Neuroscience
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Although transected central nervous system axons fail to regrow after injuries in adult mammals, they send sprouts into the scar tissue that forms at the lesion. We have investigated the relation between scar cells, laminin-like immunoreactivity and cut spinal axons in two previously characterized spinal cord lesion types. Labeling with antisera to glial fibrillary acidic protein and laminin demonstrated that the scar tissue formed after lesions in the rat and cat dorsal and ventral funiculi showed prominent gliosis and strong laminin-like immunoreactivity four days to one year postlesion. ⋯ Very few cells adhered to the spinal cord section except for the part where the scar tissue had formed, where numerous cells were attached. The PC12 cells that had adhered to the scar tissue were mainly seen in parts of the scar that showed laminin-like immunoreactivity and their neurites predominantly followed tissue showing laminin-like immunoreactivity. The close association between axonal sprouts and laminin-like immunoreactivity indicates a role for laminin in axonal growth and/or guidance in the injured spinal cord.
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Nasal and temporal retinal ganglion cells projecting to the midbrain: implications for "blindsight".
We placed pellets of horseradish peroxidase in the superior colliculus of four macaque monkeys and retrogradely labelled the retinal ganglion cells of both eyes. The ratio of labelled cells in the contralateral nasal retina and the ipsilateral temporal retina was no different from the ratio found after implants in the optic nerve, which label the entire afferent pathway. Our finding therefore invalidates the proposal that prominent differences in the properties of "blindsight" in monocular nasal and temporal visual fields arise from differences in the projection from the nasal and temporal retina to the midbrain. ⋯ At eccentricities of 3-7 mm there was a consistent and prominent difference between beta and gamma cells. The results show that at intermediate eccentricities even ganglion cells whose distal dendrites are too poorly labelled to reveal their morphological class can never the less be categorized as alpha, beta or gamma by using a combination of soma size and number of primary dendrites. This is particularly useful when attempting to classify retinal ganglion cells following microinjections into selected target nuclei of optic axons.
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A variety of metabotropic excitatory amino acid receptors are present in the thalamus. We have investigated the possibility that some of these receptors may have presynaptic effects on GABAergic inhibitory transmission in the thalamus. Inhibitory responses in ventrobasal thalamic neurons of urethane-anaesthetized rats were evoked by either air-jet stimuli to the vibrissae or by electrical stimulation of the somatosensory cortex. ⋯ As the inhibitory responses arise from the neurons of the nucleus reticularis thalami, some distance away from the site of recording and iontophoretic drug application, it is likely that the reduction of inhibition seen with L-AP4 and CCG1 is due to an action of these agonists on the terminals or axons of these inhibitory neurons. The novel antagonists of L-AP4 and CCG1, alpha-methyl-L-AP4 and alpha-methyl-CCG1, were found to block the disinhibitory actions of the agonists in a differential manner when applied iontophoretically. This suggests that there may be at least two types of receptor mediating the disinhibitory effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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In Huntington's disease striatal neurons undergo marked changes in dendritic morphology and coincidently exhibit an increase in immunoreactive calbindin D28k (calbindin), a cytosolic calcium-binding protein which is highly abundant in these neurons. Previous studies in the rat striatum have shown that excitotoxic injury, which is linked to a rise in intracellular Ca2+, mimics many of the neurochemical and neuropathological characteristics of Huntington's disease. We speculated, therefore, that the apparent increase in calbindin labeling in Huntington's disease spiny neurons may signal the response to an excitotoxic process. ⋯ This effect was blocked by the selective NMDA receptor blocker (+/-)-2-amino-5-phosphonopentanoic acid (AP-5), indicating that an NMDA receptor-mediated mechanism contributed to the change in staining pattern. Results in rats suggest that the subcellular redistribution of calbindin immunoreactivity observed in Huntington's disease spiny neurons may be related to an NMDA receptor-induced excitotoxic process. An increased availability of calbindin protein at dendrites and spines may reflect a greater demand for Ca2+ buffering precipitated by an abnormal rise in in intracellular Ca2+.
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The anterior pretectal nucleus has recently been implicated in the descending modulation of nociception. Electrical stimulation of the nucleus was found to reduce the nociceptive responses of deep dorsal horn neurons and to inhibit spinally integrated withdrawal reflexes. It is believed that at least part of the descending inhibitory effects of the anterior pretectal nucleus are mediated by reticulospinal cells of the ventrolateral medulla. ⋯ The existence of direct projections to the ventral medulla and pons correlates well with physiological data which showed that the descending, antinociceptive effects of the anterior pretectal nucleus are relayed via the rostral ventrolateral medulla. The data are also in keeping with pharmacological studies that suggested the role of catecholaminergic cells in the mediation of these descending effects. It is proposed that the rostral ventral medullary projections provide a path through which antinociceptive effects of the anterior pretectal nucleus are mediated to the spinal cord.