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Results for “Olfactory Cortex”

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PubMed1986

Desensitization to glutamate and aspartate in rat olfactory (prepyriform) cortex slice.

Olfactory cortex brain slices were subject to multiple bath applications of either glutamate or aspartate. The effectiveness of these amino acids (measured by quantitating the amplitude of lateral olfactory tract-stimulated field potentials) was progressively reduced with each successive perfusion of the agonist. However, the effectiveness of the endogenous neurotransmitter recovered to control in each intervening wash period. Thus, repeated applications of glutamate or aspartate desensitized olfactory cortex receptors to these amino acids but did not desensitize the receptors to the endogenous transmitter. These data support the hypothesis that neither glutamate nor aspartate is the neurotransmitter released from the lateral olfactory tract onto pyramidal cells of the olfactory cortex.

Animals↗
PubMedDate not supplied

Trimethyltin induced pathology in sensory neurons.

Pathologic changes in the retina, inner ear, pyriform cortex, olfactory tubercle, and dorsal root ganglia as a result of trimethyltin (TMT) intoxication were investigated. Long-Evans rats were orally intubated with TMT chloride at a dose of 6.0 mg TMT/kg b.w. Swelling of the optic fiber layer and necrotic changes in the ganglion and inner nuclear layers were observed in the retina as early as 72 hours after intoxication. Large segments of the retina were devoid of ganglion cells at later posttreatment times. The inner ear was also found to be extremely vulnerable to the toxicity of TMT. Edematous swelling of the hair cells and vacuolar changes of the spiral ganglion cells in the Organ of Corti were observed 24 hours after TMT exposure. Extensive destruction of these structures was evident 15-30 days after intoxication. Small neurons in the olfactory cortex (pyriform cortex and olfactory tubercle) also degenerated rapidly after TMT exposure. Electron microscopy demonstrated lysosomal accumulation and vacuolar changes in these nerve cells. Extensive destruction of both the pyriform cortex and olfactory cortex was observed 15 days after exposure. Although no necrotic change was observed in the neurons of the dorsal root ganglia, electron microscopy revealed extensive accumulation of lysosomes and formation of myeloid bodies both in the neuronal bodies and dorsal root fibers. Vacuolar breakdown and dissolution of the Nissl substance were found in some neurons. Thirty days after treatment, hypertrophy and hyperplasia of the neuronal mitochondria were observed. Such a change was believed to represent a compensatory response by these organelles. These findings provide the first morphological evidence of neuronal damage in the sensory neurons of both the central and peripheral nervous system following acute TMT administration.

Animals↗
PubMed1980

Thalamocortical mechanisms in odor-guided behavior. I. Effects of lesions of the mediodorsal thalamic nucleus and frontal cortex on olfactory discrimination in the rat.

The "core" subnucleus of the mediodorsal thalamic nucleus (MD) receives direct input from olfactory cortex in the rat. This part of MD projects to the frontal neocortex of the rhinal sulcus (RS), while other parts of the MD project to the anterior medial wall of the neocortex (MW). In this study, rats were tested on odor threshold, detection of specific odors, and three odor discriminations both before and after lesions of MD, MW, RS, or sham lesions. Olfactory threshold and detection ability remained unaffected by any of these lesions; however, subjects with MD and RS lesions were markedly impaired on odor discriminations. Furthermore, subjects were more profoundly impaired when the stimuli to be discriminated were novel or difficult to associate. Thus, MD and its "olfactory" projection target, RS, seem to mediate cognitive, rather than sensory aspects of odor-guided behavior in the rat.

Animals↗
PubMed1988

DSP4, a noradrenergic neurotoxin, impairs male rats' attraction to conspecific odors.

Olfactory investigation was examined in male Sprague-Dawley rats injected with 50 mg/kg of the noradrenergic neurotoxin, DSP4, 10 days before testing. In a two-choice preference test, the odor of pine shavings from the nest of a female and her litter attracted sexually experienced control males, but not drug-treated males. Further, odors from anesthetized females increased the mean number of entries made by control males, but not drug-treated males, into a cage containing pups' nest shavings. Combining a novel odor with nest shavings significantly reduced the number of entries made by both groups of males. Drug treatment decreased norepinephrine (NE) levels by 66, 62, and 68% in the olfactory cortex, olfactory bulb, and frontal cortex, respectively. Dopamine concentrations were not significantly affected. NE concentrations in the heart, and serotonin levels in the olfactory bulb, were moderately depleted (by 37 and 40%, respectively). The results support the view that central NE modulates systems regulating attraction to conspecific odors in male rats.

Adrenergic Fibers↗
PubMed1993

Effect of the non-NMDA receptor antagonist, 2,3-dihydro-6-nitro-7-sulfamoylbenzo(f)quinoxaline, on local cerebral glucose uptake in the limbic forebrain.

The present investigation examined the effect of in vivo antagonism of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor by 2,3-dihydro-6-nitro-7-sulfamoyl-benzo(f)quinoxaline (NBQX) on local cerebral glucose utilization (LCGU) using the quantitative autoradiographic 2-deoxy[14C]-glucose method in conscious rats. NBQX, at doses of 10, 30, and 60 mg/kg i.p. or three injections of 30 mg/kg i.p., did not increase LCGU in limbic areas such as the primary olfactory cortex, olfactory tubercle, hippocampus, dentate gyrus, posterior cingulate cortex, mamillary body, caudate nucleus, anterior thalamic nucleus, and nucleus accumbens. NBQX, at doses of > or = 60 mg/kg i.p., decreased LCGU in these brain areas. These data demonstrate that in vivo antagonism of the AMPA receptors by NBQX produces a pattern of alterations in metabolic activity, different from that produced by noncompetitive antagonists of the N-methyl-D-aspartate (NMDA) receptor, e.g., phencyclidine and MK-801. Combined with a lack of "phencyclidine-like" behavior produced by NBQX, these data suggest that antagonism of the AMPA receptor represents a novel mechanism to block excitatory amino acids in the CNS, which may be devoid of unwanted behavioral side effects associated with noncompetitive antagonism of the NMDA receptor.

Animals↗