Effects of grafts containing cholinergic and/or serotonergic neurons on cholinergic, serotonergic and noradrenergic markers in the denervated rat hippocampus

Cassel, J.C.; Neufang, B.; Kelche, Christian; Jeltsch, Hélène; Will, Bruno; Hertting, G.; Jackisch, Rolf

doi:10.1016/0006-8993(93)90351-m

Cited by 30 publications

(47 citation statements)

References 48 publications

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“…The neurochemical data on tissue concentrations of markers for cholinergic, serotonergic and noradrenergic innervation in the hippocampus of sham-operated and lesioned rats (Table 2) are in agreement with previous studies of our group (Cassel et al 1993Jackisch et al 1995Jackisch et al , 1999aJackisch et al , 1999b. They show that 14 months after aspirative lesions of the fimbria-fornix, the cholinergic and serotonergic innervation of the temporal half of the hippocampus was reduced by about 50% as compared to sham-operated rats.…”

Section: Release Of [ 3 H]glutamate In Hippocampal Slices Of Rats Witsupporting

confidence: 92%

“…In contrast, the hippocampal concentration of noradrenaline is diminished only initially, recovers within weeks and is even overcompensated after several months (e.g. Madison and Davis 1983;Crutcher 1987;Cassel et al 1993;Jackisch et al 1999aJackisch et al , 1999b, a phenomenon due to non-regenerative sprouting of sympathetic fibers arising from the superior cervical ganglia (see Crutcher 1987). Finally, levels of amino acid transmitters, like glutamate, aspartate, GABA or glycine, seem unaffected by lesions of afferent pathways (Jeltsch et al 1994; but see Lahtinen et al 1993aLahtinen et al , 1993b.…”

Section: Introductionmentioning

confidence: 88%

“…after an injection of atropine sulphate (4 mg/kg, i.p., 10 min prior to the injection of pentobarbital). At about 30 days of age, ten rats (LES) received bilateral aspirative lesions as described previously (Cassel et al 1993;Jackisch et al 1995). The control group (SHAM, n=7) consisted of rats which were subjected to all surgical steps except that they received no lesion.…”

Section: Methodsmentioning

confidence: 99%

“…Markers for acetylcholine and serotonin (5-HT) are significantly reduced in the hippocampus after fimbriafornix lesions and this reduction poorly recovers over time (e.g. Gage and Björklund 1986;Gasser and Dravid 1987;Cassel et al 1993;Jackisch et al 1999aJackisch et al , 1999b. In contrast, the hippocampal concentration of noradrenaline is diminished only initially, recovers within weeks and is even overcompensated after several months (e.g.…”

Section: Introductionmentioning

confidence: 95%

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Electrically evoked release of glutamate in rat hippocampal slices: effects of various drugs and fimbria-fornix lesions

Sehmisch¹,

E²,

Thorn³

et al. 2001

Naunyn-Schmiedeberg's Archives of Pharmacology

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A model of electrically evoked release of glutamate from rat hippocampus was developed and used to detect possible changes induced by lesions of hippocampal afferences. Neuronal glutamate in hippocampal slices was labelled by preincubation with [3H]glutamine. The slices were then superfused with physiological medium in the presence of the glutamate uptake inhibitor L-transpyrrolidine-2,4-dicarboxylic acid (100 microM or 3 microM) and stimulated twice electrically (S1, S2: 240 pulses, 3 Hz, 2 ms, 26-30 mA); various drugs were added before S2. In order to determine the basal and evoked outflow of [3H]glutamate only, the mixture of 3H-labelled compounds (glutamine, glutamate and GABA) was separated by ion exchange chromatography in superfusate fractions and slices. The electrically evoked overflow of [3H]glutamate was largely Ca2+-dependent and tetrodotoxin-sensitive and hence represented action potential-induced exocytotic release of [3H]glutamate. Evoked [3H]glutamate release was significantly increased by the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 0.1 microM), suggesting the presence of endogenous inhibitory adenosine, and reduced by the A1 receptor agonist N6-cyclopentyladenosine (1 microM, antagonized by DPCPX, 0.1 microM). There was no evidence for a cholinergic, serotonergic, or adrenergic modulation of the evoked release of [3H]glutamate: the corresponding selective agonists (or antagonists) were ineffective. After aspirative lesions of the septohippocampal pathways the hippocampal noradrenaline content was markedly increased, whereas cholinergic and serotonergic markers were reduced. The evoked release of [3H]glutamate in hippocampal slices of lesioned rats was significantly increased by a mechanism which still has to be determined, but which is not related to alterations in A1 receptor function. It is concluded that the present model was able to detect lesion-induced differences in electrically evoked release of [3H]glutamate, but the relationship of these differences to changes of noradrenergic, cholinergic or serotonergic hippocampal innervations remains to be established.

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Section: Release Of [ 3 H]glutamate In Hippocampal Slices Of Rats Witsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 88%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 95%

See 2 more Smart Citations

Electrically evoked release of glutamate in rat hippocampal slices: effects of various drugs and fimbria-fornix lesions

Sehmisch¹,

E²,

Thorn³

et al. 2001

Naunyn-Schmiedeberg's Archives of Pharmacology

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“…Such transplants were also found to restore metabolic (Kelly et al 1985) and neurochemical markers altered by the lesion (Björklund et al 1983;Cassel et al 1993;Emerich et al 1992;Kaseda et al 1989) and to establish electrophysiologically and morphologically normal synapses with neurons of the host brain (Clarke et al 1990;Segal et al 1985). However, there are several reports (for review, see Cassel et al 1992) suggesting that intrahippocampal grafts rich in cholinergic neurons may fail to induce the expected behavioral recovery after lesions of the septohippocampal pathways, even when such grafts show acceptable survival and have normalized the cholinergic innervation of the denervated hippocampus.…”

Section: Introductionmentioning

confidence: 99%

Behavioral effects of GM1 ganglioside treatment and intrahippocampal septal grafts in rats with fimbria-fornix lesions

1997

Self Cite

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The monosialoganglioside GM1 is a compound with neurotrophic properties found to foster functional recovery in various paradigms of brain damage. The present experiment examined whether systemic treatment with GM1 may facilitate behavioral recovery in rats with fimbria-fornix lesions and intrahippocampal grafts rich in cholinergic neurons. Among 68 Long-Evans female rats, 46 sustained a bilateral electrolytic lesion of the fimbria and the dorsal fornix and 22 were sham-operated. Fourteen days later, half the lesioned rats were subjected to intrahippocampal grafts of a fetal septal cell suspension. Starting a few hours after lesion surgery and over a 2-month period, half the rats of each surgical treatment group received a daily injection of GM1 (30 mg/kg i.p.), the other half being injected with saline as a control. All rats were subsequently tested for locomotor activity and radial maze learning. The lesions induced locomotor hyperactivity and impaired learning performances in both an uninterrupted and an interrupted radial maze testing procedure. In all rats with surviving grafts, the grafts had provided the hippocampus with a new and dense organotypic acetylcholinesterase-positive innervation pattern which did not differ between saline- and GM1-treated subjects. The scores/performances of the rats that had received only the grafts or only the GM1 treatment did not differ significantly from those of their respective lesion-only counterparts. However, in the radial-arm maze task, the grafted rats given GM1 showed improved learning performances as compared with their saline-treated counterparts: they used more efficient visit patterns under the uninterrupted testing conditions and made fewer errors under the interrupted ones. The results suggest that GM1 treatment or intrahippocampal grafts used separately do not attenuate the lesion-induced behavioral deficits measured in this experiment. However, when GM1 treatment and grafts are used conjointly, both may interact in a manner allowing part of these deficits to be attenuated.

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Fetal Hippocampal Cells Grafted to Kainate-Lesioned CA3 Region of Adult Hippocampus Suppress Aberrant Supragranular Sprouting of Host Mossy Fibers

Shetty

Turner

1997

Experimental Neurology

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Effects of grafts containing cholinergic and/or serotonergic neurons on cholinergic, serotonergic and noradrenergic markers in the denervated rat hippocampus

Cited by 30 publications

References 48 publications

Electrically evoked release of glutamate in rat hippocampal slices: effects of various drugs and fimbria-fornix lesions

Electrically evoked release of glutamate in rat hippocampal slices: effects of various drugs and fimbria-fornix lesions

Behavioral effects of GM1 ganglioside treatment and intrahippocampal septal grafts in rats with fimbria-fornix lesions

Fetal Hippocampal Cells Grafted to Kainate-Lesioned CA3 Region of Adult Hippocampus Suppress Aberrant Supragranular Sprouting of Host Mossy Fibers

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