Electrophysiological and pharmacological studies of the inhibitory projection from the cerebellar cortex to the deep cerebellar nuclei in tissue culture.
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The organization of afferents to the cerebellar cortex in the cat: projections from the deep cerebellar nuclei.
The topography of the cerebellar nucleo-cortical projection was investigated in the cat by experiments employing the horseradish peroxidase (HRP) technique or by combined HRP-autoradiographic methods. The results of the HRP studies extend previous findings showing that neurons in the deep nuclei project to the cerebellar cortex in an orderly way. Thus, it appears that the cortex of the vermis-proper receives projections from neurons located predominately in the fastigial nucleus. Intermediate and lateral zones of mid-vermal cerebellar cortex are projected on by neurons located in the interposed and dentate nuclei. Crus II receives input from neurons located predominately in the dentate nucleus, while the paramedian lobule is projected on by neurons located in a large postero-dorsal sector of the interposed nucleus and in a smaller medial strip of the dentate nucleus. Neurons in the ventral part of the dentate nucleus and the lateral part of the interposed nucleus send fibers to the paraflocculus. The nucleo-cortical pathway to the flocculus and nodulus arises largely from a population of neurons located in a ventral region stretching from the medial border of the dentate nucleus to the lateral border of the fastigial nucleus. The results of experiments using the combined HRP-autoradiographic method show that clusters of neurons in the deep cerebellar nuclei project back to the cerebellar cortical areas from which they receive input, establishing a fairly precise feedback loop between the cerebellar cortex and deep nuclei.
Afferent Pathways↗
Identification of early glial elements as the precursors of Bergmann-glia: a Golgi-analysis of the developing rat cerebellar cortex.
The developing rat cerebellar cortex was studied by the rapid Golgi procedure in 200 mu thick slices and in 1--2 mu thick semithin sections poststained with toluidine-blue. Glial cells having radial fibres directed towards the pial surface were found to be present continuously in the internal granular layer during cerebellar maturation. This cell type was identified as the developing Bergmann-glia.
Animals↗
The myelinated parallel fibers of the cerebellar cortex and their regional distribution.
In the cerebellar cortex of the Rhesus monkey and the cat, the supraganglionic plexus in the molecular layer exhibits regional differences. The plexus is very well developed in the vermal parts of the anterior lobe, but only poorly developed in the nodulofloccular lobe. Most of the fibers of this plexus are myelinated parallel fibers, which synapse in the typical manner with dendritic thorns of Purkinje cells. Only very few fibers of this plexus are recurrent collaterals of Purkinje cells. Their distribution throughout the cerebellar cortex does not display regional differences. These findings agree with physiological data on the disinhibition of Purkinje cells in different parts of the cerebellar cortex.
Animals↗
Mechanisms by which diazepam, muscimol, and other drugs change the content of cGMP in cerebellar cortex.
THE CEREBELLUM CONSISTS OF TWO PARTS: the cerebellar nuclei whose connections to the various parts of the central nervous system coordinate muscle movements, and the cerebellar cortex which exerts an inhibitory influence on the cerebellar nuclei through the release of gamma-aminobutyric acid (gammaAbu) from Purkinje cells. The activity of Purkinje cells is regulated by two excitatory inputs to the cerebellar cortex-the climbing and mossy fibers-and by a neuronal network within the cortex which inhibits the activity of Purkinje cells through the release of gammaAbu from interneurons. The net activity of Purkinje cells is related to their content of guanosine 3':5'-cyclic monophosphate (cGMP) which increases or decreases according to changes in the activity of climbing and mossy fibers as well as to changes in the activation of gammaAbu receptors. When these receptors are activated, the cGMP of Purkinje cells decreases; when they are inhibited, the cGMP increases.The cGMP content of the cerebellar cortex is altered by drugs that change either the excitatory input of climbing or mossy fibers or the inhibitory input mediated by the activation of gammaAbu receptors. Mechanisms by which various drugs alter the cerebellar content of cGMP were investigated. By using various experimental designs, it was shown that diazepam and muscimol lowered the cGMP content by activating gammaAbu receptors. In contrast, morphine and haloperidol lowered the cerebellar cortex cGMP by decreasing the excitation of mossy fibers whereas harmaline increased the cGMP by increasing the excitation of the climbing fibers.
Alkaloids↗
Mode of distribution of aminergic fibers in the cerebellar cortex of the chicken.
The cerebellar cortex of adult hens contains a dense plexus of thin varicose nerve fibers which display a formaldehyde-induced green fluorescence. This plexus is not distributed at random in the cortical layers. Within the granular layer the plexus forms a netlike pattern. The fiber branches, which have numerous varicosities, are predominantly oriented in the traverse plane of the folium. In the molecular layer the fluorescent plexus shows some variations in the convex, flat and concave portions of the folia. Many of the fluorescent branches are oriented parallel to the course of the folium. They arise from a T-division of radially oriented axons resembling parallel fibers in Golgi sections. The meshes of the fluorescent plexus in the granular layer measure 10-60 mu. In the molecular layer (top of the folia) there are about 30 fluorescent fibers per 100 mu2. The fluorescent fibers originate from the locus coeruleus and form a rostral and a caudal bundle in the cerebellar peduncle. The mode of distribution of the fluorescent fibers in the cortical layers seems to depend on the organization of the innervated tissue. Light microscopy suggests that the aminergic fibers innervate more than one class of cerebellar neurons.
Amines↗
Pharmacologically induced changes in the 3':5'-cyclic guanosine monophosphate content of rat cerebellar cortex: difference between apomorphine, haloperidol and harmaline.
Harmaline increases cerebellar 3':5'-cyclic guanosine monophosphate (cGMP) content in a dose-related manner; this increase is prevented by a pretreatment with 3-acetylpyridine (3-AP) (0.66 mmol/kg) which destroys climbing fibers and inhibits harmaline-induced tremor. The cerebellar cGMP content increases after isoniazid; this response remains unchanged in rats pretreated with 3-AP. Since isoniazid decreases cerebellar gamma-aminobuturic acid (GABA) levels, the increase in cGMP content might reflect a reduction in the availability of GABA at the level of postsynaptic receptors. Apomorphine (a dopamine receptor agonist) and haloperidol (a dopamine receptor blocker) increase or decrease the cGMP content of cerebellar cortex, respectively. Neither drug changes the guanylate cyclase activity of cerebellar homogenates; moreover their action on cerebellar cGMP content persists after 3-AP. Chloropromazine, like haloperidol, decreases the cerebellar cGMP content. The increase in cerebellar cGMP content elicited by apomorphine can be differentiated from that elicited by harmaline or isoniazid; presumably apomorphine indirectly activates mossy fibers. The decrease in cerebellar cGMP content elicited by haloperidol can be differentiated from that elicited by diazepam; perhaps haloperidol reduces the mossy fiber input to the cerebellum. We suggest that the cGMP content of cerebellar cortex fluctuates in response to changes in the afferent stimulatory input to the cerebellum; it increases when the activity of either climbing or mossy fibers is increased; it decreases when either of these two stimulatory inputs is reduced.
Alkaloids↗
The myelination of the cerebellar cortex in the cat.
The myelination of the cerebellar cortex of the cat was investigated in 61 cats aged from 3 hrs post partum to two and a half years. The first myelinated fibers appear at the time of birth in the central medullary ray. Before the onset of myelination, all fibers reach a critical diameter of about 1 micrometer. About the 14th day of life the number of oligodendrocytes in the prospective while matter increases markedly. Thereafter, the oligodendrocytes invade the inner granular layer. It therefore seems that the myelination of the cerebellar cortex proceeds from the central medullary ray towards the granular layer. At the 60th day of postnatal life, most of the afferent and efferent fiber systems are myelinated. These findings are discussed in relation to the development of function and the maturation of the electrical activity of the cerebellar circuit.
Animals↗
High potassium, veratridine and electrically induced release of taurine from the cerebellar cortex.
In the in vivo superfused cerebellar cortex of anaesthetized rats, the following stimuli were effective in evoking large increases of isotopically labelled taurine from preloaded tissue: high (40 mM) K+; rectangular, 0.1 msec electrical pulses at 1.5 mA and 500 Hz; the depolarizing veratrum alkaloid, veratridine (0.5 x 10(-5) M) and scorpion venom (10(-6) g.ml-1). Both the high K+ and electrically evoked effluxes were markedly Ca2+ dependent; the veratridine response was abolished in the presence of tetrodotoxin (10(-6) g.ml-1). The data indicate that taurine is being released from excitable cells rather than neuroglia and may therefore have some neurotransmitter-like role in the cerebellum.
Animals↗
The early ultrastructural alterations in the rabbit cerebral and cerebellar cortex after compression ischaemia.
The ultrastructural alterations in the rabbit cerebral and cerebellar cortex resulting from 30 minutes complete, permanent cerebral ischaemia were studied. The ischaemia was induced by raising the intracranial pressure (ICP) above the systolic arterial pressure (compression ischaemia). Immediately after releasing the ICP the brain was fixed by intravascular glutaraldehyde perfusion. Samples from the cerebral and cerebellar cortex were processed for electron microscopy. The ultrastructural changes were relatively minor; there was a generalised, slight intracellular oedema, most prominent in the subpial area; the nuclear chromatin was clumped, the endoplasmic reticulum and cisternae of the golgi apparatus became somewhat dilated, the inner matrix of the slightly swollen mitochondria showed increased electron lucency, and microtubules and ribosomes began to loose their compact structure. These changes, unaccompanied by any extensive volumetric change of any cellular compartment, agree well with the recently presented hypothesis of two different types of anoxic-ischaemic nerve cell injury. This cellular reaction to complete, permanent compression ischaemia represents the type of injury that is seen resulting from ischaemic insults during which no flow of fluid irrigates the ischaemically injured cells.
Animals↗
Loss of synapses in the cerebellar cortex of the senescent rat.
Numbers of synapses were compared in the cerebellar cortex of adult (12 months of age) and senescent (25 months of age) male rats of the Fisher-344 strain. The total number of axodendritic synapses was found to be 24% lower in the senescent rats as compared with adults. A differential analysis of synapses involving dendritic shafts and spines showed no significant change in numbers of synapses involving shafts, but a highly sigificant 33% decrease in numbers involving spines in senescent rats. These data suggest that the selective age-related loss of synapses involving dendritic spines (but not shafts) in the cerebellar cortex results from the impairment with advanced age of specific afferent neurons and/or a selective age-related vulnerability of dendritic spines.
Aging↗
Calcium-dependent increase in efflux of [1-3H] taurine from the superfused rat cerebellar cortex in vivo.
High (40 mM) potassium stimulation has been shown to increase the efflux in vivo of [1-3H] taurine from the superfused rat cerebellar cortex by 46%, P less than 0.001. During superfusion with calcium-free media this increase in efflux is abolished. The cellular location of [1-3H] taurine in the cerebellar cortex is not yet known, but this region of the brain contains exceptionally high levels of endogenous taurine. The calcium dependency of the release of labelled taurine raises the possibility that taurine has some neuro-humoral role in the cerebellar cortex.
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Calcium and potassium changes in extracellular microenvironment of cat cerebellar cortex.
1. Local stimulus-evoked changes in concentration of extracellular calcium ions, [Ca2+]0, and potassium ions, [K+[0, were measured in the cerebellar cortex of the cat using paired ion-selected micropipettes. 2. Repetitive stimulation of 30 s duration decreased [Ca2+]0 from a base line of 1.2 mM to as low as 0.8 mM and increased [K+]0 from 3 mM to as much as 8 mM. The magnitude of the changes was directly related to stimulus frequency. Laminar analysis showed that the greatest ion changes occurred at the level of maximum parallel fiber-Purkinje cell dendrite stimulation, but that the [Ca2+]0 changes were more localized than the [K+]0 changes. 3. Combining real-time current-source density measurement with [K+]0 determination and local manganese application, showed that the Mn blocked parallel fiber-Purkinje cell synaptic transmission, but that much of the [K+]0 changes persisted. Thus, a large part of the [K+]0 flux most probably originated in the parallel fibers. In contrast, [Ca2+]0 changes were abolished by the Mn, indicating that the decrease in this ion was probably associated with synaptic transmission or dendritic events. 4. In a few cases, spreading depression occurred in the cat cerebellar cortex. This could be accompanied by decreases in [Ca2+]0 to as low as 0.12 mM and increases in [K+]0 in excess of 48 mM. 5. These results show that significant changes in [Ca2+]0 and [K+]0 occur during cerebellar stimulation and indicate possible origins of the ion fluxes in terms of neuronal elements. This work also shows that the cerebellar cortex of the cat can support spreading depression. The present results, together with those of earlier studies on [Ca2+]0 and [K+]0 changes in the presence of aminopyridine in the cat cerebellum, suggest that synaptic or dendritic electroresponsive properties may play a role in the observed [Ca2+]0 and [K+]0 changes.
Animals↗
Mossy and climbing fibre mediated responses evoked in the cerebellar cortex of the cat by trigeminal afferent stimulation.
1. The trigeminal input to the cerebellar cortex was studied by recording mass and unitary resonses evoked by electrical stimulation of individual trigeminal cutaneous and muscle nerve branches, in cats lightly anaesthetized with sodium thiopentone. 2. The trigeminal projection area of the cerebellar cortex comprised essentially lobule HVI, but included adjacent folia of lobules HV and HVIIA. 3. Each trigeminal branch had a 'patchy' representation throughout the projection area and there was extensive convergence of individual afferents at each site. Exact combinations of convergent inputs varied between loci, the projection from the muscle nerve being weaker. No other differential representation of individual trigeminal branches was evident. 4. Responses were evoked by stimulation of both ipsi- and contralateral trigeminal afferents but contralateral projections were present at fewer sites. 5. Mass responses to stimulation of individual trigeminal branches comprised mossy fibre and climbing fibre-mediated potentials, although both components were not always present. Latencies for mossy and climbing fibre responses, evoked by ipsilateral nerve stimulation, were in the ranges 5--8 msec and 11--29 msec respectively. 6. Unitary responses of Purkinje cells activiated by trigeminal inputs also revealed convergence from individual ipsilateral afferent sources (28% influenced by one ipsilateral trigeminal branch, 48% by two branches, 17% by three branches and 7% by four branches). 7. Response patterns comprised one or more of the following: short latency (3--8 msec) simple, mossy fibre-mediated spikes, 'delayed' (10--25 msec) simple spikes and climbing fibre-mediated multiple spike bursts (9--35 msec).
Afferent Pathways↗
Ultastructural analysis on acetylcholinesterase localization in the cerebellar cortex of teleosts.
The histochemical localization of acetylcholinesterase (AChE) was studied by electron microscopy in the cerebellar cortex of the goldfish and the catfish. The patterns of enzyme distribution show noticeable differences in the two teleost species at the level of the corresponding cerebellar structures. Among the most distinctive features is the prevailing intracellular localization of enzyme activity in the goldfish and the prevailing extracellular localization in the catfish in the molecular layer and, to a lesser extent, the granular layer. Only quantitative differences in the ability to synthesize AChE can be recorded among the different cerebellar neurons in the two species, since all these neurons exhibit different amounts of enzyme activity linked to their cytoplasmic structures. Comparing the results obtained with those of previous histochemical, experimental and developmental researches, the hypothesis seems well founded that the embryonic pool of cerebellar neurons is made up of AChE-synthesizing nruroblasts which, during development, loss or maintain to a different the mechanisms for AChE synthesis. In addition the light and electron microscope histochemistry reveals at different levels of resolution that the final pattern of AChE distribution in the cerebellar cortex is the sum of different degress of AChE synthesis by cerebellar neurons and different degrees of enzyme release in extracellular spaces.
Acetylcholinesterase↗
A computational model of cerebellar cortex and peripheral muscle.
A computational model, suitable for analytical or machine simulation studies, is developed for a specific cerebellar loop, the pathway from muscle fibre stretch receptors to the cerebellar cortex and back again. The model adheres to physiological data from the cat, and employs features from several existing models, including a single neuron model developed and tested earlier. Also included is a mechanical equivalent to an idealised muscle, in this case a rectangular array of muscle fibres which map 1-to-1 onto the array of compartments which form the cerebellar cortex. Much of the literature on cerebellar models is briefly reviewed, as are several key physiological experiments.
Animals↗
Fine structure of labelled axons in the cerebellar cortex and nuclei of rodents and primates after intraventricular infusions with tritiated serotonin.
The cerebellar cortex and deep cerebellar nuclei in rats and rhesus monkey were studied after treatment with monoamine oxidase inhibitor and continuous intraventricular infusion with 10(-5) M serotonin-3H. Autoradiographs were prepared for light and electron microscopy. The cerebellum contained no labelled cells. Labelled unmyelinated axons arrive from the brain stem via the periventricular zones of the aqueduct and fourth ventricle. In the parafloccular cortex about 1 per cent of the mossy fibers are labelled, together with a small number of fine varicose axons in the molecular layer that run parallel to the folial axes (less than 0.1%). In the paravermal and vermal cortex there are few labelled fibers in the granular layer and a five-fold greater number of labelled axons in the molecular layer (about 0.5%). Apparently three systems of serotonin-containing axons are present in the cortex: mossy fibers, parallel fiber-like, and a diffuse system in granular and molecular layers. The fastigial (medial), interpositus, and dentate (lateral) nuclei, lateral vestibular and other vestibular nuclei all have numerous labelled axons. The dentate and interpositus nuclei receive labelled fibers which arrive through the superior cerebellar peduncle as well as from the periventricular area. Six morphologically different classes of labelled axon terminals have been differentiated. Class 1a, the mossy fiber rosettes, and class 1b, the CAT2 axons, have small, round, clear synaptic vesicles and large granular vesicles (lgv); class 2 axons have a distinctive collection of round granular vesicles; class 3 boutons have numerous tubular profiles, a few containing dense dots, packed in a dark axoplasmic matrix; class 4 axons have tiny 250 A granular vesicles, clear tubular profiles and occasional LGV; class 5 terminals have numerous LGV, both round and elongated, with clear round and tubular profiles; class 6 terminals have LGV, clear and granular synaptic vesicles and clear tubular profiles. All these axons have LGV 900 A in diameter with 500-600 A variably dense centers that do not fill the vesicle, and Gray's type 1 axodendritic or axasomatic synapses on postsynaptic locations in the cortex and nuclei. Labelled axons in the cortex end as mossy fibers upon granule cell dendrites in glomeruli (Class 1a) or upon dendrites of cortical interneurons, e.g. Golgi cells, basket and stellate cells, and not on Purkinje cells. ...
Animals↗
Cell number and cell density in the cerebellar cortex of man and some other mammals.
The number of cells per unit volume was determined in the cerebellar cortex of man and 19 other mammals. The cell density (i.e. the number of cells per unit volume) decreases from mammals with a low brain weight to those with a higher brain weight. This decrease in the number of cells is found to be proportional for all three layers of the cerebellar cortex. In addition, the ratio of Purkinje cells to granule cells was determined. In contrast to the decrease of all cell types with increasing brain weight, this ratio varies remarkably among the mammals and is not correlated with brain weight. In man, this ratio is 1:2991, while it is lower in all other mammals investigated. These differences in the ratio of Purkinje cells to granule cells and the decrease in cell density with increasing brain weight are discussed in relation to brain evolution.
Animals↗