Mongolian Gerbil Brain Research Articles

Chronic social defeat alters behaviors and neuronal activation in the brain of female Mongolian gerbils

Chronic social defeat has been found to be stressful and to affect many aspects of the brain and behaviors in males. However, relatively little is known about its effects on females. In the present study, we examined the effects of repeated social defeat on social approach and anxiety-like behaviors as well as the neuronal activation in the brain of sexually naïve female Mongolian gerbils (Meriones unguiculatus). Our data indicate that repeated social defeats for 20 days reduced social approach and social investigation, but increased risk assessment or vigilance to an unfamiliar conspecific. Such social defeat experience also increased anxiety-like behavior and reduced locomotor activity. Using ΔFosB-immunoreactive (ΔFosB-ir) staining as a marker of neuronal activation in the brain, we found significant elevations by social defeat experience in the density of ΔFosB-ir stained neurons in several brain regions, including the prelimbic (PL) and infralimbic (IL) subnuclei of the prefrontal cortex (PFC), CA1 subfields (CA1) of the hippocampus, central subnuclei of the amygdala (CeA), the paraventricular nucleus (PVN), dorsomedial nucleus (DMH), and ventrolateral subdivision of the ventromedial nucleus (VMHvl) of the hypothalamus. As these brain regions have been implicated in social behaviors and stress responses, our data suggest that the specific patterns of neuronal activation in the brain may relate to the altered social and anxiety-like behaviors following chronic social defeat in female Mongolian gerbils.

Astrocyte specific proteins content in the different parts of the rat and mongolian gerbil brain during ontogenesis

Astrocyte specific proteins content in the different parts of the rat and mongolian gerbil brain during ontogenesis

Species Differences in the Immunoreactive Expression of Oxytocin, Vasopressin, Tyrosine Hydroxylase and Estrogen Receptor Alpha in the Brain of Mongolian Gerbils (Meriones unguiculatus) and Chinese Striped Hamsters (Cricetulus barabensis)

Species differences in neurochemical expression and activity in the brain may play an important role in species-specific patterns of social behavior. In the present study, we used immunoreactive (ir) labeling to compare the regional density of cells containing oxytocin (OT), vasopressin (AVP), tyrosine hydroxylase (TH), or estrogen receptor alpha (ERα) staining in the brains of social Mongolian gerbils (Meriones unguiculatus) and solitary Chinese striped hamsters (Cricetulus barabensis). Multiple region- and neurochemical-specific species differences were found. In the anterior hypothalamus (AH), Mongolian gerbils had higher densities of AVP-ir and ERα-ir cells than Chinese striped hamsters. In the lateral hypothalamus (LH), Mongolian gerbils also had higher densities of AVP-ir and TH-ir cells, but a lower density of OT-ir cells, than Chinese striped hamsters. Furthermore, in the anterior nucleus of the medial preoptic area (MPOAa), Mongolian gerbils had higher densities of OT-ir and AVP-ir cells than Chinese striped hamsters, and an opposite pattern was found in the posterior nucleus of the MPOA (MPOAp). Some sex differences were also observed. Females of both species had higher densities of TH-ir cells in the MPOAa and of OT-ir cells in the intermediate nucleus of the MPOA (MPOAi) than males. Given the role of these neurochemicals in social behaviors, our data provide additional evidence to support the notion that species-specific patterns of neurochemical expression in the brain may be involved in species differences in social behaviors associated with different life strategies.

Spatial and temporal patterns of oxidative stress in the brain of gerbils submitted to different duration of global cerebral ischemia

The present study was undertaken to examine spatial and temporal patterns of oxidative stress rate in the brain of Mongolian gerbils submitted to different duration of global ischemia/reperfusion. The common carotid arteries of gerbils were occluded for 5, 10, or 15 min. We followed the temporal ischemia-induced oxidative stress rate, the most important factor that exacerbates brain damage by reperfusion, starting from 24 h up to 28 days after reperfusion. The spatial ischemia-induced oxidative stress distribution was measured parallely in different brain regions: forebrain cortex, striatum, hippocampus and cerebellum. Post-ischemic effects were followed in vivo by monitoring the neurological status of whole animals and at the intracellular level by standard biochemical assays in different brain regions. We measured superoxide production, superoxide dismutase activity, nitric oxide production, index of lipid peroxidation, and reduced glutathione. Our results revealed a pattern of dynamic changes in each oxidative stress parameter that corresponded with ischemia duration in all tested brain structures. The highest levels were obtained in the first 24 h after the insult. After that, they slowly returned to nearly control values 28 days after reperfusion (with the exception of SOD activity that returned to control values at fourth day after reperfusion). The most sensitive oxidative stress parameter was index of lipid peroxidation. Our study confirmed spatial distribution of ischemia-induced oxidative stress. Tested brain structures showed different sensitivity to each oxidative stress parameter, although their basal levels were similar. These new findings could be valuable for creation and strategy of post-ischemic therapy.

Ischemia-Responsive Protein (irp94) Gene Expression in Neurons

An increased expression of the ischemia-responsive protein gene (irp94) was detected in a Mongolian gerbil brain after an ischemic injury, particularly in the cerebral cortex and hippocampus. In a rat phaeochromocytoma tumour cell line (PC12 cells), actinomycin D blocked the irp94 gene expression but cycloheximide did not. This indicates that irp94 gene expression is transcriptionally controlled. The half-life of irp94 mRNA was estimated to be approx. 5 h using 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB). In addition, irp94 expression was enhanced by either endoplasmic reticulum (ER)-stress-inducible drugs or protease inhibitors. This suggests that irp94 gene expression is strongly associated with the unfolded protein response (UPR) in neurons.

Carnosine Protects the Brain of Rats and Mongolian Gerbils against Ischemic Injury: After-Stroke-Effect

Carnosine, a specific constituent of excitable tissues of vertebrates, exhibits a significant antioxidant protecting effect on the brain damaged by ischemic-reperfusion injury when it was administered to the animals before ischemic episode. In this study, the therapeutic effect of carnosine was estimated on animals when this drug was administered intraperitoneally (100 mg/kg body weight) after ischemic episode induced by experimental global brain ischemia. Treatment of the animals with carnosine after ischemic episode under long-term (7-14 days) reperfusion demonstrated its pronounced protective effect on neurological symptoms and animal mortality. Carnosine also prevented higher lipid peroxidation of brain membrane structures and increased a resistance of neuronal membranes to the in vitro induced oxidation. Measurements of malonyl dialdehyde (MDA) in brain homogenates showed its increase in the after brain stroke animals and decreased MDA level in the after brain stroke animals treated with carnosine. We concluded that carnosine compensates deficit in antioxidant defense system of brain damaged by ischemic injury. The data presented demonstrate that carnosine is effective in protecting the brain in the post-ischemic period.

Human neural stem/progenitor cells, expanded in long‐term neurosphere culture, promote functional recovery after focal ischemia in Mongolian gerbils

Transplantation of human neural stem cells (NSCs) is a promising potential therapy for neurologic dysfunctions after the hyperacute stage of stroke in humans, but large amounts of human NSCs must be expanded in long-term culture for such therapy. To determine their possible therapeutic potential for human stroke, human fetal neural stem/progenitor cells (NSPCs) (i.e., neurosphere-forming cells) were isolated originally from forebrain tissues of one human fetus, and expanded in long-term neurosphere culture (exceeding 24 weeks), then xenografted into the lesioned areas in the brains of Mongolian gerbils 4 days after focal ischemia. Sensorimotor and cognitive functions were evaluated during the 4 weeks after transplantation. The total infarction volume in the NSPC-grafted animals was significantly lower than that in controls. Approximately 8% of the grafted NSPCs survived, mainly in areas of selective neuronal death, and were costained with antibodies against neuronal nuclei antibody (NeuN), microtubule associated protein (MAP-2), glial fibrillary acidic protein (GFAP), and anti-2'3' cyclic nucleotide 3'-phosphodiesterase (CNPase). Synaptic structures between NSPCs-derived neurons and host neurons were observed. Furthermore, gradual improvement of neurologic functions was observed clearly in the NSPC-grafted animals, compared to that in controls. Human NSPCs, even from long-term culture, remarkably improved neurologic functions after focal ischemia in the Mongolian gerbil, and maintained their abilities to migrate around the infarction, differentiate into mature neurons, and form synapses with host neuronal circuits. These results indicate that in vitro-expanded human neurosphere cells are a potential source for transplantable material for treatment of stroke.

Developmentally induced imbalance of dopaminergic fibre densities in limbic brain regions of gerbils ( Meriones unguiculatus).

It is well established that epigenetic factors influence the maturation of neurotransmitter systems. Social isolation as well as an early intervention with methamphetamine (MA) lead to a diminished maturation of dopaminergic (DA) fibres in cortical and striatal areas in the brain of Mongolian gerbils. The aim of this study was to prove whether isolated rearing (IR) and the application of a single dose of MA on postnatal day 14 affect the maturation of DA fibres in caudal limbic areas. Therefore the DA fibre densities were quantified in the dorsolateral and ventrolateral entorhinal cortex (EC), the ventral subiculum (SUB) and in three amygdala nuclei - the basolateral (BLA), the lateral (LA) and the central (CA) nucleus. Our results showed that IR and an early MA application led to an increase of DA fibre densities in various caudal limbic areas. Whereas the BLA was affected by both IR and MA, the LA and the medial left CA were only influenced by MA in IR animals. The DA fibre surplus in the ventrolateral EC was significant in MA treated ER and IR animals in the left and right hemisphere, respectively. The SUB and the dorsolateral EC remained unaffected by both epigenetic factors. Altogether, the BLA seems to be the area which responds most sensitively to IR and MA. Previous studies in our laboratory showed a suppressive maturation of DA fibres in the prefrontal cortex (PFC) and nucleus accumbens (NAC) induced by the same set of epigenetic factors. Thus, due to the close functional connection between the PFC and limbic areas, it could be assumed that the suppressive maturation of prefrontal DA fibres implicates an enhancement of DA innervation densities in caudal limbic areas. Imbalances in the morphology and physiology of the different DA projections are suggested here to be crucial in the aetiology of schizophrenia.

Distribution of trkA in cerebral cortex and diencephalon of the mongolian gerbil after birth

TrkA is essential components of the high-affinity NGF receptor necessary to mediate biological effects of the neurotrophins NGF. Here we report on the expression of trkA in the cerebral cortex and diencephalon of mongolian gerbils during postnatal development. The expression of trkA was identified by immunohistochemical method. In parietal cortex and piriform cortex, higher levels of trkA IR (immunoreactivity) were detected at 3 days postnatal (P3) and at P9. Although trkA was not expressed till P3 in the parietal cortex, it was detectable at birth in the piriform cortex. Several regions, such as Layers I, IV & VI, did not show much expression. Layer I showed especially weak labeling. In the hippocampus, thalamus, and hypothalamus, higher levels of trkA IR were detected at P6 and P12 than earlier days. But trkA was not expressed at birth in the hippocampus, at P3 in the reticular thalamic nucleus (Rt), or neonatally in the dorsomedial hypothalamic nucleus (DM). This data shows that expression of trkA is developmentally regulated and suggests that high affinity neurotrophin-receptors mediate a transient response to neurotrophines in the cerebral cortex and diencephalon during mongolian gerbil brain ontogeny.

Changes in non-heme iron histochemistry in the ischemic brains of cats and Mongolian gerbils

We studied the changes in non-heme iron histochemistry in the ischemic brains of the cat and Mongolian gerbils. For the histochemical visualization of non-heme ferric (Fe(III)) and ferrous (Fe(II)) iron, perfusion-Perls and perfusion-Turnbull methods were used. Deeply anesthetized animals were transcardially perfused with the solution containing 1% HCl, 1% potassium ferrocyanide (perfusion-Perls method) or 1% potassium ferricyanide (perfusion-Turnbull method), and 10% formalin. In the non-ischemic animals, perfusion was performed in the cephalic direction through the abdominal aorta or through the ascending aorta within 2 min after thorachotomy and cardiotomy—incision of the right auricle and left ventricle. In the ischemic animals, perfusion was performed through the ascending aorta 10, 20 and 30 min after cardiotomy. Frozen sections of the brain were treated for 3,3′-diaminobenzidine tetrahydrochloride (DAB) intensification of Perls and Turnbull reaction product. It was demonstrated that cytoplasmic Fe(III) was reduced to Fe(II) in oligodendrocytes of ischemic brains, and that Fe(II) was concentrated in the neuronal and glial cell nuclei regardless of the presence or absence of blood supply impairment.

Superoxide dismutase activity in the mongolian gerbil brain after acute poisoning with aluminum.

In this study, the activity of total superoxide dismutase was investigated in brains of adult Mongolian gerbils (Meriones unguiculatus) treated with aluminum. AlCl3x6H20, was given "per os" in the amount of 3.7 g/kg body weight. Animals were killed 24, 48, 72 and 96 hours after the treatment and SOD activity was measured in crude mitochondrial fractions of cortex, thalamus and hippocampus. The SOD activity was significantly elevated in all investigated brain regions 24 hours after aluminum administration. The most prominent increases (up to 200% of values in control animals) were detected in thalamus and hippocampus, whereas the activity was 165% of control value in the cortex. The SOD activity returned to control values in all regions investigated forty-eight hours after poisoning. A slight secondary increases in SOD activity were observed at 72 hours, reaching 171%, 148%, and 166% of control values in the thalamus, hippocampus and cortex, respectively, 96 hours after AlCl3x6H20 administration. We conclude that Al administration causes a biphasic stimulation of SOD activity in various brain regions over 96 hours, providing evidence that oxidative stress is involved in aluminum toxicity to the brain.

Transient forebrain ischemia induces expression of serine/threonine protein phosphatase 1 mRNA in the vulnerable regions of gerbil brain

Apoptosis is thought to be implicated in delayed neuronal cell death following transient forebrain ischemia. Recently, apoptosis in neurons induced by an inhibitor of serine/threonine (ser/thr) protein phosphatases (PPs) has been reported. In this study, we investigated the effect of transient forebrain ischemia on the expression of ser/thr PPs in the brain of Mongolian gerbils. At 24 h after 5-min bilateral carotid artery occlusion, Northern blotting analysis revealed the increase of PP1 mRNA expression in the vulnerable CA1 region of the hippocampus and striatum, but not in the cortex and CA3 region. In contrast, the protein level of PP1 detected by Western blotting analysis decreased in all regions. We conclude that the inhibition in PPs expression in the vulnerable regions may affect cell death after transient forebrain ischemia.

Acetylcholinesterase Activity in the Mongolian Gerbil Brain after Acute Poisoning with Aluminum.

The aim of the present study was to evaluate the acetylcholinesterase activity in the brain of adult gerbils (Meriones unguiculatus) treated with aluminum. AlCl3 x 6H2O was given "per os" in the amount of 3.7 g/kg body weight. The animals were killed 24, 48, 72 and 96 hours after the treatment. The activities of acetylholinesterase in the mitochondrial and microsomal fractions of cortex, hippocampus and thalamus as well as plasma levels of aluminum were measured. Acetylcholinesterase activity was significantly reduced in the mitochondrial and microsomal fraction of all investigated structures. Decrease of the enzyme activity was observed in the first 24 hours, and it was most prominent 48 hours after the administration of aluminum in the mitochondrial fractions when the activity of the enzyme was 31%, 29% and 18.9% of the control value, and after 24 hours in the microsomal fractions when the activity of the enzyme was 43%, 48% and 32% of the control value in the cortex, hippocampus and thalamus, respectively. 96 hours after the administration of aluminum the activity of the enzyme was 63%, 57% and 31% of the value in the control group in mitochondrial, and 100%, 80% and 73% of the control value in microsomal fractions in cortex, hippocampus and thalamus. Plasma levels of aluminum were significantly elevated 24 hours after administration of aluminum. After 48 hours the values were doubled in comparison with the control, 72 hours later plasma concentrations of aluminum were decreased, and after 96 hours they reached the value in the control group. We can conclude that a single oral dose (LD50) of aluminum causes the changes in the brain acetylcholinesterase activity. The changes are still present when the aluminum concentration in plasma is normalized.

Effect of policosanol on cerebral ischemia in Mongolian gerbils.

Policosanol is a mixture of higher aliphatic primary alcohols isolated from sugar cane wax, whose main component is octacosanol. An inhibitory effect of policosanol on platelet aggregation and cerebral ischemia in animal models has been reported. Thus, the objective of the present study was to evaluate the effect of policosanol on cerebral ischemia induced by unilateral carotid ligation and bilateral clamping and recirculation in Mongolian gerbils. Policosanol (200 mg/kg) administered immediately after unilateral carotid ligation and at 12- or 24-h intervals for 48 h significantly inhibited mortality and clinical symptoms when compared with controls, whereas lower doses (100 mg/kg) were not effective. Control animals showed swelling (tissue vacuolization) and necrosis of neurons in all areas of the brain studied (frontal cortex, hippocampus, striatum and olfactory tubercle), showing a similar injury profile. In the group treated with 200 mg/kg policosanol swelling and necrosis were significantly reduced when compared with the control group. In another experimental model, comparison between groups showed that the brain water content of control gerbils (N = 15) was significantly higher after 15 min of clamping and 4 h of recirculation than in sham-operated animals (N = 13), whereas policosanol (200 mg/kg) (N = 19) significantly reduced the edema compared with the control group, with a cerebral water content identical to that of the sham-operated animals. cAMP levels in the brain of control-ligated Mongolian gerbils (N = 8) were significantly lower than those of sham-operated animals (N = 10). The policosanol-treated group (N = 10) showed significantly higher cAMP levels (2.68 pmol/g of tissue) than the positive control (1.91 pmol/g of tissue) and similar to those of non-ligated gerbils (2.97 pmol/g of tissue). In conclusion, our results show an anti-ischemic effect of policosanol administered after induction of cerebral ischemia, in two different experimental models in Mongolian gerbils, suggesting a possible therapeutic effect in cerebral vascular disorders.

Blood-brain barrier damage in reperfusion following ischemia in the hippocampus of the Mongolian gerbil brain.

Vascular permeability to intravenously injected horseradish peroxidase (HRP) was qualitatively examined in the hippocampus of ischemic Mongolian gerbil brains by light and electron microscopy. After 30 min of right common carotid artery occlusion followed by 90 min of reperfusion, the animal was perfused with a fixative and killed. Before the perfusion of the fixative, HRP was injected into the femoral vein. HRP was visualized with tetramethyl benzidine (TMB) and diamino-benzidine (DAB) for light and electron microscopy, respectively. Staining reaction with TMB for HRP appeared in medial or dorsal portions of the operated side of the hippocampus, especially around some vessels along the hippocampal fissure. Ultrastructural examination in the vessels along hippocampal fissure revealed that the endothelial cytoplasm contained HRP-filled vesicles or vacuoles in close proximity to the basal lamina, and seemed to be slightly electron-dense. Swollen pericytes, swollen astrocytic foot processes and perivascular cells with HRP-filled cytoplasm were also observed in that area. In this study, it was clearly demonstrated that intravascular macromolecules leaked transendothelially, through vessel walls in the hippocampal fissure, from the blood stream in the medial portions of the hippocampus during reperfusion following ischemia. These findings suggest that the blood-brain barrier in some vessels along the hippocampal fissure in the medial parts of the hippocampus is more vulnerable to ischemic insults than those in other brain areas.

MK-801, a non-competitive NMDA receptor antagonist, prevents postischemic decrease of inositol 1,4,5-trisphosphate receptor mRNA expression in mongolian gerbil brain

Changes of inositol 1,4,5-trisphosphate receptor (IP 3R) mRNA expression after transient brain ischemia and the effect of MK-801, a non-competitive N-methyl- d-aspartic acid (NMDA) receptor antagonist, on the IP 3R mRNA expression was studied in mongolian gerbil brain by in situ hybridization. Transient ischemia was induced by ligating left common carotid artery for 10 min, and the animals were allowed recovery from 15 min to 24 h. MK-801 was introduced intraperitoneally 30 min before ischemia. IP 3R mRNA expression was decreased in dentate gyrus and hippocampus from 90 min until 24 h after ischemia. MK-801 pretreatment prevented the change of IP 3R mRNA expression after ischemia. These results suggest that IP 3R mRNA expression in ischemia may be related with NMDA receptor.

Thiopental induced cerebral protection during ischemia in gerbils

Temporary interruption or reduction of cerebral blood flow during cerebrovascular surgery may rapidly result in ischemia or cerebral infarction. Thiopental has been shown to have cerebroprotective effects. However, the cerebroprotective dose of thiopental causes burst suppression of the EEG, thus this parameter cannot be used continuously for the detection of metabolic changes in the brain during thiopental anaesthesia. This study was performed in order to examine whether the multiparametric assembly (MPA), which measures energy metabolism CBF and mitochondrial (NADH) as well as extracellular ion concentrations (K +), can shed light on the mechanism of the cerebroprotective effects of thiopental. The MPA was placed on the brain of Mongolian gerbils and burst suppression of the ECoG was induced by thiopental. Cerebral ischemia was induced by occlusion of carotid arteries after burst suppression. Burst suppression of the ECoG was accompanied by a significant decrease in cerebral blood flow. In animals that received thiopental prior to ischemia, NADH increased to a lesser degree and extracellular potassium ion concentration increased to a lesser degree than in the control animals, indicating that thiopental affords protection of the brain under ischemic conditions due to improved energy metabolism. This study also demonstrates that the MPA can monitor changes occurring in the cerebral cortex even after the ECoG can no longer be used. Those findings have a significant value in the development of a new clinical monitoring device.

Histological assessment of rodent CNS tissues to EPR oximetry probe material.

The effects of the paramagnetic oxygen sensing material, lithium phthalocyanine (LiPc) and fusinite were assessed in the brain of Mongolian gerbils and the spinal columns of rats respectively, to determine if there are histologically discernible changes in the tissue surrounding the probe material. This information is essential for the evaluation of the role of EPR oximetry in the measurements of pO2 in the CNS; the technique has great potential value for such measurements because it reports on the pO2 accurately and sensitively and, after the initial placement, measurements can be made repeatedly without invasive procedures or anesthesia. Histologic assessments demonstrated the inert nature of both the fusinite and LiPc EPR probes in rodent CNS tissue over relatively long (2 month) time periods. The fusinite suspensions and LiPc crystals (size range of approximately 100-200 microns) remained well localized to the point of injection and created mild acute tissue reaction on implantation (which appeared to resolve quickly) and virtually no tissue reaction at later times. The majority of the implanted fusinite and LiPc material was present extracellularly in the brain and spinal cord. MRI provided an accurate, noninvasive assessment of probe placement and was able to investigate pathologic effects (hemorrhage, edema, necrosis) associated with the probe placement and treatment effects.

Attempted induction of blood brain barrier in vitro by co-culture of gerbil brain microvessel endothelial cells and glial cells.

The characteristics of isolated and subcultured Mongolian gerbil brain microvessel endothelial cells (BECs) were investigated, especially the disappearance of blood brain barrier (BBB) functions, and subcultured BECs were co-cultured with gerbil glial cells to assess a mass-producible BBB filter model. The subcultured cells lost specific characteristics observed in freshly isolated BECs, such as limited permeability to albumin and inulin, high gamma-glutamyl transpeptidase activity, and strong connections between individual cells. The subcultured BECs did not regain BBB functions during co-culture with glial cells, even derived from the same species. Only freshly isolated endothelial cells can be used for the BBB filter model, and a mass-producible BBB filter model may be impossible to make.

Cortical areas are revealed by distribution patterns of proteoglycan components and parvalbumin in the Mongolian gerbil and rat

Cortical areas in rodents have been basically characterized by its cytoarchitecture, connectivity or by physiological parameters. In this study we show that they are also revealed by distribution patterns of proteoglycans and parvalbumin-immunoreactivity. Brains of young adult Mongolian gerbils ( Meriones unguiculatus) and Wistar rats were cut into series of transversal sections. Proteoglycan components were detected using the N-acetylgalactosamine binding Wisteria floribunda agglutinin (WFA) and antibodies against chondroitin sulphate proteoglycan (CSPG). Differences between cortical areas were found to exist with regard to the occurrence and the density of perineuronal nets, but were also expressed in varying staining intensities for WFA and CSPG of the neuropil. Primary neocortical areas (somatosensory, auditory, visual cortex) were characterized by an intense neuropil staining in layer IV and the upper part of layer VI. Using the same methods strong labelling was also typical of the neuropil in the retrosplenial cortex, of layer Ia in the prepiriform cortex and the hippocampal CA3 field. In tangential sections cut from gerbil cortical hemispheres, some of the heavily lectin-stained cortical areas were sharply delineated from adjacent faintly labelled regions, others showed more diffuse borders. In the rat, the area-specific staining for WFA was less clearly expressed than in the gerbil. Immunocytochemistry of the calcium-binding protein parvalbumin in alternate sections showed labelling patterns of neuropil which resembled those of WFA-binding and CSPG-immunoreactivity in the entire neocortex and hippocampus. From these results it can be concluded that functional peculiarities of cortical fields may not only be determined by neuronal network parameters but also by the spatial arrangement of extracellular matrix proteoglycans.