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At least 109 records · Page 6Linked to original sources
PubMed1988

Zonation in the rat cerebellar cortex: patches of high acetylcholinesterase activity in the granular layer are congruent with Purkinje cell compartments.

The rat cerebellar cortex is built from parasagittally arranged modules with topographically ordered afferent and efferent projections. The intrinsic organization of the cerebellum is revealed by immunocytochemical staining with monoclonal antibody, mabQ113. In the cerebellum, mabQ113 recognizes a polypeptide epitope that is restricted to a subset of Purkinje cells. Antigenic Purkinje cells are clustered to form a complex pattern of parasagittal compartments. Several biochemical markers reveal a superficially similar organization of the cortex, and so it is important to determine how many independent maps are present. This report compares the mabQ113 antigen display to the patchy distribution of acetylcholinesterase (AChE). In the granular layer and the white matter of the adult cerebellar cortex there is a patchy AChE staining that includes both the hemispheres and the vermis. The staining is often not sharply resolved cytologically, but seems to be associated primarily with the synaptic glomeruli. The boundaries of these granular layer patches in the vermis correspond to the mabQ113+/mabQ113- boundaries of the overlying Purkinje cell compartments. Thus, AChE and mabQ113 antigen share a common compartmentation both in the vermis, and in the hemispheres. Both mabQ113 and AChE distributions develop postnatally in the cerebellar cortex. At birth (PO) there is neither AChE activity nor mabQ113 immunoreactivity. Both staining patterns emerge during the second postnatal week. In the vermis at P10, there is AChE activity in the granular layer and white matter, and the distribution is already patchy despite the absence of synaptic glomeruli. At the same age the mabQ113 immunoreactivity is found in all Purkinje cells rather than a subset, and the band pattern has yet to mature. There is also transient AChE staining of Purkinje cell somata and dendrites. The AChE patches clarify between P10 and P20 along with the appearance of the synaptic glomeruli and the development of differential mabQ113 staining, but there is no reason to believe that the two are causally linked. In contrast to the cerebellar cortex, AChE staining in the cerebellar nuclei matures very early and at P0 the activity is already high. Zones of high and low AChE activity are seen in all the cerebellar nuclei and may be related to the distribution of the terminal fields of the different Purkinje cell populations.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholinesterase↗
PubMed1992

Serotoninergic fibres form dense synaptic contacts with Purkinje cells in the mouse cerebellar cortex--an immunohistochemical study.

The distribution of serotonin immunoreactivity in the mouse cerebellar cortex was studied using the indirect antibody peroxidase-antiperoxidase (PAP) technique of Sternberger (1979) on epoxy embedded semithin sections. The great majority of serotonin-positive afferents distribute throughout the Purkinje cell layer and form dense synaptic contacts with the somata of the Purkinje neurons. Only a sparse immunostaining of serotoninergic fibres could be detected at the granular cell and molecular layers. The microanatomical organization of the serotoninergic projections to the mouse cerebellar cortex is quite different from that observed in other animal species. These findings suggest that in the mouse cerebellar cortex, the Purkinje cell population represents the main target for serotoninergic afferents. Our histochemical data provide morphological support for a series of electrophysiological observations which indicate serotonin as a potential modulatory neurotransmitter for Purkinje cell firing activity.

Animals↗
PubMed1989

Demonstration of axonal branching of fibres from certain precerebellar nuclei to the cerebellar cortex and nuclei: a retrograde fluorescent double-labelling study in the cat.

The projections from certain brain stem precerebellar nuclei to the cerebellar cortex and nuclei have been examined in the cat by using the retrograde fluorescent double-labelling technique. Crystalline Fluoro-Gold was implanted into the left cerebellar nuclei from the contralateral side and rhodamine-B-isothiocyanate was injected into the overlying cerebellar cortex. The inferior olive, the lateral reticular nucleus, and the reticular tegmental pontine nucleus all contained double- as well as single-labelled neurons, and it was concluded that these nuclei have a high number of neurons whose axons branch to both the cerebellar cortex and nuclei. The neurons in the paramedian reticular nucleus and the pontine nuclei proper appear to project only to the cerebellar cortex.

Animals↗
PubMed1984

Effects of Purkinje cell degeneration on the noradrenergic projection to mouse cerebellar cortex.

We have examined the effects of a genetically programmed target cell death on the noradrenergic afferent projection to mouse cerebellar cortex. We have observed that the noradrenergic axon terminals originating in in locus coeruleus are maintained in the cerebellar cortex of the Purkinje cell degeneration (pcd) mutant mouse in spite of the absence of Purkinje cells, the targets for the noradrenergic projection. The number of noradrenergic terminals in the atrophic mutant cerebellar cortex is approximately normal as assessed by counts of fibers exhibiting catecholamine fluorescence and by measurement of high affinity uptake of tritium-labeled norepinephrine (NE) by synaptosomes prepared from cerebellar cortex. An increased density of NE fibers is observed which appears to be a consequence of reduced cerebellar mass in the mutant. Although the number of noradrenergic terminals is unaffected, morphological and biochemical alterations are observed in this system. The fibers are more brightly fluorescent in mutant than in normal mice and their pattern is less orderly. The content of the endogenous transmitter, NE, is increased from 150 to 170% whereas the activity of the rate-limiting enzyme tyrosine hydroxylase (TH) is reduced to about 60% of normal values. These changes appear to be permanent as they are still present in 6 month-old mutant animals, the oldest studied. No alterations in either NE content or TH activity are found in pcd/pcd hippocampus, another target for the locus coeruleus axons.

Afferent Pathways↗
PubMed1991

Age-related structural changes in the rat cerebellar cortex: effect of choline alfoscerate treatment.

The influence of ageing and of 3 months choline alfoscerate treatment on age-related microstructural changes in cerebellar cortex was studied in 3-, 12- and 24-month-old male Sprague-Dawley rats. The number of Purkinje and granule neurons, the density of Nissl bodies in the cytoplasm of Purkinje and granule neurons and the density of silver-gold impregnated fibres within molecular and granule cells layers were assessed by neurohistological and neurohistochemical techniques associated with microdensitometry and quantitative image analysis. The number of Purkinje and granule neurons was approximately the same in rats of 3 and 12 months and significantly decreased in 24-month-old animals. The density of Nissl bodies and of fine processes of silver-gold impregnated fibres were greatest in the cerebellar cortex of rats of 12 months of age, followed in descending order by 3- and 24-month-old rats. Both the density of Nissl bodies and of silver-gold impregnated fibres were significantly lower in the cerebellar cortex of the oldest age group considered in comparison with the young and middle age groups. Treatment with choline alfoscerate, a precursor in the biosynthesis of brain phospholipids which increases bioavailability of choline in the nervous tissue, noticeably reduced the loss of Purkinje and granule neurons in rats of 24 months. Moreover, it restored the density of Nissl bodies in the cytoplasm of Purkinje and granule neurons as well as the density of silver-gold stained fibres in the molecular and in the granule cells layers to values not significantly different from those found in rats of 3 months. These findings suggest that choline alfoscerate treatment may be effective in counteracting the age-dependent disarrangement of rat cerebellar cortex. The possible mechanisms of action of the compound on the microstructural changes of cerebellar cortex occurring with age are discussed.

Aging↗
PubMed1994

Influence of treatment with L-deprenyl on the structure of the cerebellar cortex of aged rats.

Treatment with L-deprenyl increases mean and maximum life span in the rat and reverses memory and learning deficits associated with old age. Since only sparse information is available concerning the influence of L-deprenyl administration on the aging brain microanatomy, we have investigated the effect of long-term treatment with L-deprenyl on the structure of the cerebellar cortex in the aged rat. The cerebellar cortex was used since it represents a useful model for assessing age-related changes in nervous system anatomy and function. Male Sprague-Dawley rats were treated from the 19th to the 24th month of age with a daily oral dose of 1.25 mg/kg or 5 mg/kg L-deprenyl. Age-matched rats were left untreated and used as a control group. Eleven-month-old untreated rats were used as an adult reference group. The density of Purkinje and granule neuron profiles as well as the intensity of Nissl's staining within the cytoplasm of Purkinje neurons were reduced in 24-month in comparison with 11-month rats. Moreover, an increased accumulation of lipofuscin was noticeable in the cytoplasm of Purkinje neurons of old rats as well as an increase in MAO-B activity in the molecular layer of the cerebellar cortex. The two doses of L-deprenyl increased the density of both Purkinje and granule neuron profiles and the intensity of Nissl's staining in the cytoplasm of Purkinje neurons and reduced lipofuscin deposition within Purkinje neurons. The lower dose of L-deprenyl caused only a slight decrease in MAO-B activity, whereas the 5-mg/kg/day dose remarkably reduced it. These results suggest that long-term treatment with L-deprenyl counters the expression of some age-related microanatomical changes in the rat cerebellar cortex. The possible independence of the effects of the compound on age-related microanatomical changes of the cerebellar cortex and on MAO-B inhibitory activity is discussed.

Aging↗
PubMed1984

Axonal branching in the projections from the paramedian reticular nucleus to the cerebellar cortex.

Injections of fluorescent tracers into cat cerebellar cortex gave evidence of collateral axonal branching of neurons situated in the paramedian reticular nucleus. These branched reticulocerebellar projections were distributed to opposing sides of the cerebellum, in particular the anterior lobe and the ansiform lobule. No topographical organization was observed in the PRN. Less than 30% of ipsilaterally projecting reticulocerebellar fibers had contralaterally directed collateral branches. These results are in keeping with a bilateral fastigial projection to the PRN forming a feedback loop circuit through which orthostatic reflexes may be mediated.

Animals↗
PubMed1985

Trace conditioning: abolished by cerebellar nuclear lesions but not lateral cerebellar cortex aspirations.

The trace conditioning paradigm in which the conditioned stimulus-unconditioned stimulus (CS-US) interval is longer and the US and CS do not overlap requires retention of a 'trace' of the CS to associate it with the US. This task is difficult, requiring for learning about 5 times the number of trials to criterion as the standard delay task. The present study was undertaken to determine if: the cerebellar interpositus nucleus is essential in trace as well as in delay conditioning; and the lateral cerebellar cortex is involved when CS-US association over longer time intervals is required. Sixteen adult male New Zealand white rabbits had recording and in some cases lesion electrodes surgically implanted before training. They were trained daily with 126 paired trials of tone CS and airpuff US. The trace period between CS offset and US onset was 500 ms. Mean number of trials to criterion of 8/9 CRs was 466.9 trials. After a day of overtraining the animals had one of 3 surgeries: electrolytic lesion of the left cerebellar interpositus nucleus (n = 3); aspiration of the left lateral cerebellar cortex (HVI and HVIIA) and underlying cerebellar nuclei (n = 4); or aspiration of HVI and HVIIA only (n = 9). Rabbits with only HVI and HVIIA removed exhibited a transient decrease in CRs but relearned with significant savings. The amplitude, area and latency of pre- and postlesion conditioned responses (CRs) was similar. When the interpositus nucleus was damaged, the animals' capacity for CRs on the side ipsilateral to the lesion was permanently abolished. It is concluded that the cerebellar interpositus nucleus but not the overlying lateral cerebellar cortex is essential for retention of trace classical conditioning. Nevertheless, the temporary abolition of CRs by removal of lateral cerebellar cortex suggests that the cerebellar cortex does play an important role in learning and retention of the trace conditioned response.

Animals↗
PubMedDate not supplied

[The interneuronal correlations in the cerebellar cortex in the postresuscitation period].

Quantitative analysis of the neuronal populations of the cerebellar cortex was carried out in white rats after reanimation. Clinical death was modeled by 10-min clamping of the neurovascular plexus near the heart. The material for analysis was collected at the end of ischemia, 90 min, 1, 3, and 7 days after it. There are about 8 neurons of the molecular layer and 250 granular cells per pyramidal neuron in an intact cerebellar cortex of white rats. Staring from day 3 of the postreanimation period, the number of granular cells per pyramidal neuron increases, whereas the ratio of the molecular layer neurons and pyramidal neurons differs but negligibly from the control values over the entire follow-up period. Different sensitivity of various neuron populations to an ischemic exposure leads to the formation of the structural basis for the predominance of stimulating pulsation in the cerebellar cortex and reduces its inhibitory effect on the cerebellar nucleus in the postreanimation period.

Animals↗
PubMed1996

Gene expression of angiotensin II receptor subtypes in the cerebellar cortex of young rats.

Both AT1 and AT2 receptors were detected in the cerebellar cortex of 2-week-old rats by [125I]Sar1-angiotensin II binding. In contrast, using in situ hybridization histochemistry we found only AT1A and AT1B but not AT2 receptor mRNA in the cerebellar cortex of young rats. Expression of AT1A and AT1B receptor mRNA coding for either receptor subtype was found in the molecular or granular cell layers. Our results suggest that AT1 receptors may be located on dendrites of Purkinje cells expressing AT1A and AT1B receptor mRNA, whereas the AT2 receptor binding in the molecular layer may be located on nerve terminals of fibers projecting to the cerebellar, cortex from distant areas.

Animals↗
PubMed1992

Expression of tenascin in the developing and adult cerebellar cortex.

Since tenascin may influence neuronal cell development, we studied its expression pattern using immunocytochemistry, in situ hybridization, Northern blot analysis, and immunochemistry in the developing and adult mouse cerebellar cortex. Tenascin immunoreactivity was detectable in all layers of the developing cerebellar cortex. In the external granular layer, only the radially oriented processes of Golgi epithelial cells were immunoreactive, whereas the densely packed cell bodies were immunonegative. Tenascin was hardly detectable at contact sites between migrating granule cells and processes of Golgi epithelial cells. Axons of granule cells in the molecular layer were immunoreactive, whereas their cell bodies in the internal granular layer lacked detectable levels of tenascin. By in situ hybridization, only Golgi epithelial cells and astrocytes of the internal granular layer and prospective white matter, but not nerve cells, could be shown to synthesize detectable levels of tenascin mRNA in the developing mouse cerebellar cortex. Thus, tenascin in the cerebellar cortex seems to be a glia-derived molecule that becomes adsorbed to neuronal surfaces in a topographically restricted pattern in situ. Levels of tenascin protein and mRNA decreased significantly with increasing age. In the adult, tenascin immunoreactivity was weak and mainly restricted to the molecular layer and tenascin mRNA was confined to Golgi epithelial cells, indicative for a functional heterogeneity in differentiated cerebellar astrocytes. Quantitative immunoblot analysis revealed that the 225 and 240 kDa components of tenascin were developmentally downregulated at a faster rate than the 190 and 200 kDa components, corresponding to the faster downregulation of the 8 kilobase (kb) mRNA species compared to the 6 kb mRNA species as revealed by Northern blot analysis. These observations indicate a differentially regulated expression of the tenascin components. We hypothesize that glia-derived tenascin modifies the functional properties of nerve cell surfaces and that tenascin is involved in such different morphogenetic events as neurite growth and oligodendrocyte distribution.

Animals↗
PubMed1998

Temporal discrimination in the cerebellar cortex during conditioned eyelid responses.

Little is known about mechanisms used by the nervous system to encode time. In light of recent evidence, cerebellar cortex involvement in the learned timing of conditioned eyelid responses shows promise as an area of investigation into neural timing mechanisms. Lesion studies indicate that the cerebellar cortex is necessary for response timing, but do not rule out the possibility that response timing is encoded afferent to the cerebellum. To differentiate between precerebellar and cerebellar cortical timing mechanisms, rabbits were trained by pairing direct stimulation of mossy fibers in the cerebellum as the conditioned stimulus (CS) with an eyeshock unconditioned stimulus (US). We find that individual animals can produce differently timed conditioned responses when trained with a mossy fiber CS that has been paired with the US at various interstimulus intervals. The fact that differently timed responses can be conditioned using constant-frequency stimulation of an invariant subset of mossy fibers as the CS suggests that timing information in the afferent input to the cerebellum is not essential. Two rabbits trained with single-pulse stimulation in the cerebellum as the CS also learned differently timed conditioned responses; suggesting that fiber recruitment during a stimulus train does not convey the necessary temporal coding to the cerebellar cortex. Together with the lesion data, these findings suggest that the learned timing of conditioned eyelid responses occurs in the cerebellar cortex.

Animals↗
PubMed1993

Rat cerebellar cortex in vitro responds specifically to moving stimuli.

In spite of the detailed anatomical knowledge available, the functional significance of the cerebellar wiring diagram is still obscure. Since there are no variations in the anatomy throughout the whole cortical plane, it is plausible to assume that the basic operation is the same in all parts of the cerebellum. The 'wiring' suggests that local activity must depend on the spatio-temporal organization of the inputs. Neocortical input reaches the cerebellar cortex from nearly all cortical areas via mossy fibers terminating on the granular cells. We simulated such an input to the granular layer in acute slices of rat cerebellar cortex using an array of 11 stimulating electrodes. By successively switching the stimulus current from one electrode to the next, a 'moving' input to the granular layer is simulated. Our experiments show that the cerebellar cortex is specifically activated by 'moving' stimuli applied to the granular layer. The activation is a function of 'movement' direction and velocity. Thus, it enables the cerebellar cortex to act as a movement detector. Such behavior has previously been postulated on anatomical grounds [Braitenberg, J. Theoret. Neurobiol., 2 (1983) 237-241; Braitenberg, In Glickstein et al. (Eds.), Cerebellum and Neuronal Plasticity, Plenum, 1987, pp. 193-207].

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1992

[The cerebellar cortex in sudden infant death].

The author examined the cerebellar cortex in 190 post-mortem examinations, incl. 79 sudden infant deaths and 56 infants under one year with a clearly defined cause of death, six sudden deaths of toddlers and 8 toddlers with other causes of death and 41 death of subjects aged 17 months to 66 years who died from violent deaths. In 50 sudden infant deaths the authors observed a persistence of the external granular layer, as compared with a control group, in 29 infants no difference was detected. The external granular layer persisted in a 16-month-old toddler who died suddenly and in a 22-month old toddler who was drowned. A persisting external granular layer may be a supporting sign of retarded development of the cerebellar cortex in sudden infant deaths.

Adolescent↗
PubMed1984

Hereditary striatonigral and cerebello-olivary degeneration of the Kerry Blue Terrier. II. Ultrastructural lesions in the caudate nucleus and cerebellar cortex.

The character and progression of ultrastructural lesions in the caudate nucleus and cerebellar cortex were studied in four Kerry Blue Terriers afflicted with a hereditary neurodegenerative disease. In the caudate nucleus, the initial lesion was mitochondrial hypertrophy in dendrites of intrinsic neurons. Degeneration of these neurons became widespread while axons of passage and terminal boutons were spared. During the final stages, there was severe disruption of the neuropil with loss of both neurons and glia. A narrow zone bordering the lateral ventricles, however, remained unaffected. In the cerebellar cortex, the lesions involved principally Purkinje cells and progressed through a pattern of degeneration comparable to that involving intrinsic neurons of the caudate nucleus. In the later stages, there was astroglial scarring of the molecular layer. In contrast to the caudate nucleus, there was no disruption of the neuropil with loss of structure in the cerebellum. The fact that progression of lesions during the early stages of the disease in both the caudate nucleus and cerebellar cortex was similar suggested a common mechanism for the neurodegeneration .

Animals↗
PubMed1992

The physiological effects of serotonin are mediated by the 5HT1A receptor in the cat's cerebellar cortex.

Serotonin is present in a fine beaded plexus in the cerebellar cortex of several mammalian species. In the cat, serotoninergic afferents arise from neurons located within the lateral, paramedian and peri-olivary reticular nuclei (Kerr and Bishop, J. Comp. Neurol., 304 (1991) 502-515). In addition to serotoninergic afferents, these same nuclei also contain a separate population of neurons that give rise to mossy fibers to the cerebellar cortex. Physiological studies have shown that mossy fibers are excitatory to their target neurons. The intent of the present study was to determine the physiological effects of serotonin in the cat's cerebellum in an in vivo preparation and to identify the receptor(s) that mediate the observed responses. Iontophoretic application of serotonin (5HT) onto Purkinje cells reduces the spontaneous firing rate of all cells tested (n = 12). Serotonin also blocks the excitatory effects elicited by the application of aspartate in 17 of 19 units tested and of glutamate (n = 62) in all cases. In addition, 5HT potentiated the inhibitory action of GABA (n = 12). Iontophoretic application of the 5HT1A agonists, 8-OH-DPAT and ipsapirone, mimic the suppressive action of serotonin in a dose-dependent manner. This response, as well as the 5HT mediated suppression are blocked by the application of spiperone, a 5HT1A antagonist. Compounds selective for the 5HT1C,2 and 3 receptors are physiologically ineffective. The present data are in partial agreement with previous studies in the rat's cerebellar cortex.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed2000

Role of climbing fibers in determining the spatial patterns of activation in the cerebellar cortex to peripheral stimulation: an optical imaging study.

The spatial patterns of activation in the rat cerebellar cortex evoked by ipsilateral face stimulation were mapped using optical imaging based on the pH sensitive dye, Neutral Red. The aims of the study were to characterize the optical responses evoked by peripheral stimulation and test the hypothesis that the resultant parasagittal banding is due to climbing fiber activation. In the anesthetized rat Crus I and II of the cerebellar cortex were stained with Neutral Red. Epi-fluorescent changes produced by a train of stimuli (5-10s and 4-20 Hz) to the ipsilateral face were monitored in time using a fast, high resolution charge-coupled device camera. The patterns of activation were quantified using a two-dimensional fast Fourier transform analysis that removed signals with high spatial frequencies and minimized the contribution of horizontal structural elements (i.e. blood vessels). The dominant spatial pattern of activation evoked by face stimulation was that of parasagittal bands. The bands were highly frequency-dependent and were elicited most strongly by stimulus frequencies in the range of 6-8 Hz. There was a large fall-off in the response for frequencies above and below. The optical signal evoked by face stimulation built up over a period of 10s and then gradually decayed. Within a folium the individual parasagittal bands exhibited some frequency and temporal specificity. Stimulation of the contralateral inferior olive also resulted in the activation of parasagittal bands with characteristics similar to the bands evoked by face stimulation, including a preferred stimulus frequency which peaked at 10 Hz. Injection of lidocaine into the contralateral inferior olive blocked the parasagittal bands evoked by ipsilateral face stimulation, while control injections of saline had no effect. The results confirm that a parasagittal banding pattern is a dominant feature of the functional architecture of the cerebellar cortex. The parasagittal banding pattern observed with Neutral Red is due primarily to the activation of climbing fiber afferents. The frequency tuning of the responses, with the preference for peripheral stimuli of 6-8 Hz, is in agreement with previous findings that the inferior olive is inherently rhythmic. These observations support the hypothesis that inferior olivary neurons are dynamically coupled into groups that activate parasagittal bands of Purkinje cells in the cerebellar cortex. The frequency tuning also supports the hypothesis that the climbing fiber system is involved with timing. Activation of this afferent system may require stimuli with appropriate frequency content and stimuli synchronized to the rhythmicity of the inferior olive.

Action Potentials↗