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F F Ebner

Publications and source records attributed to F F Ebner.

At least 55 records · Page 3Linked to original sources
PubMed1988

The effect of thiamine deficiency on the structure and physiology of the rat forebrain.

Dietary thiamine deficiency, enhanced by pyrithiamine administration in adult rats, produces overt lesions in the brain that are especially prominent in the thalamus. The present study was undertaken to determine whether the thalamic lesions could be correlated with alterations in the physiological properties of neurons in the thalamus and somatosensory cortex. The regimen for experimentally inducing thiamine deficiency produced large lesions in the thalamus of every case; the lesions included most, if not all, of the neurons in the intralaminar thalamic nuclei. The extent of the lesion in the intralaminar thalamus was highly correlated with the loss of bilaterally synchronous spontaneous activity in the cerebral cortex. This correlation was seen in animals analyzed as early as 1-18 hr after the appearance of opisthotonus, the crisis state of thiamine deficiency, and as late as 2-9 weeks of recovery following thiamine replacement therapy. The loss of bilateral synchronous bursting neuronal activity following intralaminar thalamic lesions is consistent with the proposed role of the intralaminar thalamus as a pacemaker for rhythmic cortical activity (Armstrong-James et al., Exp. Brain Res., 1985; Fox and Armstrong-James, Exp. Brain Res. 63: 505-518, 1986). The location and size of the central lesions within the thalamus suggest that the observed neuronal loss could result from a nonhemorrhagic infarction in the ventromedial branches of the superior cerebellar arteries. Experimental thiamine deficiency also produced alterations in the receptive field properties of the somatosensory cortex neurons in all animals examined. Changes in cortical receptive field properties were correlated with the destruction of sensory relay neurons in the thalamic ventrobasal complex. The loss of the central lateral thalamic input to the cortex and the loss of somatosensory relay neurons in the ventrobasal thalamus in experimental thiamine deficiency produce alterations in cortical function which may contribute to deficits in memory and cognition analogous to those which characterize Korsakoff's psychosis in humans.

Animals↗
PubMed1987

A physiological basis for a theory of synapse modification.

The functional organization of the cerebral cortex is modified dramatically by sensory experience during early postnatal life. The basis for these modifications is a type of synaptic plasticity that may also contribute to some forms of adult learning. The question of how synapses modify according to experience has been approached by determining theoretically what is required of a modification mechanism to account for the available experimental data in the developing visual cortex. The resulting theory states precisely how certain variables might influence synaptic modifications. This insight has led to the development of a biologically plausible molecular model for synapse modification in the cerebral cortex.

Action Potentials↗
PubMed1986

Tyrosine hydroxylase is expressed by neocortical neurons after transplantation.

Tyrosine hydroxylase [TyrOHase; L-tyrosine, tetrahydropteridine:oxygen oxidoreductase (3-hydroxylating), EC 1.14.16.2], an essential enzyme in the synthesis of catecholamines, is expressed normally by neurons in the brainstem but not by those in mature neocortex. When embryonic neocortex is transplanted into adult neocortex, TyrOHase-immunoreactive cells develop and continue to be present in the transplants for the life of the host animal. The percentage of transplant neurons that express TyrOHase is highly correlated with the age of the embryonic donor tissue at the time of transplantation. Many TyrOHase-immunoreactive cells are present in transplants from embryonic day 12 (E12) embryos. The labeled cells are frequently arrayed in striking clusters of cell bodies and their processes, which ramify densely within the transplants. Moderate numbers of cells are found scattered throughout transplants from E14 donors, while E17 donors consistently develop small numbers of TyrOHase-containing cells. Tissue removed for transplantation on the day before birth (E19) never contains cells that express TyrOHase. The TyrOHase-positive cells are mostly bipolar and stellate in shape and show neither immunoreactivity for other catecholamine-synthesizing enzymes nor catecholamine fluorescence. These results provide a demonstration of continued TyrOHase synthesis in central nervous system cells that normally do not express this enzyme. Because of these and similar results with other neurotransmitter enzymes, the transplantation paradigm is particularly useful as a technique for studying the factors that regulate enzyme induction and activity during development of the nervous system.

Animals↗
PubMed1985

Postnatal changes in the distribution of acetylcholinesterase in kitten striate cortex.

We have traced the postnatal development of axons and cells in kitten striate cortex that contain acetylcholinesterase (AChE) by using a modification of Koelle's histochemical method. The maturation of AChE-positive axons was not found to be fully complete until at least 3 months of age, and was characterized by several distinct developmental trends. AChE-positive fibers in layers IVc-VI proliferate rapidly after birth until, by 4 weeks postnatal, they appear to exceed the adult density. They remain at this level as late as 8 weeks and then decrease to the adult density by 13 weeks. In contrast, the AChE-positive fibers in layer I do not show a substantial increase in density until 6 weeks of age and the adult level is not achieved before 3 months postnatal. Finally, the density of AChE-positive fibers in layers II and III appears to increase gradually from birth until the mature pattern is reached at about 6 weeks. AChE could also be localized histochemically to cell bodies whose position and appearance depended on postnatal age. Stained cells first appeared in the white matter subjacent to layer VI shortly after birth. By 2 weeks of age, most cells in layer VI were also AChE positive. The staining of these cells gradually disappears over the next 2 months until, at 3 months of age, there are no AChE-positive cells in cat striate cortex. However, a subpopulation of stained neurons appears in layer V by 1 year of age that persists throughout adulthood. The possible contributions of acetylcholine and AChE to the postnatal development of kitten striate cortex are discussed.

Acetylcholinesterase↗
PubMed1985

The projection of three extrathalamic cell groups to the cerebral cortex of the turtle Pseudemys.

Three extrathalamic subcortical inputs to the part of the cerebral cortex that is known to receive thalamic fibers in the turtle were examined in the present study. Direct projections from the locus coeruleus, the superior medial raphe nucleus, and a wide area of the basal telencephalon that lies ventromedial to the globus pallidus were demonstrated with the horseradish peroxidase method. Fluorescence histochemistry confirmed the presence of catecholamine-containing fibers in the rostral half of dorsal cortex and also demonstrated a dense network of serotoninergic fibers. Biochemical analysis showed the concentration of both monoamines to be relatively high; the norepinephrine concentration was 709 ng/g and the serotonin concentration was 1,750 ng/g. No evidence was found to suggest the existence of either a dopamine fiber projection to cortex comparable to that of mammalian neocortex or the presence of an epinephrine pathway to turtle cortex equivalent to the epinephrine-containing fibers in the pallium of amphibians. The coexistence of the projections from the thalamus with noradrenergic projections from the locus coeruleus, serotoninergic projections from the superior medial raphe nucleus, and presumably cholinergic projections from the basal telencephalon provide at least four distinct subcortical inputs to the reptilian dorsal cortex. Neither thalamic nor similar extrathalamic inputs have been demonstrated in the dorsal pallium of amphibia. Mammalian neocortex, in contrast, has even more elaborately differentiated inputs of both types. These results support the idea that thalamic and extrathalamic inputs to cortex appear at the same time in vertebrate evolution, and that both types of inputs are required for the normal development and function of neocortex.

Animals↗
PubMed1985

Glutamic acid decarboxylase activity decreases in mouse neocortex after lesions of the basal forebrain.

Glutamic acid decarboxylase (GAD) activity was measured in the cerebral cortex of animals after acute and chronic lesions to basal forebrain cholinergic nuclei. Such lesions were shown to result in an extensive depletion of cholinergic markers in parietal cerebral cortex. A statistically significant 30% decrease in GAD activity was first detected at 6 weeks postlesion and was still measurable 8 months after the lesion. These results suggest that cholinergic inputs to cortex indirectly or directly influence GABAergic transmission in cortex.

Animals↗
PubMed1985

An investigation of cholinergic circuitry in cat striate cortex using acetylcholinesterase histochemistry.

The organization of cholinergic inputs to cat striate cortex (area 17) was studied by using a histochemical stain for acetylcholinesterase (AChE). Axons were labelled in all layers of the striate cortex, with distinct plexuses occurring in layer I, lower layer III, layer IVc, and layer VI. In addition to the stained axons, a population of layer V pyramidal cells was intensely AChE-positive. Surgical undercutting eliminated virtually all of the AChE-positive axons in the striate cortex, thus indicating that this innervation arises entirely from an extrinsic source in the cat. To identify this source, cell groups projecting to area 17 were retrogradely labelled with horseradish peroxidase. Cell groups labelled with horseradish peroxidase that were also intensely AChE-positive were considered as possible candidates for providing the cholinergic input to the striate cortex. These included the basal forebrain, several intralaminar nuclei, and the lateral geniculate nucleus. Kainate lesions were then made in each of these structures to assess their individual contributions to the cortical AChE pattern. Cortical AChE was depleted only after lesions of the basal forebrain, suggesting that this is the sole source of AChE-positive axons in area 17. Because the cortically projecting cells in this region have been shown to contain choline acetyltransferase in a number of species, we postulate that the AChE-positive fibers we describe in the cat striate cortex are in fact cholinergic.

Acetylcholinesterase↗
PubMed1985

Development of cholinergic markers in mouse forebrain. I. Choline acetyltransferase enzyme activity and acetylcholinesterase histochemistry.

Measurements of choline acetyltransferase (ChAT) activity were made during the development of the neocortical cholinergic innervation, and correlated with the development of the acetylcholinesterase (AChE) staining pattern in mouse cerebral cortex and several other areas of the forebrain between the time of initial onset and maturity ChAT activity can first be measured on postnatal day 6 (P6). The enzyme reaches 40% of adult activity by P18 and adult values by 7 weeks postnatal. The onset of AChE staining varies for different regions of the forebrain and for various areas within the cerebral cortex. The earliest appearance of AChE is seen in several basal forebrain nuclei including the striatum, the ventromedial region of the globus pallidus and the hypothalamus on embryonic day 18 (E18). In neocortex and olfactory cortex, AChE-stained axons are seen in the white matter before birth, but do not enter cingulate cortex and hippocampus until P2. By P2. almost all areas of the basal forebrain and diencephalon have acquired some AChE staining pattern. The adult distribution of AChE staining is reached by 3 weeks postnatal in all areas of the forebrain. Adult cerebral cortex shows a characteristic pattern of alternating AChE dense and AChE sparse bands which vary in depth depending on the cortical area. The cortical banding pattern develops in an 'inside-out' fashion, starting in layer VI and gradually entering more superficial layers. In parallel with the AChE pattern of development in cortex, transient AChE staining can be observed in some thalamic nuclei and in some forebrain fiber systems. In the neostriatum patches of intense AChE staining first develop along the ventrolateral border, then spread throughout the whole nucleus and finally coalesce to a uniform high density over the entire neostriatum. We discuss the close spatial and temporal correspondence between AChE pattern development and reported data on synapse formation, and speculate on the role of the cortical cholinergic system in development.

Acetylcholinesterase↗
PubMed1985

Development of cholinergic markers in mouse forebrain. II. Muscarinic receptor binding in cortex.

The distribution of muscarinic receptor sites throughout the ontogeny of cerebral cortex in the BALB/c mouse have been labeled, placing special emphasis on binding site development in parietal neocortex and hippocampus. We describe a new procedure for the use of [3H]propylbenzilylcholine mustard as a muscarinic cholinergic ligand in an in vitro binding assay on brain sections. Muscarinic binding sites, as visualized by autoradiography, can be seen in cortex as early as embryonic day 18. They achieve maximal labeling density and adult distribution in neocortex by the end of the first postnatal month. The adult distribution pattern in hippocampus is reached by the second postnatal week, but the maximal density of label is not achieved until 4 weeks of age. Changes in the receptor binding pattern are illustrated at 5 different ages between birth and adulthood. We conclude that muscarinic cholinergic receptors develop late in cortical ontogeny as do other cholinergic markers. The distribution pattern of muscarinic binding sites in mouse cortex is puzzling because it does not correspond to the reported distribution of cells physiologically responsive to applied acetylcholine. These results are compared to the onset of choline acetyltransferase activity and acetylcholine esterase staining. The ontogenesis of the cortical cholinergic system is compared with other features of general cortical morphogenesis.

Age Factors↗
PubMed1985

Glutamic acid decarboxylase in the striate cortex of normal and monocularly deprived kittens.

Degeneration of the thalamic fibers in the visual cortex of turtles leads to an increase in the numerical density of cortical synapses with flattened vesicles and symmetrical membrane differentiations (Smith, L. M., and F. F. Ebner (1980) Soc. Neurosci. Abstr. 6: 328). This change correlates with an increase in the cortical activity of glutamic acid decarboxylase (GAD), the synthetic enzyme for gamma-aminobutyric acid (GABA). These data are consistent with the hypothesis that removal of thalamic input activity is the stimulus for cortical GABAergic neurons to form new synapses. Pharmacological evidence suggests that even simple environmental deprivation may induce a similar increase in the numerical density of GABAergic synapses in kitten striate cortex (Duffy, F. H., S. R., Snodgrass, J. L. Burchfiel, and J. L. Conway (1976) Nature 260: 256-257). We have examined this possibility in monocularly deprived kittens using methods to localize and measure GAD. GAD in kitten striate cortex was localized using immunocytochemistry. GAD-positive cells were found in all layers and were uniformly distributed in layers II to VI. Immunoreactivity associated with axon terminals (puncta), in contrast, was laminated with a distinct band in layer IV. Monocular deprivation (MD), by either unilateral enucleation or lid closure, had no detectable effect on the distribution of GAD in striate cortex. The band of layer IV puncta remained uniform even under conditions that produced alterations in layer IV cytochrome oxidase activity. We measured GAD activity in homogenates of striate cortex to address the possibility that MD causes an absolute change in the density of GABAergic synapses. Again, however, GAD activity in the binocular and monocular segments of striate cortex was found to be unaffected by early enucleation. These data suggest two conclusions: first, that the numerical density of GABAergic synapses in visual cortex is not regulated directly by thalamic activity, and second, that changes in GABAergic synapse density do not account for the ocular dominance shift observed in kitten striate cortex after MD.

Animals↗
PubMed1983

Mossy fibre projections into and out of hippocampal transplants.

Hippocampal primordia taken from one day old postnatal rats and grown for 1 month in the hippocampus of adult rat hosts developed hippocampal pyramids, dentate granule cells, and specific patterns of mossy fibres. In 26 cases where certain boundary conditions were precisely met, the transplant mossy fibres crossed into the host and ramified for a distance of from 0.5 mm to no more than 1 mm in the stratum oriens of the host field CA1. They formed a layer 35 micron thick adjacent to the host CA1 pyramidal cell layer. The necessary boundary conditions were: (1) direct (and "unscarred") contact between the neuropil of the transplant and the host field CA1, (2) that the hilar (and not the molecular) aspect of the transplanted dentate granule cell lamina faced the host CA1 pyramids, and (3) that some of the interface was devoid of transplant hilar cells or CA3-type pyramids interposed between the transplant dentate granules and the host CA1 pyramids. In 3 cases a converse connection was found--viz. the host mossy fibres entered the transplant. In these cases the transplants consisted entirely of pyramidal cells (with no dentate granule cells of their own), and the part of the transplant receiving the host mossy fibres was embedded directly in the host mossy fibre pathway. For the dentato-hippocampal mossy fibre system, therefore, it is shown that postsynaptic targets in the adult mammalian brain can receive specific patterns of innervation from growing axons derived from a transplant, and that cut central axons of the same type can grow and form target-specific terminal arborizations in a transplant.

Animals↗
PubMed1983

Somatostatin-like immunoreactivity in the forebrain of Pseudemys turtles.

Previous investigations of cortical organization in the brain of the turtle have revealed many features typical of mammalian neocortex. Recent evidence suggests that many neocortical neurons contain neuroactive peptides. The possibility that one such peptide, somatostatin, is found in the turtle brain was tested using immunocytochemical techniques. Intense somatostatin-like immunoreactivity was observed in many neurons and fibers in turtle cortex, as well as in several forebrain nuclei. Cortical neurons with several different dendritic configurations showed immunoreactive labelling, including bipolar, stellate and pyramidal cell types. In addition, stained cells and processes were observed in close association with the ependyma of the lateral ventricle. Other forebrain regions containing immunoreactive neurons included the dorsal ventricular ridge, the basal telencephalic nuclei and the hypothalamus. These data support the idea that peptidergic neurons existed in the pallium of an ancestor common to modern mammals and reptiles. We speculate that somatostatin plays a similar role in the normal function of all types of cortex and suggest that turtle cortex may provide a useful model for the study of this cortical neuropeptide.

Animals↗
PubMed1981

The organization of thalamic projections to the parietal cortex of the Virginia opossum.

The thalamic projections to somatic sensory-motor (SSM) cortex and adjacent cortical areas of the Virginia opossum were studied using anterograde and retrograde axoplasmic transport techniques. Large injections of horseradish peroxidase and/or tritiated amino acids were made in the parietal cortex to identify all of the thalamic nuclei that are interconnected with this large cortical area. Very restricted injections were then made in physiologically identified subdivisions of SSM cortex, in the remaining posterior portion of parietal cortex, and in the anteriorly adjacent postorbital cortex. The results show that the parietal cortex is reciprocally connected with a number of thalamic nuclei. Different combinations of these thalamic areas project to specific subregions within the parietal field. All parts of the SSM cortex, which occupies the anterior four-fifths of parietal cortex, receive input from the ventrobasal complex (VB), the ventrolateral complex (VL), the central intralaminar nucleus (CIN), the central lateral nucleus (CL), and the ventromedial nucleus (VM). We could detect no segregation of VL and VB inputs in any part of SSM cortex. Projections from all of these thalamic nuclei, except VM, show at least some degree of topographic organization. Anterior-posterior strips of SSM cortex receive input from clusters of thalamic neurons that extend dorsoventrally and rostrocaudally through VB and VL. The posterior one-fifth of the parietal cortex (the posterior parietal area) receives input from VL, the posterior nuclear complex, and the lateral complex, as well as input from CL, CIN, and VM. Postorbital cortex receives input mainly from intralaminar, midline, and medial thalamic nuclei. We conclude that the projection field of VB in the parietal cortex coincides precisely with the first somatic sensory area (SI) as defined by single unit studies (Pubols et al., '76). The VB projection field also delineates the area of the first motor (MI) representation. Thus, there is no separation of SI and MI cortex in the opossum. The posterior parietal area lies outside of SSM cortex and has thalamic connections similar to the posterior parts of parietal cortex in other mammals.

Animals↗
PubMed1981

The laminar distribution and ultrastructure of fibers projecting from three thalamic nuclei to the somatic sensory-motor cortex of the opossum.

The projections of the ventrobasal complex (VB), the ventrolateral complex (VL), and the central intralaminar nucleus (CIN) to the somatic sensory-motor (SSM) cortex of the Virginia opossum were studied with light and electron microscopic autoradiographic methods. VB, VL, and CIN have overlapping projections to SSM cortex and each one also projects to an additional cortical area. Unit responses to somatic sensory stimulation and the areal and laminar distribution of axons in cortex is different for VB, VL, and CIN, but the axons from each form similar round asymmetrical synapses, predominantly with dendritic spines. As in other mammals, VB units in the opossum have discrete, contralateral cutaneous receptive fields. VB projects somatotopically to SSM cortex and also projects to the second somatic sensory representation. Within the cortex, VB axons terminate densely in layer IV and the adjacent part of layer III. A few axons also terminate in the outermost part of layer I and the upper part of layer VI. Most VB axons terminate upon dendritic spines (86.6%), but they also contact dendritic shafts (10%) and neuronal cell bodies (3%). Neurons in VL have no reliable response to somatic stimulation under our recording conditions. VL projects to the SSM cortex and to the posterior parietal area. Throughout this entire projection field VL fibers terminate in layers I, III, and IV most densely, and sparsely in the other cortical layers. The density of termination in the mid-cortical laminae is quite sparse compared to VB, but the projection to layer I is considerably greater. Nearly all (93%) of VL axons contact dendritic spines, the remainder (7%) end on dendritic shafts. CIN is a thalamic target of ascending medial lemniscal, cerebellar, spinal, and reticular formation axons. Neurons in CIN respond to stimulation restricted to a particular body part, but typically responses may be evoked from larger areas and at longer latencies than neurons in VB that are related to the same body part. CIN neurons require a firm tap or electrical stimulation within their receptive field to elicit a response in the anesthetized preparation. CIN axons terminate throughout the entire parietal cortex, but unlike VB and VL, CIN fibers end almost exclusively in the outer part of layer I. Approximately 21% of CIN fibers contact dendritic shafts in layer I, which is twice the percentage of shafts contacted by VL or VB axons. All of the other CIN synapses are formed with dendritic spines. These experiments demonstrate three different pathways to SSM cortex. The results suggest that each projection has a unique role in controlling the patterns of activity of neurons within the SSM cortex.

Animals↗
PubMed1981

An ultrastructural and biochemical analysis of norepinephrine-containing varicosities in the cerebral cortex of the turtle Pseudemys.

The fine structure and norepinephrine content of small granular vesicle-containing profiles were studied in normal and norepinephrine-depleted cerebral cortex of the turtle, Pseudemys. The cortex was fixed for electron microscopy with the KMnO4 procedure of Koda and Bloom ('77), while the norepinephrine content was assayed wit the radioenzymatic method of Coyle and Henry ('73). Green fluorescent fibers have been described by Parent and Poitras ('74) as located almost exclusively in the outer half of the molecular layer in turtle cortex. Small granular vesicle-containing profiles are found down to 100 microns below the pial surface, but over 50% lie within 20 microns of the surface. Within the outer 100 microns of cortex, the frequency of labeled varicosities is 1.39/1,000 microns2. The average area of the norepinephrine-containing varicosities is 0.61 microns2, and there is a mean of 18.4 vesicles per single section. The average number of large plus small vesicles in an entire varicosity was estimated to be 72. Synaptic membranes are not well-preserved with KMnO4 fixation, but good examples were found of small granular vesicle-containing profiles forming both symmetrical and asymmetrical membrane differentiations. Only a small percentage of the small granular vesicle profiles were associated with a synaptic membrane differentiation in single sections. When norepinephrine-fiber synapses are seen, they usually share a postsynaptic element with another unlabeled vesicle-containing profile. Normal turtle cortex contains an average norepinephrine concentration of 1.95 micrograms/gr, which is about eight times higher than in rat cortex. The ratio of norepinephrine to dopamine is about 18 to one, suggesting that dopamine is present predominantly in a precursor pool for norepinephrine. Small granular vesicle-containing profiles were eliminated after treatment with reserpine and 6-hydroxydopamine in concentrations that were shown to reduce norepinephrine concentration by 94% and 86%, respectively. The labeled varicosities were partially depleted by midbrain hemisection and by an inhibitor of dopamine-beta-hydroxylase (FLA-63). The norepinephrine-containing varicosities are remarkably coextensive with the distribution of thalamic fibers, both in the total extent of cortex where they are found and in the depth of cortex where they terminate. The results support the idea that there is a close structural and functional association between locus coeruleus and thalamic fibers in cerebral cortex, and the apparent difference in frequency of synapses suggests that each fiber system exerts its influence on cortical cells in a different way.

Animals↗
PubMed1981

Laminar organization of efferent cells in the parietal cortex of the Virginia opossum.

The size, shape and laminar position of efferent neurons in the parietal cortex of the Virginia opossum were identified using the method of retrograde transport of horseradish peroxidase (HRP). Injection of HRP into the spinal cord, dorsal column nuclei or pontine nuclei leads to labeling of cells in layer V and occasionally in layer VI, while a large injection of HRP in the dorsal thalamus labels many cells in layer VI, with fewer cells in layer V. HRP injections in the SSM cortex label cells in layers II-VI of ipsilateral and contralateral cortical areas. However, the majority of these cortico-cortical cells are found in the supragranular layers. Examination of the size, shape and laminar position of retrogradely labeled layer V neurons after injections in each of these areas suggests that none of these features can be used to predict accurately the projection target of individual neurons. We conclude that the laminar organization of efferent cells of the opossum parietal cortex is very similar to that seen in the neocortex of other mammals, despite the complete coalescence of somatic sensory (SI) and motor (MI) areas in the opossum.

Animals↗
PubMed1980

The thalamocortical projection in Pseudemys turtles: a quantitative electron microscopic study.

Thalamic fibers in the cortex of Pseudemys turtles were studied with the electron microscope to determine the type of synaptic vesicle they contain, the type of membrane differentiation they form, and the type of processes they contact. Following unilateral removal of the thalamus, all degenerating thalamic axon terminals are located in the outer third of the molecular layer in the rostral half of general cortex. In the middle of this zone they constitute as much as 25% of all vesicle-containing profiles. The degenerated terminals appear as electron opaque profiles, most commonly with a uniform opacity. They contain round agranular vesicles and form synapses with asymmetrical membrane differentiations. They synapse mainly on dendritic spines containing mitochondria and/or membranous sacs, although some thalamic fibers contact small clear spines, dendrites, and, rarely, cell bodies. Counts show that 86% of degenerated contacts are on dendritic spines and 14% on dendritic shafts. The spines probably all belong to the dendrites of the pyramidal cells, whose somata are located in the deep cellular layer. The dendritic shafts and somata are most likely those of the aspinous stellate neurons located in the molecular layer. Although these stellate cells are not sufficiently numerous to form a cell "layer," each transverse section through thalamic recipient cortex contains about nine of these cells and they occur in a ratio of 1:37 to pyramidal cells in the underlying main cell layer. We have calculated that in a rectangular solid of turtle cortex whose dimensions are 1 mm X 1 mm X the depth from pial surface to the underlying ventricle, there are 5.2 million thalamic fiber contacts (all in the outer 100 micrometers), 15,000 pyramidal neurons in the main cell layer, and 400 stellate cells in the molecular layer. Of the 5.2 million thalamic synapses, 0.7 million contact stellate cells and 4.5 million contact pyramidal cells. Thus each stellate cell in the molecular layer receives on the average 1,800 thalamic fiber contacts, while each pyramidal cell receives only 300 thalamic fiber synapses on the distal portion of its dendrites. The calculations lead to the conclusion that individual stellate cells receive at least six times more thalamic fiber synapses than individual pyramidal cells in turtle cortex. We suggest that the stellate cells in the thalamic input zone are inhibitory and that each thalamic volley not only excites efferent pyramidal cells but is also a powerful activator of inhibitory interneurons.

Afferent Pathways↗