME and the arcuate nucleus and might influence neuroendocrine regulation.
The nucleus of the solitary tract and the dorsal vagal nucleus are richly innervated by thyrotropin-releasing hormone (TRH)-containing fibers arising from the caudal raphe nuclei. After transection of vertically oriented fibers by a horizontal knife-cut in the medulla oblongata, TRH-staining disappeared from the vagal nuclei while it increased in transected nerve fibers ventral to the knife-cut. TRH-containing cells are mainly located in the nucleus raphe pallidus and raphe obscurus. TRH-containing fibers run dorsally within the raphe and enter the dorsal vagal complex at its rostral tip. Then they turn caudally and send branches laterally. Immediately caudal to the level of the obex, several TRH-containing fibers cross over the central canal. Cells in regions other than the raphe (hypothalamus or other rostral areas, ventrolateral medulla, cranial nerves) must contribute little to the TRH innervation of the nucleus of the solitary tract and dorsal vagal nucleus, since various knife-cuts transecting all above possible connections did not alter the TRH innervation pattern or TRH concentrations of these vagal nuclei.
Concentrations of glutamate and aspartate have been measured in 45 microdissected brain areas and nuclei in rat. Both amino acids are ubiquitously present and distributed unevenly in the central nervous system. Very high glutamate levels were found in the cerebellum and the insular cortex, high levels in neocortical and limbic cortical areas, and in the nuclei of the medial hypothalamus. Aspartate is distributed rather uniformly with the highest concentration in the hypothalamic arcuate nucleus and the lowest in the midbrain central gray matter and the cerebellum. Acute formalin (pain) stress elevated glutamate and aspartate levels in the cortical areas and substantia nigra significantly, but had minor or no effects on other brain nuclei. Increased locomotor and behavioral activities due to a high dose of amphetamine resulted in a 2-5-fold increase of glutamate and aspartate concentrations, particularly in the biogenic amine-containing brain nuclei.
Variations in calcium alimentation influence the development of high blood pressure in genetic hypertensive rats. Different calcium feeding and changes in parathyroid hormone status cause altered cAMP-content in specific brain areas. All animals with high calcium diet show significant elevated cAMP-content in the locus coeruleus, irrespective of parathyroid status. These findings support the hypothesis that elevated cAMP-concentrations reflect an increased depressor activity of the locus coeruleus.
Concentrations of gamma-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).
Concentrations of taurine have been measured in 44 microdissected rat brain nuclei or areas. Taurine is ubiquitously present and distributed unevenly in the rat brain: the ratio of the highest (pyriform cortex) to lowest (midbrain reticular formation) concentrations is 4.7:1. High taurine levels were found in cerebral cortical areas, caudate-putamen, cerebellum, median eminence, and supraoptic nucleus. Acute pain stress reduced taurine levels in the hypothalamus and the lower brainstem nuclei but not in cortical areas. Increased locomotor and behavioral activities following a high dose of amphetamine elevated taurine concentrations significantly in the substantia nigra and locus ceruleus.
The source and location of serotonin in the intermediate lobe of the rat pituitary were determined by high performance liquid chromatography and immunohistochemistry. Serotonin is present in the intermediate lobe in nerve fibers and terminals, in mast cells and in elements in the blood circulating in vessels on the surface of the lobe.
The effects of anterior hypothalamic deafferentation on luteinizing hormone releasing hormone (LH-RH) fiber density in the mediobasal hypothalamus (MBH) were compared to those of a number of nonsurgical treatments which give rise to anovulatory sterility (injections of estradiol valerate, exposure to constant light, or neonatal androgen administration) in the female rat. All of the treatments used (surgical and nonsurgical) disrupted the normal 4-day pattern of estrous cyclicity. Bilateral anterior hypothalamic deafferentation markedly reduced the packing density of LH-RH fibers in the MBH. Unilateral deafferentation reduced the number of fibers on the ipsilateral side of the MBH by 31-64% and on the contralateral side by 15-40%. In contrast, none of the three nonsurgical treatments had any significant effect on the LH-RH fiber density. Electron microscopic examination revealed no morphologic, or distribution differences in MBH LH-RH fibers between control females and animals rendered anovulatory by the nonsurgical experimental procedures. These results demonstrate that estrogen, androgen, and constant light induced anovulatory sterility are not associated with any overt change in the number or morphology of LH-RH immunoreactive fibers in the MBH, suggesting that the primary lesion responsible for the failure of normal estrous cyclicity in such animals resides in the systems responsible for regulating the activity of the LH-RH neurons rather than in the LH-RH neurons themselves.
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