The Journal of comparative neurology
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Protein kinase C (PCK) is a family of isoforms that are implicated in subcellular signal transduction. The authors investigated the distribution of several PKC isoforms (PKC-alpha, PKC-beta, PKC-gamma, PKC-delta, and PKC-epsilon) within major cerebellar cell types as well as cerebellar projection target neurons, including Purkinje neurons, cerebellar nuclear neurons, and secondary vestibular neurons. PKC-alpha, PKC-beta, PKC-gamma, PKC-delta, and PKC-epsilon are found within the cerebellum. ⋯ PKC-gamma-immunolabeled axons terminated in all of the cerebellar nuclei as well as in the lateral and superior vestibular nuclei and the MVN, DVN, Psol, and NPH. The projection patterns of PKC-immunolabeled Purkinje cells were confirmed by lesion-depletion studies in which unilateral uvula-nodular lesions caused depletion of PKC-immunolabeled terminals ipsilateral to the lesion in the vestibular complex. These data identify circuitry that is unique to cerebellar-vestibular interactions.
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To understand the organization of inhibitory circuitries in the rat amygdala, the distribution of parvalbumin, calretinin, and calbindin immunoreactivity was investigated in the rat amygdaloid complex. Colocalization of various calcium-binding proteins with the inhibitory transmitter gamma-aminobutyric acid (GABA) was studied by using the mirror technique. Parvalbumin-immunoreactive (-ir) elements were located mostly in the deep amygdaloid nuclei, whereas the calretinin-ir and calbindin-ir staining were most intense in the cortical nuclei as well as in the central nucleus and the amygdalohippocampal area. ⋯ A high density of large GABA-negative calbindin-ir neurons was observed caudally in the medial division of the lateral nucleus and GABA-negative calretinin-ir neurons were observed in the magnocellular division of the accessory basal nucleus as well as in the intermediate and parvicellular divisions of the basal nucleus. These data suggest that in various amygdaloid areas, neuronal excitability is controlled by GABAergic neurons that contain different calcium-binding proteins. The appearance of basket-like plexus and cartridges in the parvalbumin preparations, but not in calretinin preparations, suggests that like in the hippocampus, the distribution of inhibitory terminals in the dendritic and perisomatic regions of postsynaptic neurons in the rat amygdala is organized in a topographic manner.
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Studies utilizing the expression of Fos protein as a marker of neuronal activation have revealed that pain of deep somatic or visceral origin selectively activates the ventrolateral periaqueductal gray (vlPAG). Previous anatomical tracing studies revealed that spinal afferents to the vlPAG arose from the superficial and deep dorsal horn and nucleus of the dorsolateral funiculus at all spinal segmental levels, with approximately 50% of vlPAG-projecting spinal neurons found within the upper cervical spinal cord. This study utilized detection of Fos protein to determine the specific populations of vlPAG-projecting spinal neurons activated by noxious deep somatic or noxious visceral stimulation. ⋯ In a second set of experiments, the combination of retrograde tracing and Fos immunohistochemistry revealed that vlPAG-projecting spinal neurons activated by deep somatic pain were located in both the upper cervical and lumbosacral cord, whereas those activated by visceral pain were restricted to the thoracic spinal cord. Thus pain arising from visceral versus deep somatic body regions influences neural activity within the vlPAG via distinct spinal pathways. The findings also highlight the potential significance of the upper cervical cord in integrating pain arising from deep structures throughout the body.
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Recent studies have described sex differences in the relative size of the hippocampus that are associated with sex differences in space use in birds and short-lived mammals. A correlation between spatial learning and increased hippocampal volume has also been demonstrated in food-caching animals. Such results suggest that sexually dimorphic spatial learning (sex differences in space use during the breeding season) and seasonal variations in food-caching behavior (spatial memory for cache locations) might correlate with morphological changes in the hippocampus of adult long-lived mammals. ⋯ There were no sex differences or seasonal variations in the relative volume or the number of neurons of any other layer of the structures forming the hippocampal complex. These results confirm the existence of sex differences in the structure of the hippocampus; however, this sexual dimorphism does not vary seasonally in adulthood and is likely to result from developmental processes. These results do not support the hypothesis that seasonal variations in food-caching behavior might correlate with morphological changes, such as variations in volume or neuron number, in the hippocampal complex of adult long-lived mammals.
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Vincristine, along with other antimitotic chemotherapeutic drugs, produces a peripheral neuropathy in humans that is accompanied by painful paresthesias, dysesthesias, and occasionally hypoesthesia, and by hyporeflexia (Holland et al. [1973] Cancer Res. 33:1258-1264; McLeod and Penny [1969] J Neurol Neurosurg Psychiatry 32:297-304; Postma et al. [1993] J Neurooncol. 15:23-27; Sandler et al. [1969] Neurology 19:367-374). Systemic administration of vincristine causes swelling of unmyelinated axons and disorientation of axonal microtubules (Tanner et al. [1998a1998a] J Comp Neurol. 395:481-492) at a time when it also produces allodynia and mechanical hyperalgesia (Aley et al. [1996] Neuroscience 73:259-265; Authier et al. [1999] Neuroreport 10:965-968) and enhanced responsiveness in C-fibers in the rat (Tanner et al. [1998b] J Neurosci. 18:6480-6491). Because slowing of A-fiber conduction velocities had also been demonstrated (Tanner et al. [1998b] J Neurosci. 18:6480-6491), and mechanical hyperalgesia can occur secondary to damage to large diameter sensory afferents (Basbaum et al. [1991] Can J Physiol Pharmacol. 69:647-651; Coggeshall et al. [1993] Pain 52:233-242; Woolf and Mannion [1999] Lancet 353:1959-1964), we sought to determine whether vincristine also induced ultrastructural changes in myelinated A-fibers. ⋯ Vincristine induced swelling of the whole nerve and an increase in the cross-sectional areas of myelinated axons but no loss of myelinated axons. There was a significant decrease in axonal microtubules, as well as microtubule disorganization, in myelinated fibers from vincristine-treated rats. In the spinal ganglion, vincristine induced swelling of large diameter sensory neurons and a build-up of neurofilaments in the cell bodies and proximal axons, suggestive of impaired anterograde axonal transport.