Dentate Fascia Research Articles

Involvement of Adhesive Puncta Adherentia Type Junctions in the Formation of Synaptic Connections between Dentate Fascia Transplants and the Recipient Brain

The dentate fascia of 20-day Wistar rat fetuses were transplanted heterotopically into the somatosensory area of the neocortex of adult rats. Granule cells in grafts projected their axons (mossy fibers) into recipient brains and established synaptic contacts with inappropriate targets. Electron microscopy was used to study the characteristics of the organization of ectopic mossy fiber synapses. These studies showed that ectopic synapses reproduced the determinant structural features of giant hippocampal synapses and induced subcellular reorganization of postsynaptic dendrites in the neocortex. Morphometric analysis showed significant increases in the number and extents of adhesive junctions, puncta adherentia, in ectopic synapses as compared with controls. These data indicate the involvement of adhesive mechanisms in the structural-chemical adaptation of target neurons to foreign axons growing from transplants.

PMO-142 Evidence refuting the Trojan-horse hypothesis of brain swelling in acute liver failure: l-type glutaminase is exclusively neuronal

IntroductionAstrocytic swelling is the characteristic feature of hyperammonemia and acute liver failure (ALF) which is thought to result from accumulation of glutamine due to the action of astrocytic glutamine synthetase...

Structural changes in the hippocampal dentate fascia in rats after action of hypoxia at the perinatal period of development

Structural changes in the hippocampal dentate fascia in rats after action of hypoxia at the perinatal period of development

248 EVIDENCE REFUTING THE TROJAN-HORSE HYPOTHESIS OF BRAIN SWELLING IN ACUTE LIVER FAILURE: L-TYPE GLUTAMINASE IS EXCLUSIVELY NEURONAL

Introduction Astrocytic swelling is the characteristic feature of hyperammonemia and acute liver failure (ALF) which is thought to result from accumulation of glutamine due to the action of astrocytic glutamine synthetase (GS). It has been suggested that glutamine may not be a benign amino acid and may act as “Trojan horse” which leads to astrocytic apoptosis as it is metabolised by Glutaminase (GLN) yielding glutamate and ammonia. In vivo proof for this hypothesis is lacking. In health, GLN is mainly neuronal and generates glutamate and GABA. The aims of the study were to define the expression of the ammonia metabolising enzymes, GS and GLN in the brain of ALF animals. Methods Two groups of CD1 mice were studied, sham: n=6; paracetamol (500 mg/kg IP): n=7. The animals were maintained normothermic and resuscitated with fluid and glucose and sacrificed at 8 h after injection of APAP or before development of coma. Arterial ammonia (COBAS) and frontal cortex brain water (dry weight technique) were measured. The brain sections were stained for GS and K and L-type GLN. Results Arterial ammonia was significantly higher in the ALF group compared with controls (345±32 vs 132±11 p=0.002) and brain water did not reach significance (83.6±2.3 vs 76.3±2.6 p=0.05). GS protein expression was observed in the astrocytes in the dentate fascia in both groups and was not different but was also seen in the oligodendrocytes only in ALF group. L-type GLN was expressed only in the neurons and not in the astrocytes and was significantly higher in the ALF animals (++++) compared with controls (+). The most marked areas were the striatum and dentate fascia and interestingly the staining was mainly cytoplasmic. K-type GLN was not different between groups and limited to brain capillaries. Conclusion Conclusion: The results of this study refute the Trojan-horse hypothesis and show for the first time increased protein expression of L-type GLN which is exclusively neuronal. From the pathophysiological perspective, this may function to generate excessive ammonia in the neuron thereby producing neuronal cell death. Competing interests None declared.

Impairments to the Establishment of the Various Hippocampal Fields in Rats as a Long-Term Consequence of Acute Perinatal Hypoxia

The aim of the present work was to study the long-term consequences of acute normobaric hypoxia during the perinatal period on the establishment of the hippocampal formation in rats. The experiments showed that hypoxia on day 2 of postnatal development led to significant damage to the structure of the hippocampal field, which showed different levels of sensitivity to the harmful factor. On day 20, all fields showed cell death and depletion of the pyramidal cell layers. The most marked neuron death occurred in fields CA4 and CA3. On day 30, a significant level of neuron death persisted in field CA4, though it decreased in field CA3 and was not seen in field CA1; neuron death in the granule layer of the dentate fascia increased. In addition, there were decreases in the sizes of pyramidal neuron bodies in all hippocampal fields. All hippocampal fields also showed activation of astrocyte reactions, which was more marked in field CA4, where gliosis persisted to prepubertal age (30 days).

Intraoperative mismanagement in anterior single-screw fixation of odontoid fractures: an analysis of 15 cases

Objective To analyze intraoperative mismanagements in anterior single-screw fixation of odontoid fractures.Methods From April 2002 to July 2010, intraoperative mismanagements happened in the treatment of 15 cases of fresh odontoid fracture with anterior single-screw fixation under C-arm fluoroscopy.They were 10 men and 5 women, aged from 22 to 65 years (average, 37 years).All the fractures were Anderson-D' Alonzo type Ⅱ.The mismanagements were characterized to find out their reasons.Results The mean follow-up time was 13.4 months (range, 6 to 47 months).All the fractures healed in an average of 14.5 week (range, 12 to 34 weeks) after operation, no severe complications were found.The intraoperative mismanagements could be elassified into 3 kinds.In the first kind, the guide pin was driven through the odontoid bone into the cranial cavity in 3 cases, resulting in one death due to serious injury to the medullary bulb.In the second kind, malreduction happened in 5 cases due to intraoperative displacement of the fracture.In the third kind, poor position and fixation of the screw happened in 7 cases because of enlargement of the screw canal after repeated correction of the guide pin direction.Conclusions The intraoperative mismanagements in anterior single-screw fixation of odontoid fractures were mostly caused by careless surgeons who made their operative assessments and plans before they read the X radiographs of their patients carefully or before they had been familiar with the operative instruments.Secondly, some mismanagements were caused by intraoperative accidents, most of which, however, could have been avoided by careful preoperative preparation and meticulous operative maneuvers. Key words: Fascia dentate; Fractures; Fracture fixation, internal; Therapeutic errors

Influence of chronic fluorosis on expression of phospho-Elk-1 in rat brains

Objective To investigate the expression and distribution of the downstream substrate of extracellular regulated protein kinase(ERK1/2) pathway, ternary complex factor phospho-Elk-1, in rat brains with chronic fluorosis, and reveal the mechanism of the impaired learning and memory ability caused by chronic fluorosis. Methods Seventy-two SD rats, weighing 100 - 120 g, were randomly divided into 3 groups, 24 in each group (half male and half female). The rats in control group were fed with tap water (fluoride < 0.5 mg/L); low- and high-dose fluoride groups were fed with tap water with different concentrations of NaF(5.0,50.0 mg/L F-, respectively). After 6 months, body weight was weighed, dental fluorosis was determined by observation and urinary fluoride and bone fluoride were detected by fluorine ion-selective electrode; the learning ability of rats was measured by navigation test of Morris water maze, and memory ability by spatial probe test in Morris water maze; the expression and distribution of phospho-Elk-1 in different brain regions were detected by immunohistochemistry method. Results In low- and high-fluoride groups, the body weight of rat[(449.2 ± 77.1), (312.8 ± 89.7)g] was significantly decreased than that of control [(635.5 ± 76.2 )g, all P< 0.05], the varying degrees of dental fluorosis were observed(x2 = 7.83, P<0.05), urinary fluoride[(2.56 ±0.91),(5.73 ±3.14)mg/L] and bone fluoride[(709.2 ± 37.4) ,(1306.3 ± 102.4) mg/kg] were significantly higher than those in controls[(0.92 ± 0.30)mg/L,(348.5 ± 89.2)mg/kg, all P< 0.05]. The escape latency of low- and high-fluoride groups[ (7.4 ± 4.1), (12.2 ± 5.7)s] was longer than that of control [(4.8 ± 2.7 )s, all P < 0.05] and the escape latency in high-fluoride group was significantly longer than that in other groups (all P < 0.05); in spatial probe test, the time of first crossing platform was longer in rats with fluorosis [(4.18 ± 1.10),(5.89 ± 0.56)s] as compared to control[(1.17 ± 0.75)s, all P< 0.05]. Expressions of phospho-Elk-1 in the hippocampus CA1(167.4 ± 8.3,163.2 ± 9.4), CA2(175.7 ± 5.0,183.3 ± 4.2), CA3(165.2 ± 11.6,162.9 ± 4.4), CA4(168.7± 6.9,169.5 ±5.3), fascia dentate (185.2 ±4.0,193.1 ±6.1) and caudate putamen( 181.4 ± 3.8, 179.8 ± 5.5) in low- and high-fluoride groups were higher than those of controls(142.4 ± 8.1,144.9 ± 8.4,143.6 ± 5.8, 116.8 ± 9.1,140.2 ± 7.8,163.1 ± 13.1, all P< 0.05). Conclusion Chronic fluorosis can cause increased expression of phospho-Elk-1 in the hippocampus and caudate putamen region of rat brains, which might be related to the mechanisms of decreased learning and memory ability of rats overexposed to fluoride. Key words: Fluoride poisoning; Brain; Transcription factor Elk-1; Learning; Memory

Involvement of the trisynaptic hippocampal pathway in generating neural representations of object–place associations (an analytical review)

A review. Possible mechanisms for generation of neural representations of object-place associations (NROPA) are analyzed in different parts of a neural network which include the hippocampus and parahippocampal complex. Streams of spatial and non-spatial information arrive to the hippocampus from the parahippocampal complex consisting of perirhinal, postrhinal and entorhinal cortical areas. We assume that, due to the absence of connections between lateral and medial areas of the entorhinal cortex, object-place associations are mostly formed in the hippocampus, but can also be generated in the perirhinal cortex due to existence of input from the postrhinal cortex. As both information streams converge on neurons of the dentate fascia and field CA3, a trisynaptic pathway through the hippocampus can play the basic role in the NROPA generation. Since the spatial information arrives in the neocortex and, therefore, reaches the parahippocampal complex and hippocampus approximately by 20 ms earlier than the "non-spatial" stream, only spatial information is processed firstly in the dentate fascia and field CA3. Generation of NROPA in the dentate fascia starts later, due to returning excitation from field CA3c. In the dentate fascia, signals from the NROPA are transferred into field CA3, where the activated neuronal pattern is superimposed by information arriving from the entorhinal cortex. As a result, more complex NROPA are formed in field CA3 and send signals to field CA1. In the dorsal (ventral) part of the field CA1, the activated neuronal pattern is superimposed by non-spatial (spatial) information arriving from the lateral (medial) part of the entorhinal cortex. As a result, a higher-order NROPA are generated. In the parahippocampal cortex, the generation ofNROPA can be a consequence of the activity transferred from the dorsal part of the hippocampal CA1 field.

Acquisition of an Active Avoidance Reaction in Rats and Morphological Changes in the Hippocampus in Pentylenetetrazol Kindling

The relationship between measures of active avoidance behavior and morphological changes in the hippocampus was studied in rats after kindling induced by administration of pentylenetetrazol. Pentylenetetrazol kindling impaired the acquisition of the avoidance reaction and increased the number of intersignal reactions without altering the acquisition of the avoidance reaction in the shuttle box in rats. The numbers of neurons in the hippocampus (fields CA1 and CA3) and dentate fascia decreased, while the numbers of damaged neurons increased. Inverse correlations between seizure severity and the numbers of neurons in hippocampal fields CA1 and CA3 and the dentate fascia were seen in rats subjected to kindling. Rats of this group also showed positive correlations between seizure severity and the numbers of damaged neurons in field CA1 and the dentate fascia. There were no correlations between measures of convulsive activity or the number of cells in hippocampal zones and measures of the acquired avoidance behavior. Control animals showed negative correlations between the numbers of damaged cells in field CA1 and the dentate fascia and the characteristics of avoidance behavior in the first and third training sessions.

Neuroprotection by hypothalamic peptide proline-rich peptide-1 in Aβ25–35 model of Alzheimer's disease

Background This work sought to determine the effects of hypothalamic proline-rich peptide (PRP)-1 in a rat model of Alzheimer's disease. Methods Complex histochemical, electrophysiologic, and behavioral analyses were performed on intact or diseased Wistar rats (n = 28). Pathologic conditions were induced by bilateral intracerebroventricular injection of amyloid peptide Aβ25–35. The diseased rats received systemic administration of PRP-1 or placebo control. Results Aβ25–35 caused cellular neurodegeneration with marked glial reaction in the hippocampal complex and almost full destruction of the dentate fascia, which was not observed in conditions of PRP-1 administration after Aβ25–35 injection. Hippocampal neurons of intact animals responded to high-frequency (tetanic) stimulation of entorhinal cortex of ipsilateral cerebral hemisphere by tetanic and posttetanic potentiation of a different intensity and duration, which was accompanied by posttetanic depression. Aβ25–35 led to significant changes in the level and pattern of hippocampal neuronal activity, indicating the absence of both tetanic and posttetanic activity. Poststimulus activity manifestations rarely occurred and rapidly decreased after repeated trials. This indicated the focal character of lesion. Regular administration of PRP-1 for 4 weeks resulted in optimal restoration of electrophysiologic parameters. PRP-1 maintained the initial learning level achieved in a behavioral study in a Morris water maze. Conclusions Systemic administration of PRP-1 possesses neuroprotective effects and can prevent the neurodegeneration in hippocampus induced by Aβ25–35. This suggests that PRP-1 could be a potential therapeutic agent for specific neurodegenerative diseases.

Seizures Beget Seizures in Temporal Lobe Epilepsies: The Boomerang Effects of Newly Formed Aberrant Kainatergic Synapses

Do temporal lobe epilepsy (TLE) seizures in adults promote further seizures? Clinical and experimental data suggest that new synapses are formed after an initial episode of status epilepticus, however their contribution to the transformation of a naive network to an epileptogenic one has been debated. Recent experimental data show that newly formed aberrant excitatory synapses on the granule cells of the fascia dentate operate by means of kainate receptor-operated signals that are not present on naive granule cells. Therefore, genuine epileptic networks rely on signaling cascades that differentiate them from naive networks. Recurrent limbic seizures generated by the activation of kainate receptors and synapses in naive animals lead to the formation of novel synapses that facilitate the emergence of further seizures. This negative, vicious cycle illustrates the central role of reactive plasticity in neurological disorders.

A study on the correlation between IL1RAPL1 and human cognitive ability

This study aimed to investigate the effects of IL1RAPL1 on the human cognitive ability. Four genetic marker sites, i.e., DXS1218, DXS9896, rs6526806 and rs12847959 on IL1RAPL1 were genotyped in 332 Qinba Mountain Area children. Meanwhile, a cognition test with a C-WISC scale was performed to study the relationship of genotype with cognition test scores. Results indicated that genotypes of DXS1218, DXS9896 and rs12847959 were associated with memory/concentration factor intelligence quotient (IQ) (P=0.027, 0.042, 0.029, respectively). DXS1218 also associated with full IQ, verbal IQ, and performance IQ (P=0.006, 0.014, 0.006, respectively). rs12847959 were related to verbal comprehension factor and perceptual organization factor IQ (P=0.021, 0.043, respectively). Further study on rat brain revealed that Il1rapl was mainly expressed in memory/concentration-associated encephalic regions, such as hippocampus, dentate fascia, osmesis perithelium, and piriform cortex. mRNA expression levels of Il1rapl in brains of rats with different learning and memory abilities showed significant difference. Combined data suggested that IL1RAPL1 affected human cognitive ability to some extent, especially the memory and concentration capability.

Late expression of FosB transcription factor in 4-aminopyridine-induced seizures in the rat cerebral cortex

In this study, the immunolocalization of FosB transcription factor was investigated in acute and chronic experimental models of seizures induced by 4-aminopyridine. Wistar rats were injected intraperitoneally daily with 5mg/kg 4-aminopyridine for 1, 4, 8 and 12 days and sacrificed 24h after the last injection. Corresponding control groups received the solvent of 4-aminopyridine. Immunohistochemistry revealed an increase in FosB immunolabelling in the frontal cortex in 4-aminopyridine-treated animals compared to controls, both in acute and chronic time course groups. The dentate gyrus displayed elevated FosB immunopositivity only after repeatedly applied convulsant (4-aminopyridine), i.e. following 4, 8 and 12 days of treatment, but no significant immunolocalization was observed in the hippocampus proper. The neuronal localization of FosB after 12 days of 4-aminopyridine-induced convulsions was analysed by means of FosB-parvalbumin double immunolabelling. The increased number of double-labelled cells was significant in the frontal cortex, hilum of the dentate fascia and region CA1 of the hippocampus. We conclude that the studied neocortical and allocortical areas showed a different pattern of FosB immunolocalization, which suggests a relative deficiency of transcriptional regulation in the Ammon's horn and may be responsible for distinct response to seizure-induced cellular insult.

Involvement of neuropeptide mechanisms in the process of integration of heterotopic dental fascia transplants with recipient brains

Embryonic dentate fascia was transplanted into the somatosensory area of the neocortex of adult rats. Ultrastructural and morphometric analyses of giant synapses formed by the granule neurons of transplants with inappropriate neuronal targets in the recipient brains were performed after nine months. As compared with intact synaptic terminals in the control hippocampus, there were differences in the quantity and distribution of large synaptic vesicles with electron-dense centers storing neuropeptide cotransmitters. The proportion of peptidergic vesicles (of the total number of vesicles) in ectopic giant synapses was 5.8 +/- 0.6%, compared with 3.3 +/- 0.6% in controls. Accumulations of large, dense vesicles close to the active zones of aberrant connections were seen almost 7.9 times more often than in controls. These results show that neuropeptide transmitters are critical for maintaining synaptic connections between heterotopic dentate fascia transplants and recipient brains.

Amyotrophic lateral sclerosis with dementia showing clinical parkinsonism and severe degeneration of the substantia nigra: Report of an autopsy case

An autopsy case of amyotrophic lateral sclerosis with dementia (ALS-D) showing clinically overt parkinsonism and severe degeneration of the substantia nigra is reported. The patient was a 78-year-old man who died after a 2-year clinical course characterized by parkinsonism that was responsive to Levodopa (L-DOPA) treatment. Motor neuron symptoms and dementia were not apparent ante-mortem. The autopsy demonstrated the severe degeneration of the substantia nigra without alpha-synucleinopathy-related changes. Finely granular mineralization of necrotic neurons was a unique finding in the substantia nigra. The mild loss of spinal anterior horn cells, the appearance of several Bunina bodies and the degeneration of the hippocampal subiculum and temporal cortex were also noted. A small number of ubiquitinated intra-cytoplasmic inclusions were found in neurons of the dentate fascia of the hippocampus and the temporal and frontal cortices. Although the degeneration of the substantia nigra is a common finding in ALS-D, patients seldom develop clinically overt parkinsonism. This case indicates that patients with ALS-D rarely present with predominantly parkinsonian clinical features and these symptoms and signs can be improved by L-DOPA treatment.

Causes of neuronal heterotopia other than migration disturbances

A differentiated form of cerebellocortical fragments (case 1) in the white matter or even in the cerebellar dentate nucleus, found in a fetus with trisomy 13, may be due to an auto-transplantation accompanied by a penetrating vessel. A similar condition was observed in the Ammon's horn (case 2) incidentally as a heterotopic tissue fragment of the dentate fascia. Further cause of heterotopia may be speculated as a mechanical separation by a surrounding and developing tissue part in case of organized, differentiated cerebellocortical heterotopia in the white matter (cases 3-5) which were clinically silent. Migration disturbances are not the only cause of neuronal heterotopia since the structure of heterotopia is differentiated and organized by tissue components.

Alterations of seizure-induced c- fos immunolabelling and gene expression in the rat cerebral cortex following dexamethasone treatment

We examined the effects of dexamethasone on the expression of the inducible transcription factor c-fos in 4-aminopyridine (4-AP) seizures. Induction of c-fos mRNA due to 4-AP-elicited convulsion was detected by means of the polymerase chain reaction (PCR) in samples from the neocortex. Adult male rats were pretreated with different doses of dexamethasone (0.5, 1, 3, 5mg/kg body weight); 1h later 5mg/kg 4-AP was injected intraperitoneally. Controls received the solvent of dexamethasone. Pretreatment with dexamethasone provided significant symptomatic protection against 4-AP-induced convulsions. Immunohistochemistry was used to evaluate the presence of the c-fos protein. The number of Fos-immunoreactive nuclei per section area was measured in the neocortex and hippocampus. Pretreatment with dexamethasone resulted in a dose-dependent, significant decrease of seizure-induced Fos-protein immunoreactivity in the neocortex, in the hilum of the dentate fascia, as well as in regions CA1-3 of the hippocampus, compared to control animals. Brains processed for mRNA isolation and PCR, displayed a significant increase of c-fos mRNA following the 4-AP treatment, while pretreatment with dexamethasone did not prevent or decrease this boosted c-fos mRNA expression. We conclude that seizure-induced c-fos expression and intracellular Fos-protein localization are mediated by transmitter and receptor systems, and dexamethasone significantly decreases Fos immunoreactivity, probably by regulating the intracellular traffic of the protein. We also conclude that dexamethasone does not interfere with the genomic regulation of c-fos mRNA synthesis.

Pentylenetetrazol kindling in rats: Is neurodegeneration associated with manifestations of convulsive activity?

Structural changes in neurons and measures of oxidative stress were studied in the hippocampus of rats tolerant (ST) and sensitive (SS) to developing clonic-tonic seizures in conditions of pentylenetetrazol kindling. Sequences of 11 injections of pentylenetetrazol significantly decreased the number of normal neurons in hippocampal field CA1 in SS rats, this effect being seen in both hippocampal field CA1 and the dentate fascia in ST rats. Decreases in the numbers of normal neurons were accompanied by increases in the numbers of damaged cells in field CA4 in rats of both groups. After 21 injections, decreases in the numbers of normal neurons were seen in field CA1 in both SS and ST rats, while the numbers of damaged neurons were significantly greater than control only in ST rats in fields CA1 and CA4. The glutathione level was significantly lower in the hippocampus in both groups of rats than in controls. Thus, rats " tolerant" to developing convulsions show signs of oxidative stress and neurodegenerative changes in the hippocampus. This suggests that oxidative neuron damage leading to neurodegeneration in the pentylenetetrazol kindling model is not directly associated with convulsive activity.

Pick’s disease with Pick bodies combined with progressive supranuclear palsy without tuft‐shaped astrocytes: A clinical, neuroradiologic and pathological study of an autopsied case

We report clinical, neuroradiologic features, and neuropathologic findings of a 76-year-old man with coexistent Pick's disease and progressive supranuclear palsy. The patient presented with loss of recent memory, abnormal behavior and change in personality at the age of 60. The symptoms were progressive. Three years later, repetitive or compulsive behavior became prominent. About 9 years after onset, he had difficulty moving and became bedridden because of a fracture of his left leg. His condition gradually deteriorated and he developed mutism and became vegetative. The patient died from pneumonia 16 years after the onset of symptoms. Serial MRI scans showed progressive cortex atrophy, especially in the bilateral frontal and temporal lobes. Macroscopic inspection showed severe atrophy of the whole brain, including cerebrum, brainstem and cerebellum. Microscopic observations showed extensive superficial spongiosis and severe neuronal loss with gliosis in the second and third cortical layers in the frontal, temporal and parietal cortex. There were Pick cells and argyrophilic Pick bodies, which were tau- and ubiquitin-positive in neurons of layers II-III of the above-mentioned cortex. Numerous argyrophilic Pick bodies were observed in the hippocampus, especially in the dentate fascia. In addition, moderate to severe loss of neurons was found with gliosis and a lot of Gallyas/tau-positive globus neurofibrillary tangles in the caudate nucleus, globus pallidus, thalamus, substantia nigra, locus coeruleus and dentate nucleus. Numerous thorned-astrocytes and coiled bodies but no-tuft shaped astrocytes were noted in the basal ganglion, brainstem and cerebellar white matter. In conclusion, these histopathological features were compatible with classical Pick's disease and coexistence with progressive supranuclear palsy without tuft-shaped astrocytes.

Features of the expression of the c-Fos gene along the rostrocaudal axis of the hippocampus in common voles after rapid training to solve a spatial task

The level of expression of the c-Fos protein in neurons was used as a measure of the activation of transcription in the hippocampus of common voles (Microtus arvalis Pall.) after rapid spatial training. Stained Fos-positive cells were counted on 20 brain sections along the rostrocaudal axis of the hippocampus. Voles were trained to find the exit to their home cages through one of the arms of a modified eight-arm radial maze (using a 2-h series of six trials on one day). Animals were initially trained to leave the home cage via an arm not connected to the maze. Voles of the "active" control group were passed through the isolated arm into the home cage six times on the experimental day. Animals for the "passive" control for c-Fos levels were collected from their home cages. Significant increases in c-Fos expression in voles trained in the maze and the active control group, as compared with passive controls, were seen in all areas studied (hippocampal fields CA1 and CA3 and the dentate fascia). At the same time, a significant increase in the number of c-Fos-positive neurons in voles trained in the maze, as compared with the active controls, was noted only in the caudal hippocampus, no differences being seen in the rostral part. The greatest levels of activation were seen in the dentate fascia and field CA3. These results provide evidence for the heterogeneous functioning of the hippocampus along the rostrocaudal axis during training of voles to solve a spatial task.