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C Nitsch

Publications and source records attributed to C Nitsch.

At least 37 records · Page 2Linked to original sources
PubMed1993

Opposite effects of intranigral ibotenic acid and 6-hydroxydopamine on motor behavior and on striatal neuropeptide Y neurons.

Unilateral lesions of the basal ganglia circuit induce a disequilibrium of motor processing, most obviously expressed by the resulting circling behavior. Compensatory events, which reduce the motor asymmetry, could be accompanied by changes in neurotransmitter/modulator parameters in the involved brain regions. In the present investigation, the effects of an interruption of the striato-nigro-thalamic loop by ibotenic acid (IBO)-induced lesions of total substantia nigra (SN) on circling behavior and on striatal neuropeptide Y (NPY) neurons were compared with those after the selective destruction of the dopaminergic nigrostriatal projection with 6-hydroxydopamine (6-OHDA). Directly after the operation, IBO-lesioned rats showed a high circling rate to the side contralateral to the lesion, whereas 6-OHDA-lesioned rats showed ipsiversive circling. With the lesion-induced development of dopamine receptor supersensitivity, 6-OHDA-treated rats, when stimulated with the dopaminergic agonist apomorphine, change their circling direction to the contralateral side. Complete IBO lesions of the SN abolished this effect: rats continued to circle to the contralateral side. These observations suggest that not only the dopaminergic denervation of the striatum but also the imbalance in the activity of the thalamo-cortical projection (reduced after 6-OHDA, augmented after IBO) are instrumental in determining the degree and direction of circling. Quantification of NPY-immunoreactive neurons in striatum revealed a decrease in 6-OHDA lesioned rats after 3 days on the side contralateral to the lesion, an effect even more pronounced after 4 month's survival time. IBO-induced lesions of the SN had an opposite effect on NPY-immunoreactivity in the striatum: neuron counts were lower on the ipsi- than on the contralateral side. In addition, a time-dependent variation in total number of NPY-neurons was noted: during the early postoperative periods an increase, followed by a prolonged decrease to values below 50% of the controls after 4 months. Taken together, these results provide evidence that a dopaminergic deafferentation and its consequences on the nigro-thalamo-cortical loop will determine NPY expression in the striatal interneurons. In particular, it is suggested that the number of striatal NPY-neurons and the imbalance in cortical activity are tightly coupled in terms of a negative correlation.

Animals↗
PubMed1993

Absence of calcium-induced LTP-like response in the dentate area of seizure-prone gerbils and its relation to parvalbumin in the entorhinal perforant path synapse of this species.

Mongolian gerbils (Meriones unguiculatus) are genetically predisposed to seizures, for which an involvement of hippocampal hyperexcitability and disinhibition has been suggested. The response in vitro of the hippocampal synaptic circuit upon exposure to an elevated extracellular calcium concentration is well known in the rat, and its dependence on inhibitory and excitatory transmission has been thoroughly studied. The purpose of the present investigation was to compare the influence of elevated extracellular calcium on inhibitory and excitatory transmission in the dentate area and the CA1 field of gerbil and rat hippocampal slices. Elevated calcium induced in the CA1 area of both animal species a long-term potentiation (LTP)-like response. Upon calcium exposure in the dentate area a decrease in population spike amplitude occurred in both gerbil and rat slices, indicating a similar degree of synaptic inhibition in the two species. However, in contrast to the effects known in the rat, elevated extracellular calcium failed to enhance the excitatory postsynaptic potential in the gerbil dentate area. This difference may depend on the species-specific, selective presence of the calcium-binding protein parvalbumin in perforant path terminals of the gerbil, which may be relevant to the susceptibility to seizures of this animal species.

Animals↗
PubMed1993

Comparison by means of a computer-supported device of the enlarging characteristics of two different instruments.

Numerous studies report different results when testing endodontic instruments with similar and/or different research protocols. However, objective studies that could eliminate the factors inherent to the operator have not yet been developed. Simulated root canals in clear casting resin were used as models. The Canal Master U and Flexogate were tested by using a double exposure photographic technique. A computer-aided device capable of reproducing three-dimensional enlarging movements and irrigation of the simulated canals was developed. The enlarging movements were programmed according to the step-back and step-down techniques. The enlarging of simulated root canals with this device proved to be constant and reproducible. Standard deviations were kept low and were dependent on the degree of canal curvature. The enlarged simulated root canals showed that both instruments could be kept centered in the path of the root canal. Results showed only a few significant differences between the effective material removed and a theoretical ideal amount of removed material.

Dental Cavity Preparation↗
PubMed1992

Differential Ca2+ binding properties in the human cerebellar cortex: distribution of parvalbumin and calbindin D-28k immunoreactivity.

The distribution of the Ca(2+)-binding proteins parvalbumin (PV) and calbindin D-28k (CaBP) was investigated in the human cerebellar cortex. Purkinje cells contain both PV and CaBP. PV but not CaBP stains stellate and basket cells in the molecular layer. In the granular layer Golgi neurons can be subdivided into a majority, devoid of both Ca(2+)-binding proteins, and a scanty population which appears to be PV- and CaBP-immunoreactive. Thus GABAergic neurons in the human cerebellar cortex show selective differences in their Ca(2+)-binding properties, and these differences might reflect a heterogeneity in the processing of Ca(2+)-mediated events.

Aged↗
PubMed1992

Ibotenic acid-induced calcium deposits in rat substantia nigra. Ultrastructure of their time-dependent formation.

The excitotoxin ibotenic acid (IBO) induces local calcium deposits upon injection into rat substantia nigra. Their formation has been investigated at the ultrastructural level in a time course study from 2 days to 8 weeks survival. Potassium bichromate stain was used to visualize pathological calcium accumulation. Two days after IBO application, reaction product for calcium was observed in mitochondria of degenerating perikarya and dendrites, but not in axons, boutons or glia. Four days after the lesion, calcium stain was found, in addition, in a seemingly free form in a few dendrites, especially those still contacted by intact boutons and not sequestrated by invading glia. Two days later, most of these calcium-accumulating dendrites were separated by astroglia from their synaptic partners. At the border between glia and dendrite a fibrillar matrix was formed which further accumulated calcium. During the following weeks this matrix enlarged stepwise and was infiltrated with calcium, thus giving a picture resembling the annual growth rings of trees. The evolving bodies incorporated smaller deposits in their vicinity, finally representing the large concretions seen at the light microscopic level from the 4th postoperative week onward. Similarities and dissimilarities of these observations with the results from other ultrastructural studies on excitotoxin lesions are detailed. It is suggested that the different outfit of neuronal subpopulations and of glia with ligand-gated and metabotropic glutamate receptors in the single brain region, as well as the local response repertoire of glial cells towards the excitotoxic injury with the subsequent formation of a calcium-accumulating matrix provide the molecular basis for the formation of calcium deposits.

Animals↗
PubMed1992

High frequency of ciliated neuropeptide Y-immunoreactive neurons in rat striatum.

An analysis of the ultrastructure of neuropeptide Y-immunoreactive neurons in rat striatum revealed the presence of a cilium in half of the neurons serially sectioned in part, and in a quarter of the neurons observed in single sections. It is speculated that the cilium is a developmental remnant, i.e., a sign of the less differentiated state of the NPY-containing neurons compared with the other neurons, and that this could explain the plasticity of this type of neuron after lesions.

Animals↗
PubMed1992

The prolonged presence of glia-derived nexin, an endogenous protease inhibitor, in the hippocampus after ischemia-induced delayed neuronal death.

The presence of glia-derived nexin and glia fibrillary acidic protein (GFAP) was investigated in the hippocampus of Mongolian gerbils (Meriones unguiculatus) after transient forebrain ischemia. Bilateral clamping of the common carotid arteries for 7 min resulted in selective degeneration of CA1 pyramidal cells after a delay of three to four days, the so-called delayed neuronal death. Immunoreactivity for glia-derived nexin was found in astrocytes of all CA1 layers and was detectable until day 90 (the longest survival time studied). Astroglial reactivity was demonstrated in parallel by staining for GFAP. The co-localization of glia-derived nexin and GFAP was confirmed by double immunocytochemistry. Ultrastructural studies showed the exclusive presence of glia-derived nexin in astrocytes, in the vicinity of degenerating and preserved neuronal structures. Perivascular glia was intensely stained, but endothelial cells were devoid of immunoreactivity. Glia-derived nexin is a potent protease inhibitor with in vitro neurite-promoting activity. During adulthood, it is mainly present in the olfactory system, where receptor neurons are constantly being replaced. The ability of astrocytes to renew the expression of glia-derived nexin after selective delayed neuronal death and the prolonged presence of the protease inhibitor in a zone where degeneration occurs in the immediate neighborhood of preserved neuronal elements indicate that glia-derived nexin may play a role in structural rearrangements of the central nervous system.

Amyloid beta-Protein Precursor↗
PubMed1991

The perforant path in the seizure sensitive gerbil contains the Ca(2+)-binding protein parvalbumin.

The Mongolian gerbil (Meriones unguiculatus) is used as a model in epilepsy studies. Structural abnormalities in the hippocampus and in its GABAergic system have been correlated with this affliction. A reliable marker of a subpopulation of GABAergic neurons is the Ca2+ binding protein parvalbumin (PV). Here we show that, whereas PV is present in the same population of hippocampal interneurons in gerbil as described in the rat, in the gerbil, PV-immunoreactivity is also found in the outer molecular layer of the hippocampus. Ultrastructural analysis revealed that it is located there in axospinous boutons with asymmetric synaptic junctions, i.e. the terminals of the entorhinal perforant path. Upon ablation of the intensely PV-immunoreactive entorhinal cortex, PV-staining is completely absent in its hippocampal termination zones. Thus, in gerbil hippocampus (but not in the rat, mouse, cat and man) PV is contained in a presumably excitatory projection. This outstanding feature of the limbic system of the gerbil implies different functional properties related to Ca2+ mediated processes, and could be of relevance for the seizure sensitivity of this animal species.

Animals↗
PubMed1990

Lesion patterns of vasoactive intestinal polypeptide-containing neurons in the myenteric plexus induced by clamping or transsection of rat jejunum.

The acute reactions of vasoactive intestinal polypeptide (VIP)-containing neurons in the myenteric plexus of the rat jejunum in response to circumferential clamping or transection/reanastomosis were evaluated in a detailed time course of up to ten days. Whereas in sham-operated controls VIP immunostaining was confined exclusively to varicose fibers, either clamping or transection induced the appearance of strongly VIP-immunoreactive beaded neuronal processes and neuronal perikarya in the oral part of the lesion one day postoperatively. After five days strongly immunostained varicose fibers orientated in the longitudinal axis of the gut towards the lesion reappeared suggestive of the onset of regenerative processes.

Animals↗
PubMed1990

Two different types of dynorphin-A-immunoreactive terminals in rat substantia nigra.

The opioid peptide dynorphin A (1-17) is the third transmitter identified in the striatonigral projection, the other two being gamma-aminobutyric acid (GABA) and substance P. The ultrastructural features of the dynorphinergic terminals in substantia nigra/pars reticulata were studied using pre-embedding immunocytochemistry with the classical peroxidase-antiperoxidase-diaminobenzidine-method; these features were compared with GABAergic boutons visualized with an immunogold method. Two distinct types of dynorphin-A-immunoreactive boutons could be identified: (1) type A (81%) possessing characteristics similar to the GABAergic nerve endings in this region, i.e., large pleomorphic vesicles and symmetric synaptic contacts; (2) type B (19%) displaying asymmetric synaptic zones and small, mostly round vesicles. These results are in agreement with physiological studies suggesting a dual action of dynorphin A in substantia nigra.

Animals↗
PubMed1990

Calcium deposits develop in rat substantia nigra but not striatum several weeks after local ibotenic acid injection.

The excitotoxin ibotenic acid (IBO) was used to place local circumscript lesions in rat substantia nigra (SN). Four to six months after the injection we found in the neuron depleted SN basophilic deposits resembling calcium concretion. Additional experiments revealed that calcium deposits, as verified with the alizarin red stain, were first detectable after a delay of 4 weeks. They increased in number, size and extent over the following 12 weeks, but remained confined to the boundaries of SN. Injection of at least 3.5 micrograms IBO was necessary for induction of deposits. In striatum, 14 micrograms IBO did not cause clearly identifiable concretions. Thus, IBO-induced lesions are not stationary but mature, and the long-term effects can be different in different brain regions. These observations may have some relevance for considerations on the cause of the idiopathic nonarteriosclerotic calcifications.

Animals↗
PubMed1990

Ultrastructure of the dynorphin-immunoreactivity in rat brain hippocampal mossy fiber system.

In rat hippocampus, the opioid peptide dynorphin A (1-17) is present in a subpopulation of the mossy fiber terminals, as shown by ultrastructural immunocytochemistry. The immunoreactive boutons exhibit all features characteristic for giant mossy fiber boutons, as e.g. inclusions of neighboring giant boutons which may or may not be dynorphin A-positive. At early survival times after selective lesioning the mossy fiber system with colchicine, lysosomes indicative for the proceeding degeneration are present in boutons still immunoreactive for dynorphin A as well as in non-immunoreactive boutons. This observation provides evidence that the dynorphinergic terminals are in fact the endings of the granule cells.

Animals↗
PubMed1989

GABAergic hippocampal neurons resistant to ischemia-induced neuronal death contain the Ca2(+)-binding protein parvalbumin.

Bilateral transient occlusion of carotid arteries in gerbils for 7 min results in delayed neuronal cell death in hippocampal field CA1. Local gamma-aminobutyric acid (GABA)ergic neurons survive the ischemic insult. Here we show that interneurons in gerbil hippocampus are parvalbumin-immunoreactive, that they contain the GABA-synthetizing enzyme glutamic acid decarboxylase (GAD), and that they are resistant to the effects of ischemia, being present up to 28 days after the insult. It might be concluded that the presence of the Ca2+-binding protein parvalbumin protects the GABAergic neurons from the deleterious consequences of ischemia-induced excitotoxin-mediated Ca2+-influx.

Animals↗
PubMed1989

Preservation of GABAergic perikarya and boutons after transient ischemia in the gerbil hippocampal CA1 field.

Using an antibody directed against the gamma-aminobutyric acid (GABA)-synthetizing enzyme glutamate decarboxylase (GAD) the fate of the GABAergic innervation was investigated in the hippocampal field CA1 of gerbils up to 14 days after a bilateral transient 5-min occlusion of carotid arteries. As described previously, the CA1 pyramidal cells were subject to the ischemia-induced delayed neuronal death, the first signs of which were detectable after 2 days and which was fully developed after 4 days. Local GAD-immunoreactive neurons and boutons, however, exhibited no changes in their distribution and morphology over the whole 14-day period investigated, as studied both at the light and electron microscopic level. Thus, it can be assumed that the increased excitation observed during the development of delayed neuronal death, is not due to a loss of GABAergic neuronal profiles. The resistance of the GABAergic neurons to the ischemic insult is discussed in relation to the presence of Ca2+-binding proteins in this class of neurons, and the long persistence of innervation in an area nearly devoid of postsynaptic targets is considered.

Animals↗
PubMed1988

Immunocytochemical demonstration of GABAergic synaptic connections in rat substantia nigra after different lesions of the striatonigral projection.

Vibratome sections of rat substantia nigra (SN) topically injected with colchicine were processed for glutamate decarboxylase (GAD) immunocytochemistry to reveal GABAergic neurons using electronmicroscopic procedures. Both, GAD-immunoreactive neurons and non-immunoreactive neurons receive a dense innervation of GAD-immunoreactive nerve terminals. In an attempt to clarify the origin(s) of this GABAergic input, the projections between caudate-putamen (CP) and SN were lesioned by circumscribed ibotenic acid injections in CP, or by complete hemitransection either at the level of the globus pallidus or at the frontal pole of SN. In addition, the axonal transport was blocked by local injection of colchicine. After survival times from 40 h to 7 days, the interrelations of GAD-immunoreactive neurons and of unstained neurons with degenerated and preserved boutons were investigated. Striatal terminals contact GAD-negative (presumably dopaminergic) neurons, and, at least as frequently, the GABAergic pars reticulata neurons. Numerous GAD-immunoreactive boutons are apparently intact after the different types of lesions; also the spared GABAergic boutons synapse on both, GAD-positive and GAD-negative neurons. Thus, at the level of SN the striatonigrostriatal loop as well as the striatonigrothalamic (-tectal) projections are under the control of inhibitory axon collaterals of the GABAergic pars reticulata neurons.

Animals↗