PubMed · 1013346
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W Storm van Leeuwen. 1976. EEG and behavior.. https://doi.org/10.1016/s0079-6123(08)61000-6
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The objective of this study was to identify cortical areas that project to the lateral nucleus of the macaque monkey amygdaloid complex. Discrete injections of the fluorescent retrograde tracers Fast blue and Diamidino yellow were placed into different locations within the lateral nucleus. Retrogradely labeled cells were mapped using a computer-aided digitizing system. In the frontal cortex, low numbers of retrogradely labeled cells were observed in medial and orbitofrontal regions (areas 10, 11, 12, 13, 13a, and 14). In the anterior cingulate cortex, low to moderate numbers of retrogradely labeled cells were located in areas 25, 24, and 32. In the insula, there were moderate to high numbers of retrogradely labeled cells in agranular and dysgranular regions. The parainsula cortex also demonstrated a moderate to high number of retrogradely labeled cells. In the temporal lobe, retrogradely labeled cells were most numerous in the rostral (polar) portion of the perirhinal cortex. Large numbers of labeled cells were also located throughout more caudal portions of the perirhinal regions as well as in the entorhinal cortex, area TE, and the superior temporal gyrus. Fewer retrogradely labeled cells were observed in the cortex along the dorsal bank of the superior temporal sulcus, in the parahippocampal cortex, and in area TEO. Although retrograde tracers can provide only limited evidence for topography, we nonetheless noted that the density of retrogradely labeled cells in a cortical area reliably depended on the location of the tracer injection in the lateral nucleus.
Exposure to stressful or fear-inducing environmental stimuli activates descending antinociceptive systems resulting in a decreased pain response to peripheral noxious stimuli. Stimulating mu opioid receptors in the basolateral nucleus of the amygdala (BLA) in anesthetized rats produces antinociception that is similar to environmentally induced antinociception in awake rats. Recent evidence suggests that both forms of antinociception are mediated via projections from the amygdala to the ventral periaqueductal gray (PAG). In the present study, we examined the types of neurochemicals released in the ventral PAG that may be important in the expression of antinociception produced by amygdala stimulation in anesthetized rats. Microinjection of a mu opioid receptor agonist into the BLA resulted in a time dependent increase in tail flick latency that was attenuated by preadministration of a mu opioid receptor or a neurotensin receptor antagonist into the ventral PAG. Microinjection of a delta(2) opioid receptor antagonist or an NMDA receptor antagonist into the ventral PAG was ineffective. These findings suggest that amygdala stimulation produces antinociception that is mediated in part by opioid and neurotensin release within the ventral PAG.
The excitatory amino acid glutamate has been implicated in the neurodegeneration associated with several different central nervous system diseases. Treatment with kainic acid (KA), a glutamate analog known to activate the AMPA/KA subtype of glutamate receptor, has been widely used as a model of epilepsy. Long term temporal studies of its neuropathological effects, however, are lacking. In this study, two techniques were used to directly visualize and characterize the neuropathology that occurred over a 2-month period following KA-induced status epilepticus in adult female Sprague-Dawley rats. Post-injection survival was 2, 4, 8 h, 2 days, 2 weeks, or 2 months. Labeling with Fluoro-Jade B (FJB), a fluorescent green dye that labels the cell body, dendrites, axons and axon terminals of degenerating neurons, was observed within the cortex, hippocampus, thalamus, basal ganglia, and amygdala by 4 h post-treatment. The highest level of labeling was seen in the piriform cortex, hippocampus, and thalamus. Myelin changes in the rat forebrain following KA treatment were also examined using the myelin-specific Black-Gold (BG) stain. Varicose myelinated fibers were observed in the same regions as FJB positive neurons, although these changes were evident by the 2-h survival time-point. Both stains showed a temporal progression of brain damage throughout the affected areas. By 2 months post-treatment, few degenerating neurons could be detected and abnormal myelin was absent in most regions. As myelin changes can be seen prior to neuronal degeneration, and oligodendrocytes express functional AMPA/kainate-type glutamate receptors, the neurodegeneration and myelin pathologies may occur as independent events. Thus, researchers should consider the temporal and multiple effects of kainic acid to optimize conditions for their endpoint of interest when designing experiments.