Biomedical subjects

K M Carnes

Publications and source records attributed to K M Carnes.

7 recordsLinked to original sources

PubMed1994

Colocalization of excitatory and inhibitory neurotransmitter markers in striatal projection neurons in the rat.

The principle neuronal output of the neostriatum comes from medium spiny neurons that project from the caudate/putamen to the globus pallidus and substantia nigra. Although current evidence generally indicates that gamma-aminobutyric acid (GABA) is the principal neurotransmitter in this pathway, this cannot account for the excitatory synaptic activity present among cultures of striatal neurons or the short latency excitatory postsynaptic potentials which often proceed or obscure inhibitory activity evoked by striatal stimulation. In this study, retrograde transport of [3H]D-aspartate has been used to demonstrate striato-pallidal and striato-nigral neurons that possess a high-affinity uptake system for glutamate and aspartate and are therefore putatively glutamatergic. Injections of [3H]D-aspartate into the globus pallidus or substantia nigra, pars reticularis of the rat retrogradely labeled medium-sized neurons throughout the rostral-caudal extent of the neostriatum. To characterize this population further, adjacent sections were immunoreacted with antibodies to either GABA, glutamic acid decarboxylase (GAD), calbindin, or parvalbumin prior to autoradiographic processing. Under these conditions, autoradiographically labeled neurons displayed positive immunoreactivity for GABA, GAD, or calbindin. Autoradiographic label did not colocalize with parvalbumin immunoreactivity. The colocalization of anatomical markers of GABAergic and glutamatergic neurotransmission raises the possibility that both neurotransmitters are functionally expressed within single striatal projection neurons.

Animals↗

PubMed1990

Sources of presumptive glutamatergic/aspartatergic afferents to the magnocellular basal forebrain in the rat.

The distribution of presumptive glutamatergic and/or aspartatergic neurons retrogradely labeled following injections of [3H]-D-aspartate into the magnocellular basal forebrain of the rat was compared with the distribution of neurons labeled by comparable injections of the nonspecific retrograde axonal tracer wheat germ agglutinin conjugated to horseradish peroxidase. Cells retrogradely labeled by wheat germ agglutinin-horseradish peroxidase were found in a wide range of limbic and limbic-related structures in the forebrain and brainstem. In the telencephalon, labeled neurons were seen in the orbital, medial prefrontal, and agranular insular cortical areas, the amygdaloid complex, and the hippocampal formation. Labeled cells were also seen in the olfactory cortex, the lateral septum, the ventral striatopallidal region, and the magnocellular basal forebrain itself. In the diencephalon, neurons were labeled in the midline nuclear complex of the thalamus, the lateral habenular nucleus, and the hypothalamus. In the brainstem, labeled cells were found bilaterally in the ventral midbrain, the central gray, the reticular formation, the parabrachial nuclei, the raphe nuclei, the laterodorsal tegmental nucleus, and the locus coeruleus. A significant fraction of the afferents to the magnocellular basal forebrain appear to be glutamatergic and/or aspartatergic. Only a few of the regions labeled with wheat germ agglutinin-horseradish peroxidase were not also labeled with [3H]-D-aspartate in the comparable experiments. Most prominent among the non-glutamatergic/aspartatergic projections were those from fields CA1 and CA3 of the hippocampus, the hilus of the dentate gyrus, the dorsal subiculum, the tuberomammillary nucleus, and the ventral pallidum. In addition, most of the lateral hypothalamic and brainstem projections to the magnocellular basal forebrain were not significantly labeled with [3H]-D-aspartate. In addition to these inputs, a commissural projection from the region of the contralateral nucleus of the horizontal limb of the diagonal band was confirmed with both wheat germ agglutinin-horseradish peroxidase and the anterograde axonal tracer Phaseolus vulgaris leucoagglutinin. This projection did not label with [3H]-D-aspartate or [3H]-GABA, suggesting that it is not glutamatergic/aspartatergic or GABAergic. Furthermore, double labeling experiments with the fluorescent retrograde tracer True Blue and antibodies against choline acetyltransferase indicate that the projection is not cholinergic.

Afferent Pathways↗

PubMed1988

Arthrographic surface anatomy of the carpal triangular fibrocartilage complex.

In a review of 364 radiocarpal and 123 distal radioulnar joint arthrograms we identified 44 (12%) patients with contrast defects at either the proximal or distal surface of the carpal triangular fibrocartilage complex (TFCC). Differences in their arthrographic characteristics distinguished two separate groups of patients; one with similar and another with dissimilar appearing TFCC surface contrast collections. Thirty-one of our 44 patients had similar appearing, isolated radial-sided collections at either the proximal or distal TFCC surfaces. Our arthrographic, demographic, and historical study of these patients suggests that the collections are not caused by traumatic partial TFCC tears but represent a normal anatomic variant, probably a synovial recess at the radial TFCC attachment. Arthrography and dissection of a limited number of cadaveric specimens confirmed this conclusion. The second group included the remaining 13 patients. This group had contrast collections at either the proximal or distal TFCC surface, which varied in location and appearance. This smaller group is more likely to represent those uncommon patients with partial TFCC defects caused by tears.

Adolescent↗

PubMed1988

Prefrontal-limbic epilepsy: experimental functional anatomy.

Nonconvulsive seizures from prefrontal cortex in humans cause complex behavioral, motor, and autonomic manifestations. In order to gain insight into the possible anatomical basis of these phenomena, we have studied experimental seizures from medial and lateral prefrontal-limbic cortex and the amygdaloid complex in rat. Small injections of penicillin or electrical stimulation were used to induce seizures, and the [14C]deoxyglucose technique was employed to map pathways of seizure spread. Analysis of results indicates that prefrontal-limbic cortex and amygdala exhibit strong bilateral reciprocal interaction. Mild seizures from these different areas activated both unique and similar pathways and targets. With increasing strength of discharge from these areas, there was a convergence of the subcortical pattern of activation in medial and midline thalamic nuclei and bilateral substantia nigra. These studies suggest that complex epileptic phenomena in humans evoked from a prefrontal seizure focus relate to activation of cortical and subcortical functional limbic anatomy.

Amygdala↗

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

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↗

PubMedDate not supplied

Two methods of catecholamine depletion in kitten visual cortex yield different effects on plasticity.

As first clearly demonstrated by the experiments of Wiesel and Hubel, the developing visual cortex is exquisitely sensitive to sensory deprivation. Temporary closure of one eye of a kitten during a critical period that extends from 3 weeks to 3 months of age results in a dramatic cortical reorganization such that most neurones, originally binocularly driven, are dominated exclusively by the open eye. Recently, attention has been directed to chemical factors which may influence the degree of plasticity during the critical period. The work of Kasamatsu and pettigrew suggests that cortical catecholamines, especially noradrenaline (NA), are essential for the normal plastic response to visual deprivation. In an effort to clarify the role of NA in visual cortical plasticity, we have monocularly deprived kittens whose cortex had been depleted of catecholamines by the neurotoxin 6-hydroxydopamine (6-OHDA). We used two strategies to deplete cortical NA: the first, pioneered by Kasamatsu el al., utilized osmotic minipumps to deliver 6-OHDA to visual cortex; the second involved systemic neonatal injections of 6-OHDA, a technique which has proved effective in rodents. We found, using high-pressure liquid chromatography (HPLC), that both techniques produced a substantial reduction in the level of cortical NA. However, single unit recording in area 17 revealed that the plastic response to monocular deprivation (MD) was only diminished in the kittens depleted by minipump.

Animals↗