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C J Frederickson

Publications and source records attributed to C J Frederickson.

At least 37 records · Page 2Linked to original sources
PubMed1991

Zinc containing projections to the bed nucleus of the stria terminalis.

A retrograde tracing method that selectively labels the perikarya of zinc-containing neurons was used to identify the neurons that supply zinc-containing fibers to the bed nucleus of the stria terminalis in the rat. In agreement with prior lesion studies, retrograde tracing indicates that neurons in amygdalar and periamygdalar regions are the major sources of the zinc-containing innervation of the bed nucleus complex. Zinc-containing neurons in the presubiculum and prosubiculum were also retrogradely labeled from the BNST, whereas cells of the subiculum proper did not label. Light and occasional retrograde labeling of some CA1 and CA2 neurons and limbic cortical neurons was also observed, but the possibility of transport from regions bordering BNST injections (septum, caudate-putamen) could not be excluded in the latter cases.

Animals↗
PubMed1991

Applications of piezoelectric fluid jetting devices to neuroscience research.

Piezoelectric pumps or "jets" are used in industry for precise dispensing of small volumes of fluids. In the present work we have tested the feasibility of using these piezoelectric devices for dispensing fluids in neurobiological research. In one experiment, 70 picoliter (pl) droplets of histochemical reagent were jetted onto discrete targets of frozen tissue sections, and qualitative and quantitative histochemical studies were done on the small (170 microns diameter) circle of tissue wet by the droplets. In the second experiment, 70 pl droplets of neuroactive drugs were jetted onto brain tissue slices while recording single neurons extracellularly in vitro, and the effects of the drugs were found to vary systematically as a function of the number of drops and the distance between drop application and the recorded neuron. The results indicate that piezoelectric jets could have wide application for dispensing fluids in neurobiological research.

Administration, Topical↗
PubMed1990

A retrograde transport method for mapping zinc-containing fiber systems in the brain.

A method for selectively labeling the CNS neurons that give rise to zinc-containing axonal boutons is described. Focal intracerebral infusions of selenium anions are used to produce a precipitate (presumably ZnSe) in zinc-containing axonal boutons at the injection site, and within 24-48 h, the precipitate is transported to the neurons of origin of those boutons. Silver enhancement is used to render the ZnSe visible in sections prepared for the light or electron microscope. No evidence of retrograde labeling is apparent in neurons that do not contain zinc in their boutons. Thus, the method provides a chemically specific technique for retrograde tracing of zinc-containing pathways in the CNS.

Animals↗
PubMed1990

In situ binding of bouton zinc reversibly disrupts performance on a spatial memory task.

Neurons with zinc in the presynaptic vesicles innervate much of the telencephalon, but the functional significance of the vesicular zinc has never been established. The present work shows that reversible binding of zinc by drug infusion into the hippocampus produces a time-locked and selective disruption of hippocampal-dependent spatial-working memory. A role for vesicular zinc in neurotransmission or neuromodulation is implied.

Animals↗
PubMed1990

Possible role of zinc in the selective degeneration of dentate hilar neurons after cerebral ischemia in the adult rat.

The fluorescent dye 6-methoxy-8-p-toluene sulfonamide quinoline (TSQ) was used to monitor the distribution of zinc in the hippocampus and fascia dentata of adult rats subjected to 20 min of cerebral ischemia. In normal brains TSQ stains only neuropil, in particular the mossy fiber layers in the dentate hilus (CA4) and CA3, but within 2 h after ischemia, TSQ-fluorescent cells were observed in the dentate hilus. At longer survival times TSQ-positive cells stained positively with acid fuchsin, a sign of cellular degeneration. At the same time a decrease in the TSQ fluorescence of the mossy fiber terminals in the dentate hilus (CA4) and the CA3 mossy fiber layer was noted. The observations suggest that zinc many play a role in the selective death of dentate hilar neurons after cerebral ischemia.

Aminoquinolines↗
PubMed1990

Labeling of the neurons of origin of zinc-containing pathways by intraperitoneal injections of sodium selenite.

Intraperitoneal injections of sodium selenite result in the formation of zinc-selenium complexes in zinc-containing axonal boutons ("Timm stainable boutons"), and the zinc-selenium precipitate can be rendered visible in histological sections by silver enhancement. In this work we present evidence, in the rat, that zinc-selenium precipitates formed in vivo after intraperitoneal injections of sodium selenite are translocated by colchicine-sensitive retrograde transport to neural perikarya when animals are allowed to survive 12-24 h after the selenite administration. Silver enhancement renders the perikaryal precipitates visible and thus demonstrates the perikarya of all zinc-containing neurons in the CNS simultaneously. Large populations of zinc-containing neurons identified by the method are found in layers II, III, and VI of all neocortical areas, in the superficial and deep layers of the prepyriform areas and, with a high degree of regional differentiation, in the retrosplenial, entorhinal, para- and presubicular cortices, the hippocampal formation and the amygdaloid complex. Zinc-containing cells were absent from the caudate-putamen, nucleus accumbens and septal complex. Labeled zinc-containing cells are absent in non-telencephalic parts of the brain. The findings indicate that the zinc-containing circuitry of the brain mainly serves in telencephalic information processing.

Animals↗
PubMed1990

Zinc-containing neurons in hippocampus and related CNS structures.

Recent advances in metallohistochemistry have substantiated the identification of a distinct class of neurons in the brain, the zinc-containing neurons. These neurons sequester peculiar amounts of zinc in their presynaptic boutons and show both high-affinity uptake and calcium- and impulse-dependent release of the cation. It is thought that the zinc may act to stabilize the storage of certain macromolecules in presynaptic vesicles, but there is also mounting evidence that zinc released from vesicles can produce a broad spectrum of neuromodulatory effects upon target cells. Zinc-containing neurons are found predominantly in limbic and cerebrocortical regions, and a possible role of these neurons in the modification of synaptic strength is considered.

Animals↗
PubMed1989

Amygdaloid efferents through the stria terminalis in the rat give origin to zinc-containing boutons.

Many regions of the basal forebrain are innervated by zinc-containing axonal boutons. In the present work, the lesion/degeneration method, coupled with histochemical staining for zinc-containing boutons, was used to determine the origins and efferent pathways of these zinc-containing projections to the basal forebrain. Knife cuts of the stria terminalis or extensive electrolytic lesions of the amygdala resulted in the bleaching of the staining for zinc (Timm stain) and terminal degeneration (Fink-Heimer method) ipsilaterally in the following areas: granule cell layer of the accessory olfactory bulb, shell of nucleus accumbens, bed nucleus of the stria terminalis, striohypothalamic nucleus, retrochiasmatic area, ventromedial hypothalamic nucleus (in the cell-sparse shell), medial tuberal nucleus, terete hypothalamic nucleus, and ventral premammillary nucleus. Small lesions made with ibotenic acid in the posteromedial part of the amygdalohippocampal area caused bleaching of the stain for zinc in the accessory olfactory bulb, in the medial zone of the bed nucleus of the stria terminalis, and in the ventral premammillary nucleus. Lesions in either the ventral subiculum or the anterolateral part of the amygdalohippocampal area caused bleaching in the ventromedial hypothalamic nucleus. Lesions in the hippocampus or in the neocortex did not produce bleaching of the stain for zinc in the above-mentioned terminal fields. The present results agree with previous studies on amygdaloid efferents and suggest that neurons in the amygdalohippocampal area and, possibly, in the ventral subiculum give origin to zinc-containing boutons.

Amygdala↗
PubMed1989

Translocation of zinc may contribute to seizure-induced death of neurons.

Rats were subjected to seizures induced by kainic acid, and the resulting changes in CNS zinc staining were studied with the toluene sulfonamide quinoline fluorescence method. Seizures caused a loss of zinc staining from presynaptic boutons in many limbic and cerebrocortical regions. Simultaneously, the postsynaptic neurons that were degenerating (acidophilic) in those regions as a result of the seizure developed intense fluorescence for zinc. A possible role for zinc in the death of the postsynaptic neurons is suggested.

Amygdala↗
PubMed1989

Evidence from dithizone and selenium zinc histochemistry that perivascular mossy fiber boutons stain preferentially "in vivo".

This paper describes a perivascular staining pattern that is obtained when dithizone or sodium selenite are used to label zinc intravitally. Our observations indicate that the perivascular staining is a result of zinc labeling in mossy fiber boutons adjacent to capillaries and suggest that there might be a special blood brain barrier in the mossy fiber regions.

Animals↗
PubMed1989

Darkfield illumination improves microscopic detection of metals in Timm's stained tissue.

Deposits of trace or toxic metals can be quickly identified by light microscopical surveys of tissue sections stained for metals by variants of Timm's silver enhancement method. The present work shows that the small, isolated silver grains that label isolated deposits of metal in tissue are undetectable in brightfield light microscopy but are easily detected in darkfield microscopy. Darkfield illumination is therefore recommended for improving the detection of trace or toxic metals in tissue.

Animals↗
PubMed1988

Loss of zinc staining from hippocampal mossy fibers during kainic acid induced seizures: a histofluorescence study.

A quinoline fluorescence method for staining zinc in axonal boutons was used to study the effects of kainic acid (KA) induced seizures upon zinc in the boutons of hippocampal mossy fibers. Compared to untreated rats, rats given KA (10-12 mg/kg) and undergoing sustained seizures showed a marked loss of zinc fluorescence in the mossy fiber regions. The reduced fluorescence was detectable within 3 h of KA administration, was most pronounced at 12-24 h, and was still noticeable up to 48 h after KA. The findings suggest that zinc is released rapidly from mossy fiber boutons during seizures.

Animals↗
PubMed1988

Zinc-containing fiber systems in the cochlear nuclei of the rat and mouse.

Zinc-containing neurons are cells which sequester zinc in the vesicles of their axonal boutons; such zinc-containing fiber systems have been previously shown to innervate many limbic and cerebrocortical brain regions. The present study of rats and mice shows that zinc-containing axons also innervate the cochlear nuclei, forming two morphologically-distinct projection systems. One zinc-containing pathway innervates the molecular stratum of the dorsal nucleus, supplying a diffuse, even band of neuropil staining throughout the stratum. The other pathway projects sparsely to the various small cell (granule cell) regions of the nuclei where the zinc-positive elements form scattered clusters and threads of bouton-like puncta amidst the granule neuron somata. Preliminary observations indicate that the pattern is the same in the cat as in the rat and mouse.

Animals↗
PubMed1987

Quantification of hippocampal noradrenaline and zinc changes after selective cell destruction.

Deafferentation of septo-hippocampal projections results in sprouting of sympathetic noradrenergic (NA) fibers into the hippocampus. To determine whether dentate granule cells are necessary for the initiation and/or direction of this sprouting, both NA intensity and zinc density were microspectrophotometrically quantified at 10 or 30 days after selective neurotoxin lesions of either granule cells or CA3 pyramidal cells, and electrolytic lesions of medial septum. Groups with elevated zinc density at 10 days also had significantly higher NA levels at 30 days. Destruction of granule cells eliminated the rise in zinc and prevented the NA increase. The zinc increase may be related to a nerve growth factor-like protein responsible for the initiation of sympathetic sprouting.

Adrenergic Fibers↗
PubMed1987

A quinoline fluorescence method for visualizing and assaying the histochemically reactive zinc (bouton zinc) in the brain.

A histochemical method for staining CNS zinc by the stoichiometric formation of zinc: quinoline fluorescent chelates is described. Four congeners of quinoline have been tested, and two found to be useful for histochemistry. The procedure is a one-step method, suitable for fresh-frozen and fixed tissue sections alike. The quinoline fluorescence selectively labels the CNS regions (such as hippocampus, amygdala) shown by prior histochemical procedures to be rich in histochemically reactive zinc in axon boutons and therefore appears to be a specific marker for the bouton zinc. Microfluorometric data indicate that the fluorochrome can be used for quantitative estimates of CNS zinc pools as well as qualitative studies of localization.

Animals↗
PubMed1987

A comparison of the electrophysiological and pharmacological properties of serotonin-containing neurons in the nucleus raphe dorsalis, raphe medianus and raphe pallidus recorded from mouse brain slices in vitro: role of autoreceptors.

The potential role of autoreceptors in regulating the activity of serotonin-containing nucleus raphe dorsalis (RD), raphe medianus (RM) and raphe pallidus (RPA) neurons was examined by recording the activity of these neurons under a variety of conditions both in vivo and in vitro. Raphe neurons recorded in vivo displayed the characteristic slow, rhythmic discharge pattern previously described for rat and cat raphe cells. The activity of these neurons was suppressed in a dose-dependent manner by tryptophan, LSD and chlorimipramine administered intravenously. There were no significant changes in the spontaneous discharge rate of raphe neurons over time when recorded in vitro, even though tissue serotonin and its metabolite, 5-hydroxyindoleacetic acid, decreased dramatically. RPA neurons fired significantly faster than either RD or RM neurons both in vivo and in vitro. Prior depletion of brain serotonin by p-chlorophenylalanine administration resulted in no significant change in raphe unit activity recorded in vitro. Elevation of brain serotonin by monoamine oxidase inhibition produced a total inhibition of raphe unit activity in vitro. Similarly, increasing the concentration of serotonin in the tissue slice by adding serotonin directly to the incubation medium resulted in a profound, though transitory, depression of unit activity. This depressant effect of serotonin was rapidly reversible upon drug wash-out. Serotonin receptor blockers, methiothepin, cypoheptadine, and methysergide, produced no significant change in unit activity. The serotonin reuptake blocker, fluoxetine, produced a total inhibition of raphe unit activity in all three nuclei in vitro. These data suggest that excess serotonin suppresses the activity of raphe neurons, apparently by an action on autoreceptors, but that a deficiency, or normal concentration, of serotonin does not influence the spontaneous activity of these cells. The data also show that RD and RM are much more sensitive to the depressant effects of serotonin than the caudal RPA neurons. More generally, these studies provide a data base for examining the electrophysiological and pharmacological characteristics of serotonergic neurons in the three major serotonin-containing nuclei in mouse brain. The mouse has proven to be a much easier species than the rat to use in these types of studies, based on the finding that mouse brain slices are more viable in vitro than are rat brain slices.

Action Potentials↗
PubMed1987

Zinc-containing 7S-NGF complex. Evidence from zinc histochemistry for localization in salivary secretory granules.

7S-NGF is a pro-protein containing a neurotrophic subunit, beta-NGF, which has been localized by immunocytochemistry to the granules of granular convoluted tubule (GCT) cells in certain murine salivary glands [Watson et al., Anat Rec (1985) 213:365]. The 7S-NGF pro-protein contains zinc and is stabilized by zinc ions [Pattison and Dunn, Biochemistry (1976) 15:3696]. In the present work, dithizone, toluene sulfonamide quinoline (TSQ), and neo-Timm's methods for zinc were used to determine whether zinc histochemistry could be used to visualize the zinc associated with the 7S-NGF complex and, if so, whether zinc histochemistry might corroborate the reported localization of the 7S-NGF complex in GCT secretory granules. The results indicate that intensity of zinc staining varies with the reported variations in NGF levels in different salivary glands, and that the zinc is selectively concentrated in the GCT secretory granules. We suggest that zinc histochemistry may be a useful marker for the presence of the zinc-stabilized 7S-NGF pro-protein.

Animals↗