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K Fuxe

Publications and source records attributed to K Fuxe.

At least 163 records · Page 9Linked to original sources
PubMed1997

Increased potency of neuropeptide Y to antagonize alpha2-adrenoceptor function in the nucleus tractus solitarii of the spontaneously hypertensive rat.

The regulation by neuropeptide Y of alpha2-adrenoceptors in the nucleus tractus solitarii was evaluated in the adult normotensive Wistar Kyoto rat and the adult spontaneously hypertensive rat. The microinjection of a submaximal dose of l-noradrenaline (800 pmol in 50 nl) alone into the nucleus tractus solitarii produced a significant reduction in the mean arterial blood pressure in either strain. The threshold dose (1 pmol in 50 nl) of neuropeptide Y(1-36) for the vasodepressor response in the Wistar Kyoto rat was five times higher than that (0.2 pmol in 50 nl) in the spontaneously hypertensive rat. Furthermore, neuropeptide Y(1-36) at 0.2 pmol in 50 nl could significantly counteract the vasodepressor response to l-noradrenaline (800 pmol in 50 nl) in the spontaneously hypertensive rat, but not in the Wistar Kyoto rat, in which 1 pmol in 50 nl of neuropeptide Y(1-36) must be employed to counteract the vasodepressor response to l-noradrenaline (800 pmol in 50 nl), although the vasodepressor responses are of a similar magnitude. The in situ hybridization and quantitative receptor autoradiographical experiments showed that the alpha2A-adrenoceptor messenger RNA levels and the B(max) value of the alpha2-adrenoceptor agonist [3H]p-aminoclonidine binding sites measured in the nucleus tractus solitarii of the spontaneously hypertensive rat were substantially lower than those in the Wistar Kyoto rat. The quantitative receptor autoradiographical results were consistent with the cardiovascular results and showed that in the spontaneously hypertensive rat, neuropeptide Y(1-36) at 1 nM led to a significant increase in the K(d) value of [3H]p-aminoclonidine binding sites. In the Wistar Kyoto rat, neuropeptide Y(1-36) produced this effect only at 10 nM. The present study provides evidence for an increase of the potency of neuropeptide Y(1-36) to antagonistically modulate alpha2-adrenoceptors in the nucleus tractus solitarii of the spontaneously hypertensive rat. This enhanced antagonistic action may partly be related to a reduction in the number of alpha2A-adrenoceptors in the nucleus tractus solitarii of the spontaneously hypertensive rat, since a decrease has been observed in the alpha2A-adrenoceptor messenger RNA levels and the alpha2-adrenoceptor binding sites in the spontaneously hypertensive rat. This increased potency of neuropeptide Y(1-36) to antagonize alpha2-adrenoceptor function in the nucleus tractus solitarii of the spontaneously hypertensive rat may contribute to the development of high blood pressure in this hypertensive strain.

Adrenergic alpha-2 Receptor Agonists↗
PubMed1997

Localization of angiotensin II AT1 receptor-like immunoreactivity in catecholaminergic neurons of the rat medulla oblongata.

There exist at least two distinct subtypes of angiotensin II receptors in the brain, namely the AT1 and AT2 subtypes. The high density of angiotensin II AT1 receptors is present in the medulla oblongata. The AT1 subtype of angiotensin II receptors mainly mediates central cardiovascular events. In the present study a polyclonal antibody against the angiotensin II AT1 receptor and a monoclonal antibody against tyrosine hydroxylase were employed to evaluate the possible presence of angiotensin II AT1 receptor-like immunoreactivity in the catecholaminergic neurons of the rat medulla oblongata by means of the double colour immunofluorescence technique. A weak, diffuse cytoplasmic angiotensin II AT1 receptor-like immunoreactivity was observed in almost all the catecholaminergic cell bodies of the A2, C1, C2 and C3 cell groups, except those of the A1 cell group containing moderately intense, diffuse cytoplasmic angiotensin II AT1 receptor-like immunoreactivity, occasionally found in the noradrenergic dendrites of the A1 cell group. There was a higher density of the angiotensin II AT1 receptor-like immunoreactive profiles in the A2 cell group area than in other catecholaminergic cell group areas. In addition, the angiotensin II AT1 receptor-like immunoreactivity was seen in non-catecholaminergic neurons. The present results provide evidence for the existence of the specific angiotensin II AT1 receptor-like immunoreactivity in the noradrenergic and adrenergic neurons of the rat medulla oblongata known to have a cardiovascular role. Thus, the findings support the view that angiotensin II AT1 receptors in the medulla oblongata participate in cardiovascular control and indicate a cellular substrate for the documented interaction between the angiotensin II and adrenergic transmission lines in cardiovascular function at the level of the nucleus tractus solitarii.

Adrenergic Fibers↗
PubMed1997

Prenatal corticosterone treatment induces long-term changes in spontaneous and apomorphine-mediated motor activity in male and female rats.

The potential influence of glucocorticoids on fetal brain development was investigated after corticosterone administration via pellets to pregnant rats during the last trimester of gestation. We examined both spontaneous motor activity and dopamine-mediated motor responses to apomorphine, a D1, D2 and D3 receptor agonist, given at a postsynaptic dose (1 mg/kg, s.c.) to both prepubertal and adult male and female offspring. Prenatal corticosterone was found to produce the following alterations in the offspring. (1) Prepubertal stage: Male offspring: a statistically significant (P < 0.05) increase was observed in spontaneous rearing, motility and locomotion (activity measured during the first 30 min) without changes in apomorphine-induced motor responses. Female offspring: a reduction (P < 0.05) only in spontaneous rearing activity was observed during the exploratory phase (activity measured during the first 10 min) without significant changes in apomorphine-induced motor responses. (2) Adult stage: Male offspring: the exploratory activity to the novel environment was increased (P < 0.05) without significant changes in apomorphine-induced motor activity. Female offspring: an increase (P < 0.05) in spontaneous locomotion was observed during the first 30 min of testing without significant changes in exploratory activity to the novel environment. However, the apomorphine-induced motility and locomotion were reduced (P < 0.05) during the first 30 min. These observations indicate that prenatal corticosterone induces both short-term and long-term changes in spontaneous motor activity as well as long-lasting alterations in dopamine receptor response in the motor network mechanisms controlled by DA receptors. These changes are in part age and sex-dependent. The possible relationship between prenatal programming of the mesolimbic and nigrostriatal dopaminergic pathways by corticosterone and the observed changes in motor function is discussed.

Animals↗
PubMed1997

Adenosine A2A agonists: a potential new type of atypical antipsychotic.

The systemic intraperitoneal (i.p.) administration of the adenosine A2A agonist CGS 21680 was found to dose-dependently antagonize spontaneous and amphetamine-induced (1 mg/kg i.p.) motor activity with similar ED50 values (about 0.2 mg/kg). The ratios between the ED50 values for induction of catalepsy and for antagonizing amphetamine-induced motor activity for CGS 21680, haloperidol, and clozapine were 12, 2, and > 30, respectively. Furthermore, CGS 21680 was comparably much stronger than haloperidol or clozapine at antagonizing the motor activity induced by phencyclidine (2 mg/kg subcutaneously) than motor activity induced by amphetamine (1 mg/kg i.p.). In conclusion, the present results show a clear "atypical" antipsychotic profile of the adenosine A2A agonist CGS 21680 in animal models.

Adenosine↗
PubMed1997

GABA-dopamine receptor-receptor interactions in neostriatal membranes of the rat.

Recent evidence has shown in membrane preparations that the binding of one ligand to its receptor is able to modify the binding parameters of a second receptor (receptor-receptor interactions), allowing the modulation of incoming signals onto a neuron. To further understand the gamma-amino-butyric acid (GABA)-dopamine (DA) interactions in the neostriatum we have carried out experiments to explore whether an activation of the GABA(A) receptor could affect the binding characteristics of the D2 DA receptor in membrane preparations of the rat neostriatum. The results show the GABA (30-100 nM) significantly increases the dissociation constant of the high affinity (KH) D2 DA binding site (labelled with the selective D2 DA receptor antagonist [3H]raclopride and that such an effect is fully counteracted by the GABA(A) receptor antagonist bicuculline (1 microM). It is suggested that such putative GABA(A)/D2 receptor-receptor interactions may take place in the somato-dendritic membrane of the striato-pallidal GABA neurons and that it may modulate the inhibitory effects of DA on these neurons, mediated via D2 receptors.

Animals↗
PubMed1997

Differential effects of intrastriatal neurotensin(1-13) and neurotensin(8-13) on striatal dopamine and pallidal GABA release. A dual-probe microdialysis study in the awake rat.

In the present dual-probe microdialysis study the effects of intrastriatal perfusion with the tridecapeptide neurotensin(1-13) [NT(1-13)] and its active fragment NT(8-13) on striatopallidal GABA and striatal dopamine release were investigated. The modulatory action of NT(1-13) on D2 receptor-mediated inhibition of striatal and pallidal GABA release was also studied. Both intrastriatal NT(1-13) (100 nM) and NT(8-13) (100 nM) increased striatal (139 and 149% respectively) and pallidal (130 and 164%) GABA release, and this effect was antagonized by intrastriatal perfusion with the neurotensin receptor antagonist SR48692 (100 nM). A similar increase (155%) in striatal dopamine release was observed following intrastriatal NT(1-13) (100 nM), but not NT(8-13) (100 and 500 nM). However, at the highest concentration studied (1 microM) NT(8-13) was associated with a rapid increase (130%) in striatal dopamine release. In a second study intrastriatal NT(1-13) (10 nM) counteracted the inhibition of striatal and pallidal GABA release induced by pergolide (500 and 1500 nM). The inhibitory action of the D2 agonist was restored when SR48692 (100 nM) was added to the perfusion medium. These results suggest that in the neostriatum the neurotensin receptor located postsynaptically on the striatopallidal GABA neurons seems to differ from the neurotensin receptor located on dopaminergic terminals, as indicated by the relative lack of effect of NT(8-13) on striatal dopamine release. Furthermore, the ability of NT(1-13) to counteract the pergolide-induced inhibition of both striatal and pallidal GABA release strengthens the evidence for antagonistic receptor-receptor interaction between postsynaptic striatal neurotensin and D2 receptors located on striatopallidal GABA neurons.

Animals↗
PubMed1997

Localization of neuropeptide Y Y1 mRNA in the human brain: abundant expression in cerebral cortex and striatum.

Many neurobiological functions have been ascribed to the NPY Y1 receptor subtype, but autoradiographic analysis has failed to detect Y1 binding sites in most human brain areas, in contrast to the rat. We examined the regional distribution of Y1 mRNA-containing cells in the post-mortem human brain to clarify if there is a major species difference in terms of the existence of Y1 receptors in the human telencephalon, in particular the striatum and cortex. In situ hybridization experiments revealed widespread distribution of Y1 mRNA signals in all layers of most limbic and neocortical regions, predominantly in layer IV (most cortical regions) and layer VI. The striatum showed moderate Y1 receptor mRNA expression levels with intensely expressing cells localized to the nucleus accumbens. The highest Y1 receptor mRNA expression was apparent within the dentate gyrus, and the lowest in the subiculum, parahippocampal gyrus, cerebellum, and thalamus. In vitro autoradiography using [125I]Leu31Pro34-PYY and [125I]PYY with NPY (13-36) or Leu31Pro34-NPY, confirmed the presence of low Y1-like binding in the human brain despite abundant Y1 mRNA expression. However, using a rat model of the human autopsy process, it was apparent that the inability to reveal high Y1- versus Y2-like receptors in the human brain was related in part to marked reductions of Y1-like, but not Y2-like, receptors within a 4 h post-mortem delay. Altogether, the results indicate that the Y1 receptor gene is abundant in the human brain and this receptor may have important roles in cognitive, limbic and motor function.

Adult↗
PubMed1996

The vigilance promoting drug modafinil decreases GABA release in the medial preoptic area and in the posterior hypothalamus of the awake rat: possible involvement of the serotonergic 5-HT3 receptor.

The effect of modafinil on endogenous gamma-aminobutyric acid (GABA) release in the medial preoptic area (MPA) and posterior hypothalamus (PH) and the role of local 5-HT3 receptors in this effect was investigated in the awake rat using in vivo microdialysis. Modafinil (30-100 mg/kg i.p.) dose-dependently decreased GABA release from the MPA, while only the 100 mg/kg dose markedly reduced GABA release in the PH. The modafinil (100 mg/kg) induced inhibition of GABA release in the MPA and the PH was partially counteracted by the 5-HT3 receptor antagonist MDL72222 (1 microM) when perfused locally alone or together with the non-selective 5-HT receptor antagonist methysergide (1 microM). Thus, the reduction of GABA transmission induced by modafinil in the MPA and in the PH, at least in part, involves local 5-HT3 receptors. The GABA release inhibition by modafinil in the above areas may be relevant for its vigilance promoting action.

Animals↗
PubMed1996

Adenosine A2A receptors modulate the binding characteristics of dopamine D2 receptors in stably cotransfected fibroblast cells.

In membrane preparations from rat striatum, where adenosine A2A and dopamine D2 receptors are coexpressed, stimulation of adenosine A2A receptors was found to decrease the affinity of dopamine D2 receptors for dopamine agonists. We now demonstrate the existence of this antagonistic interaction in a fibroblast cell line (Ltk-) stably transfected with the human dopamine D2 (long-form) receptor and the dog adenosine A2A receptor cDNAs (A2A-D2 cells). In A2A-D2 cells, but not in control cells only containing dopamine D2 receptors (D2 cells), the selective adenosine A2A agonist 2-[p-(2-carboxyethyl)-phenethylamino]-5'-N-ethyl-carboxamido adenosine (CGS 21680) induced a 2-3-fold decrease in the affinity of dopamine D2 receptors for dopamine, as shown in competition experiments with dopamine versus the selective dopamine D2 antagonist [3H]raclopride. By contrast, activation of the constitutively expressed adenosine A2B receptors with 5'-N-ethyl-carboxamidoadenosine (NECA) did not modify dopamine D2 receptor binding. In A2A-D2 cells CGS 21680 failed to induce or induced only a small increase in adenosine-3',5'-cyclic-monophosphate (cAMP) accumulation. In D2 cells NECA- or forskolin-induced adenylyl cyclase activation was not associated with any change in dopamine D2 receptor binding. These results indicate that adenylyl cyclase activation is not involved in the adenosine A2A receptor-mediated modulation of the binding characteristics of the dopamine D2 (long-form) receptor.

Animals↗
PubMed1996

Intrastriatally injected c-fos antisense oligonucleotide interferes with striatonigral but not striatopallidal gamma-aminobutyric acid transmission in the conscious rat.

Antisense c-fos oligonucleotides injected into the neostriatum of conscious rats selectively inhibited c-fos expression associated with compensatory increases in striatal c-fos mRNA levels and also with increased expression of junB and NGFI-A mRNA, probably as a result of regulatory phenomena. Dual probe in vivo microdialysis was used to investigate gamma-aminobutyric acid (GABA) release in the substantia nigra and the globus pallidus, which represent the terminal sites of the dopamine D1 receptor regulated striatonigral and the dopamine D2 receptor regulated striatopallidal GABA pathways, respectively. Intrastriatal infusion of the c-fos antisense oligonucleotide profoundly decreased dialysate GABA levels in the ipsilateral substantia nigra within 60 min but did not influence the dialysate GABA levels in the globus pallidus compared with the sham and control oligonucleotide treated groups. The site of action of the antisense oligonucleotides was mainly restricted to striatal neurons as shown by the distribution of locally injected fluoresceine isothiocyanate and radiolabeled oligonucleotides. The findings demonstrate a facilitatory role for c-fos mediated gene regulation in striatonigral GABA transmission and strengthen the evidence that the regulation of neurotransmission is different in the striatonigral and striatopallidal GABA pathways.

Adenosine Triphosphate↗
PubMed1996

Centrally infused galanin-(1-15) but not galanin-(1-29) reduces the baroreceptor reflex sensitivity in the rat.

It has been demonstrated previously that central administration of the N-terminal galanin fragment (1-15) elicits hypertension and tachycardia and antagonizes the hypotensive effect of the parent molecule galanin-(1-29). In order to further clarify the role of galanin in central cardiovascular control, the possible modulation of the baroreceptor reflex by both galanin molecules has been studied. Different groups of rats were injected in the lateral ventricle with subthreshold doses of galanin-(1-15) (0.1 nmol/rat, or 0.3 nmol/rat), with subthreshold doses of galanin-(1-29) (0.1 nmol/rat, and 0.3 nmol/rat) or with an effective dose of galanin-(1-29) (3.0 nmol/rat). The baroreceptor reflex was elicited by intravenous injections of different doses of L-phenylephrine before and after the intraventricular administration of galanin peptides. The changes of the bradycardic responses after galanin peptide injections as well as the modifications of the baroreceptor reflex sensitivity were evaluated. Intraventricular injections of galanin-(1-15) significantly inhibited the reflex bradycardia elicited by intravenous L-phenylephrine and thus decreased the baroreceptor sensitivity. However, neither subthreshold doses of galanin-(1-29) nor its effective dose were able to modulate these cardiovascular responses. From these data it may be suggested that the galanin fragment (1-15) plays a more important role in central cardiovascular regulation than galanin-(1-29), possibly acting on a specific receptor subtype which exclusively recognizes N-terminal fragments of galanin, and exists on cardiovascular areas of the central nervous system.

Adrenergic alpha-Agonists↗
PubMed1996

Adenosine A1 receptor blockade selectively potentiates the motor effects induced by dopamine D1 receptor stimulation in rodents.

An antagonistic interaction between adenosine A1 and dopamine D1 receptors has previously been found in the basal ganglia. However, direct evidence for a selective adenosine A1 antagonist-induced potentiation of dopamine D1-mediated motor activation is lacking. The systemic administration of the adenosine A1 antagonist 8-cyclopentyl-1,3-dimethylxanthine significantly potentiated the motor activating properties of the systemically administered dopamine D1 agonist SKF 38393 in both reserpinized mice and unilaterally 6-hydroxy-dopamine-lesioned rats. However, 8-cyclopentyl-1, 3-dimethylxanthine did not modify the motor effects of the dopamine D2 agonist quinpirole. The present work shows that an antagonistic interaction between adenosine A1 and dopamine D1 receptors may be involved in the motor activating effects of adenosine antagonists, like caffeine.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1996

The non-peptide neuropeptide Y Y1 receptor antagonist BIBP3226 blocks the [Leu31,Pro34]neuropeptide Y-induced modulation of alpha 2-adrenoceptors in the nucleus tractus solitarii of the rat.

The potential blockade of the neuropeptide Y (NPY) Y1 receptor agonist [Leu31,Pro34]NPY-induced modulation of the characteristics of alpha 2-adrenoceptor agonist [3H]p-aminoclonidine binding sites by a selective non-peptide NPY Y1 receptor antagonist BIBP3226, was studied in the nucleus tractus solitarii of the rat by means of quantitative receptor autoradiography. [Leu31,Pro34]NPY at a concentration of 10 nM significantly increased the Kd value of [3H]p-aminoclonidine binding sites in the nucleus tractus solitarii without influencing the Bmax, suggesting the existence of an antagonistic modulation by NPY Y1 receptors of alpha 2-adrenoceptors in the nucleus tractus solitarii. BIBP3226 at 100 nM fully blocked the [Leu31,Pro34]NPY-induced increase in Kd of the [3H]p-aminoclonidine binding sites. The present results therefore provide evidence, by use of a NPY Y1 receptor antagonist, for the existence of a NPY Y1/alpha 2 receptor interaction in the nucleus tractus solitarii.

Animals↗
PubMed1996

Evidence for receptors for hyaluronan in discrete nerve cell populations of the brain.

Evidence is presented, based on immunoblotting, immunohistochemistry and double immunolabelling procedures, for the existence of hyaluronan receptor immunoreactivity in discrete nerve cell populations of the rat brain, present within the zona compacta and the zona reticulata of the substantia nigra, the ventral tegmental area the locus coeruleus, the mesencephalic trigeminal nucleus, the nucleus of the trapezoid body, the motor trigeminal nucleus and the lateral cerebellar nucleus. With preimmune serum control, this hyaluronan receptor immunoreactivity could not be demonstrated. Double immunofluorescence immunocytochemistry, using a well-characterized hyaluronan receptor antiserum, together with the tyrosine hydroxylase antiserum, in the presence or absence of detergent, demonstrated the existence of hyaluronan receptor immunoreactivity in dopamine nerve cells of the substantia nigra and the ventral tegmental area and in noradrenaline nerve cells of the locus coeruleus, previously shown not to stain for hyaluronan. In all the nerve cells, the immunoreactivity had the appearance of punctate bodies mainly located in the cytoplasm of the perikarya of the above nerve cell populations as also shown by confocal laser microscopy in the mesencephalic trigeminal nucleus. Based on these observations, it is concluded that hyaluronan receptors exist in discrete nerve cell populations of the brain, including many noradrenaline and dopamine neurones. In all nerve cells, it is located intracellularly in bodies possibly representing clustered hyaluronan receptors undergoing endocytosis. The results open up the possibility that hyaluronan receptors may reduce high concentrations of hyaluronic acid in the surrounding matrix, thereby facilitating communication between adjacent neurones. Intracytoplasmatic hyaluronic acid may also be of special importance for neuronal plasticity, in view of the ability of hyaluronic acid to activate protein kinase activity and/or by influencing the architecture of the cytoskeleton.

Animals↗
PubMed1996

Subacute toluene exposure increases DA dysfunction in the 6-OH dopamine lesioned nigrostriatal dopaminergic system of the rat.

The potential neurotoxicity of the solvent toluene to the nigrostriatal dopaminergic system was assessed in a rat model of Parkinson's disease. Rats, 1 day after a unilateral injection of 6-hydroxydopamine (6-OH DA) into the substantia nigra, inhaled air or different concentrations of toluene (80, 300 or 1000 ppm), 6 h/day for 3 days. The animals were sacrificed 2 days after the last exposure and biochemical measurements of catecholamines and 3,4-dihydroxyphenylacetic acid (DOPAC) were performed in the neostriatum and substantia nigra. Toluene at 80 and 1000 ppm significantly enhanced the depletion of striatal DOPAC levels induced by the lesion and produced at 80 and 300 ppm a trend for intensifying the 6-OH DA-induced depletion of striatal DA stores. The alterations induced after the combined challenge to the dopaminergic nigrostriatal system may reflect endangering actions of toluene.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1996

Expression of cytochrome P45011B1 mRNA in the brain of normal and hypertensive transgenic rats.

Cytochrome P45011B1 (11 beta-hydroxylase) was detected in the brain of male rats by in situ hybridization methods. Normal Sprague-Dawley rats were compared to the transgenic strain TGR(mRen2)27, characterized by the expression of the murine Ren-2d renin gene and the development of severe hypertension. Specific riboprobes were generated by in the vitro transcription of a 152 base-pair long cDNA template 35S-labeled riboprobes were hybridized to cryostat sections from adrenal glands and from two different levels of the brain using standard protocols and varying washing conditions. After exposure of the radiolabeled sections to X-ray film, the signals were quantified and compared. Following autoradiography and counterstaining, cytochrome P45011B1 mRNA was clearly localized in the zona fasciculata/reticularis of the adrenal cortex and in distinct layers of the cerebral cortex. High signal densities were obtained in the layers II-IV of the neocortex and in the layer II of the piriform cortex, although the concentrations of cytochrome P45011B1 mRNA were remarkably lower in the central nervous system as compared to adrenal glands. As revealed by the semi-quantitative analysis, there was a slight increase in adrenal 11 beta-hydroxylase mRNA in the transgenic rats, whereas the brain seems to express nearly the same amount of this enzyme in both strains. The cytochrome P45011B1 mRNA expression in distinct cells, probably nerve cells, and especially in regions with high densities of glucocorticoid receptors points to a possible function of brain derived corticosterone in receptor activation.

Adrenal Glands↗
PubMed1996

Basic fibroblast growth factor expression and tenascin C immunoreactivity after partial unilateral hemitransection of the rat brain.

Basic fibroblast growth factor (bFGF) gene expression as well as its immunoreactivity were studied after partial unilateral hemitransection of the rat brain during a time course of 24 h, 72 h, 7 and 14 days. The mechanical injury resulted in a global increase of bFGF gene expression at the 24-h time interval. This global increase was seen at the ipsilateral site at the level of the lesion as well as rostral to the lesion in the ipsilateral hemisphere. The upregulation in bFGF gene expression was in most of the areas investigated due to an upregulation in glial cells as seen by means of nonradioactive in situ hybridization compared with immunocytochemistry for glial fibrillary acidic protein (GFAP). Basic FGF immunoreactivity (IR) was increased around the lesion in glial cell nuclei 7 days after the injury. This increase was also detected in GFAP positive glial cells surrounding small vessels in the lesioned area. Moreover, in the present paper we demonstrate increased tenascin immunoreactivity in the lesioned area 7 days after injury. The tenascin IR was increased at the edges of the lesion as well as in vessel like structures. The tenascin IR was partially codistributed with GFAP IR in the lesioned area. The lesion was also characterized by an increase in vimentin IR as well as in laminin IR. It is suggested that the observed changes in the expression of bFGF, matrix proteins (laminin, tenascin) and intermediate filaments (vimentin) are involved in (a) tissue repair, (b) protection of neuronal cells from excitotoxic influences and (c) formation of new vessels in the lesioned area.

Animals↗