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Biomedical subjects

E G Jones

Publications and source records attributed to E G Jones.

At least 91 records · Page 5Linked to original sources

Deaf and hearing mothers' interactions with normally hearing infants and toddlers.

The purpose of this study was to compare the interactions between Deaf mothers and their normally hearing infants and toddlers with the interactions between hearing mothers and their normally hearing infants and toddlers. The Nursing Child Assessment Teaching Scale (NCATS), modified to credit Deaf mothers and their children for both spoken and signed communications, was used to assess mother-child interactions. There were no statistically significant differences in scores on the NCATS Parent subscales, NCATS Child subscales, or in total NCATS scores of the Deaf mother/child dyads compared with the hearing mother/child dyads. Implications for clinical practice are discussed.

Adult↗

Foster parents' early adaptation to the placement of a child with developmental disabilities in their home.

Eight foster parents of children with developmental disabilities (DD) were interviewed about their early adaptation to placement of the child in their homes. Analysis using a grounded theory methodology showed important adaptations in the physiological, role function, interdependence, and self-concept modes of adaptation. Parents described less attention to their own physical health, dominance of the parenting role over all other roles, decreased social interactions, and a sense of personal satisfaction in response to placement of a child with DD in their homes. Implications for nursing practice are included.

Adaptation, Psychological↗

Deaf and hearing parents' interactions with eldest hearing children.

Observational methods were used to gather data from 54 individuals in 9 Deaf-parented families and 9 hearing-parented families whose eldest hearing children were aged 7 to 11 years old. Transcripts of parent/child dyadic interactions during a vacation planning activity were analyzed using Condon, Cooper and Grotevant's (1984) Individuation Code. Repeated measures ANOVAS were conducted with the independent variables of the parent's gender (mother versus fathers) and group membership (Deaf-parented versus hearing-parented families) on the percentage of communication that reflected self-assertion, separateness, permeability, and mutuality. There were no significant differences between children from Deaf-parented families versus children from hearing-parented families. There was a significant main effect for parents in communication reflecting self-assertion; namely hearing parents had a higher percentage of self-assertive communication than Deaf parents.

Adolescent↗

Selective alterations in gene expression for NMDA receptor subunits in prefrontal cortex of schizophrenics.

NMDA receptor antagonists can induce a schizophrenia-like psychosis, but the role of NMDA receptors in the pathophysiology of schizophrenia remains unclear. Expression patterns of mRNAs for five NMDA receptor subunits (NR1/NR2A-D) were determined by in situ hybridization in prefrontal, parieto-temporal, and cerebellar cortex of brains from schizophrenics and from neuroleptic-treated and nonmedicated controls. In the cerebral cortex of both schizophrenics and controls, mRNAs for NR1, NR2A, NR2B, and NR2D subunits were preferentially expressed in layers II/III, Va, and VIa, with much higher levels in the prefrontal than in the parieto-temporal cortex. Levels of mRNA for the NR2C subunit were very low overall. By contrast, the cerebellar cortex of both schizophrenics and controls contained very high levels of NR2C subunit mRNA, whereas levels for the other subunit mRNAs were very low, except NR1, for which levels were moderate. Significant alterations in the schizophrenic cohort were confined to the prefrontal cortex. Here there was a shift in the relative proportions of mRNAs for the NR2 subunit family, with a 53% relative increase in expression of the NR2D subunit mRNA. No comparable changes were found in neuroleptic-treated or untreated controls. These findings indicate regional heterogeneity of NMDA receptor subunit expression in human cerebral and cerebellar cortex. In schizophrenics, the alterations in expression of NR2 subunit mRNA in prefrontal cortex are potential indicators of deficits in NMDA receptor-mediated neurotransmission accompanying functional hypoactivity of the frontal lobes.

Autoradiography↗

Laminar patterns of expression of GABA-A receptor subunit mRNAs in monkey sensory motor cortex.

Radioactive complementary RNA probes, made from monkey-specific cDNAs specific for the alpha 1, alpha 2, alpha 4, alpha 5, beta 1, beta 2, and gamma 2 subunits of the gamma-aminobutyric acid A (GABAA) receptor were used for in situ hybridization histochemistry of the primary motor, somatosensory, and anterior parietal areas of the cerebral cortex in macaque monkeys. mRNAs for the alpha 1, beta 2, and gamma 2 subunit polypeptides, which form receptors with the full range of classical properties, are expressed at much higher levels in all areas and show laminar- and sublaminar-specific concentrations. alpha 2, alpha 4, alpha 5, and beta 1 subunit transcripts are expressed at much lower levels but also display individual, laminar-specific concentrations; alpha 5 expression, in particular, is highly expressed in layer IV in the somatosensory and parietal areas and in a layer IV-like band in the motor cortex. In layers in which expression of a particular transcript is high, all neurons may express the gene, but in layers in which expression is moderate, it is possible to detect differences in the degree of labeling of individual neurons for a particular mRNA, and some neurons may not express certain subunit transcripts in detectable amounts. These findings indicate the variability in expression of different GABAA receptor subunits in the cerebral cortex. Laminar differences may indicate the assembly of functional receptors from different arrangements of available subunits in different classes of cells.

Animals↗

Representation of the face and intraoral structures in area 3b of the squirrel monkey (Saimiri sciureus) somatosensory cortex, with special reference to the ipsilateral representation.

Studies of the representation of the trigeminal nerve in the thalamus and cerebral cortex of mammals have revealed representations of both contra- and ipsilateral intraoral structures. However, the relative extent of both representations is subject to considerable species variation. The present study employed microelectrode mapping and anatomical tracing to investigate the location and extent of the ipsilateral representation in area 3b of the somatosensory cortex of squirrel monkeys. A small region, approximately 2 mm2, was found to be responsive to stimulation of ipsilateral intraoral structures. This region was located on the anteromedial border of area 3b, surrounded by the representation of the contralateral roof of the mouth. This region corresponded to areas of intense anterograde labeling following injections placed in the ventromedial portion of the ventral posterior medial nucleus of the thalamus at the only sites where neural responses could be elicited by stimulation of ipsilateral intraoral structures. The amount of thalamus and cortex given over to the ipsilateral representation in the squirrel monkey is small compared with that of the macaque monkey. This difference may be related to the lack of cheek pouches in the squirrel monkey, and therefore a different strategy for eating. The representation of the contralateral lower lip in area 3b was split by the representation of the contralateral upper lip. This split representation is in agreement with previous studies of the trigeminal representation in area 3b of the macaque monkey and may be a general feature of the representation of the trigeminal nerve in area 3b of primate cerebral cortex.

Afferent Pathways↗

Editing for an AMPA receptor subunit RNA in prefrontal cortex and striatum in Alzheimer's disease, Huntington's disease and schizophrenia.

Animal studies and cell culture experiments demonstrated that posttranscriptional editing of the transcript of the GluR-2 gene, resulting in substitution of an arginine for glutamine in the second transmembrane region (TM II) of the expressed protein, is associated with a reduction in Ca2+ permeability of the receptor channel. Thus, disturbances in GluR-2 RNA editing with alteration of intracellular Ca2+ homeostasis could lead to neuronal dysfunction and even neuronal degeneration. The present study determined the proportions of edited and unedited GluR-2 RNA in the prefrontal cortex of brains from patients with Alzheimer's disease, in the striatum of brains from patients with Huntington's disease, and in the same areas of brains from age-matched schizophrenics and controls, by using reverse transcriptase-polymerase chain reaction, restriction endonuclease digestion, gel electrophoresis and scintillation radiometry. In the prefrontal cortex of controls, < 0.1% of all GluR-2 RNA molecules were unedited and > 99.9% were edited; in the prefrontal cortex both of schizophrenics and of Alzheimer's patients approximately 1.0% of all GluR-2 RNA molecules were unedited and 99% were edited. In the striatum of controls and of schizophrenics, approximately 0.5% of GluR-2 RNA molecules were unedited and 99.5% were edited; in the striatum of Huntington's patients nearly 5.0% of GluR-2 RNA was unedited. In the prefrontal white matter of controls, approximately 7.0% of GluR-2 RNA was unedited. In the normal human prefrontal cortex and striatum, the large majority of GluR-2 RNA molecules contains a CGG codon for arginine in the TMII coding region; this implies that the corresponding AMPA receptors have a low Ca2+ permeability, as previously demonstrated for the rat brain. The process of GluR-2 RNA editing is compromised in a region-specific manner in schizophrenia, in Alzheimer's disease and Huntington's Chorea although in each of these disorders there is still a large excess of edited GluR-2 RNA molecules. Disturbances of GluR-2 RNA editing leading to excessive Ca2+ permeability, may contribute to neuronal dysfunction in schizophrenia and to neuronal death in Alzheimer's disease and Huntington's disease.

Aged↗

Subdivisions of macaque monkey auditory cortex revealed by calcium-binding protein immunoreactivity.

The aim of this investigation was to characterize auditory areas of the primate cerebral cortex on the basis of chemoarchitecture. Cortical areas of the supratemporal plane were delineated in Macaca fuscata (M. fuscata) by immunocytochemical staining for parvalbumin, staining for cytochrome oxidase, examination of cyto- and myeloarchitecture, and retrograde tracing of corticocortical connections. Comparative observations were made on Macaca fascicularis (M. fascicularis). Differential staining of fiber plexuses, probably of thalamic origin, identifies a central core zone of dense immunostaining and a surrounding zone of moderate-to-dense immunostaining composed of anteromedial, lateral, and posteromedial fields. Outside the second zone, there is a third anterolateral zone of weaker immunoreactivity, and, outside that zone, there is a fourth zone in which immunoreactivity is virtually absent. Differences in parvalbumin immunostaining in the auditory fields may reflect differences in relative contributions of thalamic inputs from parvalbumin-immunoreactive cells in the medial geniculate complex. The central core zone and the surrounding three fields can be correlated with major auditory fields previously defined by multiunit mapping and thalamocortical connectivity. The core zone contains a large principal field and an anterior extension. The pattern of corticocortical connections between these and adjoining fields suggests that the anteromedial, lateral, and posteromedial fields represent first steps in three streams of connections passing outward from auditory into association cortex. M. fuscata has an unusually large auditory cortex that is more deeply placed in the lateral sulcus in comparison to that of M. fascicularis. A small annectant gyrus provides a guide to the position of the primary auditory area.

Animals↗

Auditory thalamocortical pathways defined in monkeys by calcium-binding protein immunoreactivity.

This study investigated differentiation of Macaca fuscata auditory thalamus into chemically defined nuclei forming relays to auditory cortical areas. The thalamus was stained immunocytochemically for parvalbumin and 28 kDa calbindin in normals and in brains in which retrogradely transported tracers were injected into middle layers of auditory cortical areas or applied to the cortical surface. Parvalbumin- and calbindin-immunoreactive cells show a complementary distribution in ventral, anterodorsal, posterodorsal, and magnocellular medial geniculate nuclei. The ventral nucleus has a high density of parvalbumin cells and few calbindin cells, and the anterodorsal nucleus has a high density of parvalbumin cells and moderate numbers of calbindin cells. Both nuclei have a dense parvalbumin-immunoreactive neuropil formed by terminations of fibers ascending in the brachium of the inferior colliculus. The posterodorsal nucleus has approximately equal proportions of parvalbumin and calbindin cells; neuropil staining is weak but contains terminations of calbindin-immunoreactive fibers ascending in the midbrain tegmentum. The magnocellular nucleus contains domains of parvalbumin and calbindin cells. Parvalbumin cells in the ventral nucleus project to a central core of auditory cortex with densest parvalbumin immunoreactivity. Those in anterodorsal and posterodorsal nuclei project to surrounding auditory fields with less dense parvalbumin immunoreactivity; those in the magnocellular nucleus project widely to auditory and other fields. Injections of middle cortical layers label a large majority of parvalbumin cells in the ventral, anterodorsal, or posterodorsal nuclei and in the magnocellular nucleus. Superficial deposits label calbindin cells only, usually in more than one nucleus, implying a widespread projection system.

Animals↗

Patchy and laminar terminations of medial geniculate axons in monkey auditory cortex.

The object of this study was to identify the terminal distributions of thalamocortical axons arising in chemically characterized subdivisions of the medial geniculate complex. Large injections of wheat germ agglutinin-conjugated horseradish peroxidase or small injections of Phaseolus vulgaris leucoagglutinin were made in the medial geniculate complex of Macaca fuscata. The terminal distributions of labeled axons in the cortex were correlated with auditory cortical fields demonstrable by different intensities of immunoreactivity for parvalbumin. Fibers from the ventral nucleus terminated mainly in layer IV and deep portion of layer III (IIIB), with additional terminations in layers I-IIIA and in layer VI. In layers IIIB-IV, a major terminal plexus was formed by a small number of dense patches, 300-500 microns in diameter, surrounded by smaller satellite patches. The patches conformed to a similarly lobulated pattern of parvalbumin fiber immunoreactivity. Terminations of some individually labeled thalamocortical fibers were restricted to a single patch, whereas others innervated more than one patch by collateral branches. Fibers from the dorsal nuclei ending in areas of less dense parvalbumin immunoreactivity surrounding the primary auditory cortex formed much larger terminal patches centered largely in layer IIIB. Fibers from the magnocellular nucleus had relatively few terminal branches but innervated extremely wide areas by collaterals of single axons. Two types of axons arose from the magnocellular nucleus, one terminating preferentially in middle cortical layers and the other exclusively in layer I. These may arise respectively from parvalbumin- and calbindin-immunoreactive cell populations in the magnocellular nucleus.

Animals↗

Synaptic distribution of afferents from reticular nucleus in ventroposterior nucleus of cat thalamus.

This study was aimed at determining the synaptic circuitry that contributes to the alterations in thalamic function that accompany changes in behavioral states. The somatosensory sector of the thalamic reticular nucleus (RTN) was identified by microelectrode recording in cats and injected with Phaseolus vulgaris-leucoagglutinin (PHA-L). The axons of labeled RTN cells gave rise to collaterals within the RTN and continued into the dorsal thalamus where they terminated predominately in the ventral posterior lateral nucleus (VPL). After small injections in the upper limb representation of RTN, most labeled terminations in VPL were confined to its medial part, suggesting the presence of a topographic organization in the projection. Terminations were concentrated in localized, focal aggregations of boutons. Combined electron microscopic immunocytochemistry, using immunogold labeling for gamma-aminobutyric acid (GABA), showed that the PHA-L labeled boutons were GABA-positive terminals that ended in symmetrical synapses. Eighty-two percent of these synapses were on dendrites of relay neurons, 8.5% on dendrites of interneurons, and 9.3% on somata. The terminals of RTN axons form the majority of axon terminals ending in symmetrical synapses in VPL. Their concentration on relay neurons probably underlies the capacity of the RTN projection to reduce background activity of VPL relay neurons in the awake state and to maintain oscillatory behavior of these neurons in drowsiness and early phases of sleep.

Animals↗

Expression patterns and deprivation effects on GABAA receptor subunit and GAD mRNAs in monkey lateral geniculate nucleus.

The expression and regulation of seven GABAA receptor subunit gene transcripts were examined in the adult monkey lateral geniculate nucleus. In situ hybridization histochemistry was used to localize mRNAs of the genes encoding monkey-specific alpha 1, alpha 2, alpha 4, alpha 5, beta 1, beta 2, and gamma 2 subunits. The highest levels of expression in the nucleus were for alpha 1, beta 2, and gamma 2 subunit transcripts. The levels were substantially higher in the magnocellular than in the parvocellular layers. Alpha-2, alpha 4, alpha 5, and beta 1 subunit mRNAs were expressed at much lower levels, and magno- and parvocellular layers had approximately equal levels of expression. Following 4- or 21-day periods of monocular deprivation induced by intravitreal injections of tetrodotoxin, levels of the alpha 1, alpha 2, alpha 4, alpha 5, beta 1, and beta 2 mRNAs were decreased in the deprived geniculate laminae. Adjacent sections hybridized with probes specific for 67-kDa glutamic acid decarboxylase (GAD) mRNA also showed decreased levels of expression in deprived laminae after the 21-day deprivation period. Levels of gamma 2 receptor subunit mRNA were unaffected by monocular deprivation. In our previous studies, a clearly significant downregulation is observed for this subunit transcript in the visual cortex of monkeys deprived for equivalent times. The differential expression and responses to deprivation in the lateral geniculate nucleus suggest region-specific regulation of GABAA receptor subunit genes.

Animals↗

Distribution of four types of synapse on physiologically identified relay neurons in the ventral posterior thalamic nucleus of the cat.

This study was aimed at providing quantitative data on the thalamic circuitry that underlies the central processing of somatosensory information. Four physiologically identified thalamocortical relay neurons in the ventral posterior lateral nucleus (VPL) of the cat thalamus were injected with horseradish peroxidase and subjected to quantitative electron microscopy after pre- or postembedding immunostaining for gamma-aminobutyric acid to reveal synaptic terminals of thalamic inhibitory neurons. The four cells all had rapidly adapting responses to light mechanical stimuli applied to their receptive fields, which were situated on hairy or glabrous skin or related to a joint. Their dendritic architecture was typical of cells previously described as type I relay cells in VPL, and they lacked dendritic appendages. Terminals ending in synapses on the injected cells were categorized as RL (ascending afferent), F (inhibitory), PSD (presynaptic dendrite), and RS (mainly corticothalamic) types and were quantified in reconstructions of serial thin sections. RL and F terminals formed the majority of the synapses on proximal dendrites (approximately 50% each). The number of synapses formed by RL terminals declined on intermediate dendrites, but those formed by F terminals remained relatively high, declining to moderate levels (20-30%) on distal dendrites. RS terminals formed moderate numbers of the synapses on intermediate dendrites and the majority (> 60%) of the synapses on distal dendrites. Synapses formed by PSDs were concentrated on intermediate dendrites and were few in number (approximately 6%). They formed synaptic triads with F terminals and rarely with RL terminals. On somata, only a few synapses were found, all made by F terminals. The total number of synapses per cell was calculated to be 5,584-8,797, with a density of 0.6-0.9 per micrometer of dendritic length. Of the total, RL terminals constituted approximately 15%, F terminals approximately 35%, PSD terminals approximately 5%, and RS terminals approximately 50%. These results provide the first quantitative assessment of the synaptic architecture of thalamic somatic sensory relay neurons and show the basic organizational pattern exhibited by representatives of the physiological type of relay neurons most commonly encountered in the VPL nucleus.

Animals↗

Gene expression for glutamic acid decarboxylase is reduced without loss of neurons in prefrontal cortex of schizophrenics.

BACKGROUND: Up-regulation of gamma-aminobutyric acidA (GABAA) receptors and decreased GABA uptake in the cerebral cortex of schizophrenics suggest altered GABAergic transmission, which could be caused by primary disturbance of GABA synapses or by decreased production of the transmitter. Decreased production could be due to a shutdown in GABA production or to loss of GABA neurons caused by cell death or their failure to migrate to the cortex during brain development. METHODS: To discriminate between these possibilities, we quantified levels of messenger RNA (mRNA) for the 67-kd isoform of glutamic acid decarboxylase (GAD), the key enzyme in GABA synthesis, and the number and laminar distribution of GAD mRNA--expressing neurons in the dorsolateral prefrontal cortex (DLPFC) of schizophrenics and matched controls, using in situ hybridization-histochemistry, densitometry, and cell-counting methods. These data were compared with the total number of neurons, the number of small, round or ovoid neurons 8 to 15 microns in diameter, and overall frontal lobe volume. As a control, mRNA levels for type II calcium-calmodulin-dependent protein kinase (CamIIK) were quantified. RESULTS: Schizophrenics showed a pronounced decrease in GAD mRNA levels in neurons of layer I (40%) and layer II (48%) and an overall 30% decrease in layers III to VI. There were also strong overall reductions in GAD mRNA levels. The CamIIK mRNA levels showed no significant differences between samples. No differences were found in the total number of neurons nor in small, round or ovoid neurons, which should include a majority of the GABA cells. Prefrontal gray and white matter volume did not differ significantly between controls and schizophrenics. CONCLUSIONS: The prefrontal cortex of schizophrenics shows reduced expression for GAD in the absence of significant cell loss. This may be brought about by an activity-dependent down-regulation associated with the functional hypoactivity of the DLPFC. The lack of significant alterations in cell numbers in the DLPFC and frontal lobe volume in schizophrenics also implies that overall cortical neuronal migration had not been compromised in development. Previous reports of altered neuronal distribution in the subcortical white matter of schizophrenic brains in comparison with that of controls may indicate disturbances of migration or programmed cell death in the cortical subplate, leading to altered connection formation in the overlying cortex of schizophrenics and activity-dependent down-regulation of neurotransmitter-related gene expression.

Adult↗

Cortical development and neuropathology in schizophrenia.

Epidemiological studies suggest that perturbations occurring during pregnancy can increase the incidence of schizophrenia among offspring. Examination of the neuropathology of the brains of some schizophrenics suggests that a defect in the later phases of cerebral cortical development, notably the last phases of neuronal migration and the establishment and refinement of patterns of cortical connections, may be involved. Most of these studies are conjectural, and the relationship between primary lesions and potential secondary retrograde and anterograde effects in the circuitry linking the prefrontal cortex, basal forebrain, mediodorsal thalamus and medial temporal cortex is unknown. Our hypothesis, based on neuromorphological and gene expression studies, is that a disturbance of migration or in the pattern of preprogrammed cell death in the subplate zone of the developing cerebral cortex causes a failure to establish normal patterns of connections in the overlying cortex. This compromised circuitry subsequently decompensates, leading to schizophrenic symptoms and activity-dependent manifestations of altered gene expression for neurotransmitter- and receptor-related molecules.

Cerebral Cortex↗

Decreased expression of the alpha subunit of Ca2+/ calmodulin-dependent protein kinase type II mRNA in the adult rat CNS following recurrent limbic seizures.

Calcium/calmodulin-dependent protein kinase type II (CamKII) is a ubiquitous brain enzyme implicated in a wide variety of neuronal processes. Understanding CamKII has become increasingly complicated with the recent identification of multiple gene transcripts coding for separate subunits. Previous studies have shown that mRNA for the alpha subunit of CamKII can be increased by reduction of afferent input. In this study we have examined the regulation of alpha CamKII mRNA following increased activity due to seizures. Using in situ hybridization with a cRNA probe against the rat alpha CamKII sequence we found reduced levels of hybridization following limbic seizures induced by lesions of the hilus of the dentate gyrus. Hybridization was most dramatically reduced in the granule cells of the dentate gyrus and the pyramidal cells of hippocampal region CA1. There were also significant reductions in hybridization in the superficial layers of neocortex and piriform cortex. In each of these region hybridization was decreased in the molecular layers which is consistent with the reported dendritic localization of alpha CamKII mRNA. All changes in mRNA content were transient, with maximal reductions at 24 h following lesion placement and a return to control levels by 96 h. These findings demonstrate the negative regulation of alpha CamKII mRNA by seizure activity and raise the possibility that synthesis of this kinase may be regulated by normal physiological activity.

Animals↗

Developmental and regional expression pattern of a novel NMDA receptor-like subunit (NMDAR-L) in the rodent brain.

A novel NMDA receptor-like (NMDAR-L) cDNA was isolated that contained an open reading frame coding for a predicted polypeptide of 1115 amino acids that shares approximately 27% identity with NMDA receptor subunits. In situ hybridization experiments indicated that NMDAR-L mRNA was expressed in the developing rodent CNS. On postnatal day 1 (P1), NMDAR-L mRNA expression was pronounced in the entorhinal cortex, the subiculum and the thalamus, in layer V of the developing neocortex, in the superior and inferior colliculi, and various regions of the hindbrain, excluding the cerebellum. On P5, NMDAR-L mRNA was expressed in layer V of the neocortex, in the entorhinal cortex, in the subiculum, and in the thalamus. On P14, NMDAR-L mRNA was expressed in layers II-VI of the neocortex, in the entorhinal and piriform cortex, in the subiculum and CA1 field, and in the nucleus of the lateral olfactory tract. In the adult brain, NMDAR-L mRNA was detected predominately in the nucleus of the lateral olfactory tract. Injection of NMDAR-L cRNA into Xenopus oocytes did not lead to the expression of homomeric glutamate-activated channels. However, coinjection of the triple combination of NMDAR-L with NMDAR1 and NMDAR2B cRNAs led to a striking decrease in the current magnitude compared to currents obtained after coexpression of the double combination of NMDAR1 with NMDAR2B. While the function of NMDAR-L remains to be established, its developmental and regional expression pattern suggests that NMDAR-L may influence axonal outgrowth and synaptogenesis during brain development.

Aging↗

Extent of intracortical arborization of thalamocortical axons as a determinant of representational plasticity in monkey somatic sensory cortex.

The extent of intracortical arborization of individual thalamocortical axons in area 3b of the somatic sensory cortex and the degree of overlap in the cortical projections of relay cells in the ventral posterior nucleus of the thalamus were examined in macaque monkeys. Paired intracortical deposits of Fast blue (FB) and Diamidino yellow (DY) separated by 100-1500 microns were made by inserting crystals of dye into the tracks of tungsten microelectrodes used to record receptive field data on area 3b cells. Each injection gave retrograde labeling of one or more clusters of cells extending in elongated anteroposterior arrays through the ventral posterior medial (VPM) or ventral posterior lateral (VPL) nucleus. Double-labeled cells were only found when the distance between the centers of the dye deposits was less than 600 microns. With interdeposit distances greater than 600 microns, most clusters of retrogradely labeled cells had a majority of cells labeled by FB or DY. However, even with interdeposit distances of 1-1.5 mm the labeled clusters also contained significant numbers of cells labeled with the other dye. These results and an accompanying regression analysis indicate that the extent of intracortical arborization of single thalamocortical axons in area 3b is no greater than 600 microns. However, adjoining cells in the same part of the thalamic body representation can project to cortical targets as discrepant as 1.5 mm. It is proposed that the fine grain of the cortical representation depends upon inputs from the majority population of each thalamic cell cluster.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗