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L Jennes

Publications and source records attributed to L Jennes.

89 records · Page 5Linked to original sources
PubMed1982

Neurotensin: topographical distribution in rat brain by immunohistochemistry.

The anatomical distribution of neurotensin perikarya and fibers in rat brain, spinal cord, and pituitary has been studied by immunohistochemistry. Neurotensin immunoreactivity is widely distributed throughout the brain, especially in forebrain and midbrain limbic structures, but also in the pons, medulla, and spinal cord. Areas with low immunoreactivity, or lack of it, stand out and include most of the hippocampus, isocortex, ventromedial and dorsomedial hypothalamic nuclei, somatomotor nuclei, cerebellum, and dorsal column nuclei. Strong neurotensin immunoreactivity is found in accumbens-caudate-putamen, central and medial amygdaloid nuclei, ventrolateral septum, pars lateralis of the nucleus of the stria terminalis, paraventricular, periventricular, and lateral hypothalamus, median eminence, thalamic intralaminar and periventricular nuclei, ventral tegmentum, central gray, certain raphe nuclei, locus ceruleus, nucleus parabrachialis medialis and lateralis, nucleus of the solitary tract and area postrema, spinal and trigeminal substantia gelatinosa, as well as certain cells in the anterior pituitary. The anatomical data suggest the existence of neurotensin circuits for (1) the control of autonomic-endocrine functions, involving the nucleus tractus solitarii, area postrema, nucleus ambiguus, nucleus parabrachialis, nucleus paraventricularis, nucleus centralis amygdalae, and pars lateralis of the bed nucleus of the stria terminalis; and (2) for the transmission and modulation of certain somatosensory qualities, involving the spinal substantia gelatinosa, trigeminal sensory nuclei, and thalamic intralaminar nuclei.

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PubMed1982

Neurotensin: topographical distribution of brain sites involved in hypothermia and antinociception.

When administered into the cerebroventricular system of the rat, neurotensin (NT) produces a variety of effects, including a decrease in colonic temperature and an increase in nociceptive threshold. The previous study described in detail the localization of immunohistochemical NT in the rat brain. In this study, bilateral injections of NT were made into 223 separate loci in the rat brain an a map was generated showing the brain regions where NT produced a decline in colonic temperature and an increase in hot plate response latency. It was found that some of the brain areas which contain immunohistochemically identified NT responded to locally administered NT. Further, most NT-sensitive brain loci contain NT cell bodies as well as fibers. Areas in the brain where NT produced an antinociceptive response were not the same areas where NT evoked hypothermia. An antinociceptive response was consistently produced after NT injection into the nucleus amygdaloideus centralis, rostral area praeoptica medialis, the ventral thalamus dorsomedial and medial to the lemniscus medialis, rostral mesencephalic periventricular gray, and medial pontine formatio reticularis. Less-consistent antinociception was also observed in the mesencephalic formatio reticularis and the caudal diagonal band of Broca. Hypothermia was induced by NT in the area praeoptica medialis contiguous with the area anterior hypothalami, nucleus ventralis tegmenti (Tsai), floor of the fourth ventricle, and tractus spinalis nervi trigemini. Less profound hypothermia was also produced in the posterior hypothalamus. The fact that all these responsive brain areas contain NT indicates that the microinjection of NT may be mimicking the effects of endogenously released NT, thus supporting the possible physiological significance of NT as an endogenous modulator of body temperature or nociceptive sensory information.

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PubMed1982

Centrifugal innervation of the retina by luteinizing hormone releasing hormone (LHRH)-immunoreactive telencephalic neurons in teleostean fishes.

In cichlid, poecilid and centrarchid fishes luteinizing hormone releasing hormone (LHRH)-immunoreactive neurons are found in a cell group (nucleus olfactoretinalis) located at the transition between the ventral telencephalon and olfactory bulb. Processes of these neurons project to the contralateral retina, traveling along the border between the internal plexiform and internal nuclear layer, and probably terminating on amacrine or bipolar cells. Horseradish peroxidase (HRP) injected into the eye or optic nerve is transported retrogradely in the optic nerve to the contralateral nucleus olfactoretinalis where neuronal perikarya are labeled. Labeled processes leave this nucleus in a rostral direction and terminate in the olfactory bulb. The nucleus olfactoretinalis is present only in fishes, such as cichlids, poecilids and centrarchids, in which the olfactory bulbs border directly the telencephalic hemispheres. In cyprinid, silurid and notopterid fishes, in which the olfactory bulbs lie beneath the olfactory epithelium and are connected to the telencephalon via olfactory stalks, the nucleus olfactoretinalis or a comparable arrangement of LHRH-immunoreactive neurons is lacking. After retrograde transport of HRP in the optic nerve of these fishes no labeling of neurons in the telencephalon occurred. It is proposed that the nucleus olfactoretinalis anatomically and functionally interconnects and integrates parts of the olfactory and optic systems.

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PubMed1981

LHRH systems in brain of platyfish.

The luteinizing hormone-releasing hormone (LHRH) system of the platyfish Xiphophorus has been studied using immunohistochemistry and retrograde transport of horseradish peroxidase (HRP). Three different populations of LHRH-positive cell bodies are present in the brain, one in the ventral telencephalon at the border to the olfactory bulb (nucleus of olfactoretinalis), one lateral to the n. preopticus (nucleus preopticus basalis lateralis) and one in the midbrain. LHRH neurons from the nucleus olfactoretinalis project via the medial olfactory tract to the olfactory bulb and to olfactory nerves. A second projection from this nucleus enters the optic tract, crosses in the optic chiasm, and courses rostrally in the outer layer of the optic nerve to the retina, where LHRH-positive nerve fibers terminate near amacrine and bipolar cells. HRP injections into the eye or into the cut optic nerve result in retrograde transport of the enzyme to the contralateral LHRH nucleus olfactoretinalis. Projections from LHRH neurons in the lateral preoptic region can be followed medially to surround the interhemispheric ventricle and laterally to border the optic tract. At the level of the postoptic commissure, LHRH fibers condense to form a fascicle which reaches the pituitary stalk to arborize throughout the hypophysis. LHRH fibers, probably in part from the midbrain LHRH neurons, project to the optic tectum, torus semicircularis, corpus and valvula of the cerebellum, as well as to the medulla oblongata. Associations of LHRH projections with sensory systems and with endocrine-autonomic systems in hypothalamus-pituitary and lower brain stem suggest a role in the modulation and integration of sensory, autonomic, behavioral and hypophyseotrophic functions.

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PubMed1980

Changes in the LHRH-immunoreactivity of hypothalamic structures during late pregnancy and after parturition in the guinea pig.

LHRH-immunohistochemistry and radioimmunoassay of the gonadotropins were used to demonstrate changes in the LHRH content of the hypothalamus during late pregnancy and after parturition in the guinea pig. Immediately after parturition a decrease in the amount of LHRH-associated fluorescence was observed in the medial preoptic area. Only 12 h later similar changes were found in the median eminence. In the precommissural region no obvious changes were noted in the quantity of LHRH-immunoreactive "terminals" and "synapses". The radioimmunoassay of the gonadotropins shows an increase of LH shortly after parturition which reaches the level of a preovulatory rise, whereas the amount of FSH does not vary significantly. The role of the medial preoptic area and the OVLT in the regulation of the estrous cycle through LHRH is discussed.

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PubMed1980

LHRH-systems in the brain of the golden hamster.

Vibratome sections of male hamster brains were treated immunohistochemically with LHRH antiserum, and the anatomical distribution of LHRH immunoreactive cells and nerve fibers was assessed. LHRH-cell bodies are found in the ventral hypothalamus that includes its preoptic, anterior and central parts, in the septum, the olfactory tubercle, the main and accessory olfactory bulb, and the prepiriform cortex. In addition, extracerebral LHRH-neurons and ganglia exist in LHRH-positive nerves at the ventromedial surface of the olfactory tubercle and bulb as well as in olfactory nerves. Dense networks of LHRH-immunoreactive fibers are found in all regions where LHRH-cell bodies exist. Intraseptal connections reach the organum vasculosum of the lamina terminalis, the subfornical organ, and the lateral ventricle. Dorsolateral projections from the septum can be traced via the fimbria hippocampi and alveus to the ventral hippocampus, via the stria terminalis to the amygdala and piriform cortex. Ventrolateral projections extend from the level of the olfactory tubercle and preoptic-anterior hypothalamic area via the ventral amygdalofugal pathway to the prepiriform and piriform cortex as well as the amygdala. Dorsal supracallosal projections via the stria longitudinalis are seen in the induseum griseum and the cingulate cortex. Caudal efferents reach the havenula, interpeduncular nucleus, midbrain raphe, and central gray of the rostral fourth ventricle via the stria medullaris and fasciculus retroflexus and by a ventral projection via the periventricular and subventricular hypothalamus. A major portion of this ventrocaudal projection gives rise to a dense network in the median eminence. Anatomical relationships of LHRH-fibers to certain regions of the inner ventricular and outer brain surface are noted.

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PubMed1979

Scanning and transmission electron microscopy of intraventricular dendrite terminals of hypothalamic cerebrospinal fluid contacting neurons in Triturus vulgaris.

A scanning (SEM) and transmission electron microscopic (TEM) study of the ventricular wall of the hypothalamus of Triturus vulgaris was performed with special regard to the intraventricular dendrite terminals of the cerebrospinal fluid (CSF) contacting neurons of the preoptic area (magnocellular and parvocellular preoptic nuclei), the infundibular lobe (anterior periventricular nucleus, infundibular nucleus), and the paraventricular organ. In the preoptic area and infundibular lobe, the terminals were knob-like or club-shaped, of various sizes (diameter about 0,5 to 3,0 micrometer) and located immediately above the ependyma. Ultrastructurally, they may contain dense-core vesicles of varying sizes. The CSF contacting dendrite endings of the paraventricular organ built up a supraependymal labyrinthic layer which could be divided into a rostral crest-like part and a caudal flat and broad division. In both parts, three main types of terminals of various size and shape could be distinguished: a) ramifying, b) elongated, and c) bulb-like dendrite endings which also differed by their TEM structure. The bulk-like terminals, first of all the small ones, originated from the distal part of the nucleus of the organ (nucleus organi paraventricularis) while the other two types took their origin from its intra- and subependymal part. In all areas investigated, each intraventricular dendrite ending gave rise to a solitary cilium (type 9 X 2 + 0). It differed from the ependymal kinocilia by both SEM and TEM characteristics. In the paraventricular organ, the neuronal cilia were hidden inside, or below the supraependymal layer of terminals. There were intraventricular axons which formed synapses on CSF contacting dendrite endings of both parts of the paraventricular organ. Free intraventricular neurons, further ependymal areas heavily or scarcely ciliated, were described. The CSF contacting dendrite terminals were predominantly present near ventricular recesses and in regions where the ependyma was scarcely ciliated.

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PubMedDate not supplied

Inhibition by MIF-I of alpha-MSH induced increase of intraocular pressure and miosis in rabbits.

The effects of intracameral (i.c.) administration of MIF-I on the ocular response to alpha-MSH were tested in rabbits. In confirmation of previous studies, i.c. alpha-MSH significantly increased intraocular pressure (IOP) and reduced pupillary diameter (PD). Concomitant administration of alpha-MSH and MIF-I antagonized both the IOP increase and miosis induced by alpha-MSH. Aqueous humor (AH) dynamics studies revealed that alpha-MSH increases IOP, possibly, by decreasing AH outflow. The decreased AH outflow induced by alpha-MSH was antagonized by concurrent administration of MIF-I and alpha-MSH. MIF-I did not affect IOP or PD when administered alone. These results add more support for a role of alpha-MSH in ocular function, and suggest that the ocular response to alpha-MSH may be subject to inhibitory control by MIF-I.

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PubMedDate not supplied

Pupillary response to atrial natriuretic factor in rabbits.

This study was designed to evaluate the pupillary and intraocular pressure (IOP) response to exogenously administered atrial natriuretic factor (ANF) in rabbits. Dose-response studies were conducted by administering intracameral (i.c.) ANF (0.1-5 micrograms). The effect of route of administration was evaluated by administering ANF (5 micrograms/kg) intravenous (i.v.) subcutaneous (s.c.) and intraperitoneal (i.p.). In a final study, normal rabbit serum or ANF antiserum were administered i.c. In all studies, pupillary diameter (PD) and IOP were evaluated. Intracameral administration of ANF (0.1-5 micrograms) produced a significant (P less than 0.01) dose-dependent unilateral miosis without affecting IOP. Peripheral (i.v., s.c., i.p.) administration ANF did not affect PD or IOP. Finally, ANF antiserum did not affect PD significantly. These data suggest that ocular, but not circulating ANF may contribute to regulate pupillary function. The mechanism of the miotic response to ANF probably involves interactions with other autonomic neurotransmitters because immunoneutralization of endogenous ocular ANF was without measurable effect.

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PubMedDate not supplied

Antagonism of neurotensin induced miosis by thyrotropin-releasing hormone (TRH) in rabbits.

In previous studies we have shown that thyrotropin-releasing hormone (TRH) antagonizes many of the neural effects of neurotensin (NT). This study, evaluated the ability of TRH and two TRH analogs: 3 methyl-His-TRH and Phe2-TRH to affect NT-induced miosis in rabbits. In confirmation of previous findings, NT (30 micrograms) produced a significant miosis. The high (60 micrograms), but not the low (30 micrograms) dose of TRH significantly antagonized NT (30 micrograms)-induced miosis. Of interest was the observation that 3 methyl-His-TRH and Phe2-TRH were more effective than native TRH in blocking NT-induced miosis. The inhibitory effect of 3 methyl-His-TRH on the miotic response to NT exhibited long duration (approximately 60 min) when compared to native TRH and Phe2-TRH. TRH or the TRH congeners had no appreciable effects on pupillary diameter when administered alone. These findings indicate that TRH antagonizes the miotic response to NT, and suggest a hitherto undescribed peptide-peptide interaction involved in regulation of iris motility.

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PubMedDate not supplied

Receptor-mediated uptake of GnRH agonist and antagonists by cultured gonadotropes: evidence for differential intracellular routing.

The binding and uptake of the GnRH agonist D-Lys6-GnRH and of the antagonists [N-Ac-D-(pyro)-Cl-Phe1,2-D-Trp3-Lys6-D-Ala10]-GnRH and D-p-Glu1-D-Phe2-D-Trp3-D-Lys6-GnRH by dispersed pituitary gonadotropes was studied with electron microscopy. The peptides were coupled to colloidal gold markers with a diameter of 6 or 20 nm which were incubated separately or together for time periods between 15 and 180 min. Both antagonists could be found after 45 and 180 min at 37 degrees C in lysosomes as well as at the plasma membrane of gonadotropes. Co-incubation of both antagonists or of agonist and either antagonist resulted in uptake of the conjugates into separate lysosomes as well as mixed together into the same lysosome. Localization of the antagonists in structures associated with the Golgi apparatus was not observed at the time points studied. The results show that both GnRH agonist- and antagonist-conjugates are biologically active and that they are internalized by the gonadotropes via receptor mediated endocytosis. The failure to detect antagonist conjugates in the Golgi apparatus may indicate that passage through this organelle requires activation of the receptors by agonists and that the uptake of antagonist into lysosomes due to normal membrane protein turnover.

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PubMedDate not supplied

Focal ellipsoid deposits in the atrial myocytes of Syrian hamster.

A peculiar hyaline sarcoplasmic inclusion in the atrial myocytes of old female Syrian hamsters is described. This type of inclusion resembles that described in rare human cardiomyopathy. They have also been described in other rodents and have been speculated eventually to contain atrial natriuretic factor (ANF). The present study demonstrated that they are fibrillar in nature, however, and do not contain ANF-immunoreactive product. Because their morphologic aspect is analogous to that described in human heart and in the pathology of other contractile tissues, it is suggested that they probably consist of intermediate filaments and/or associated macromolecules.

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