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Burton Slotnick

Publications and source records attributed to Burton Slotnick.

9 recordsLinked to original sources

Olfactory performance of rats after selective deafferentation of the olfactory bulb by 3-methyl indole.

Rats trained to detect propyl acetate and valeric acid and to discriminate between propyl acetate and amyl acetate and between valeric acid and butyric acid were injected with a low dose of 3-methyl indole, a treatment that produces well-defined and selective deafferentation of the olfactory bulbs. Treatment completely deafferented most but not all bulbar loci for aliphatic acids and at least disrupted those for propyl and amyl acetate. In posttreatment tests, experimental rats performed somewhat but not significantly more poorly than controls and about as well on the acid detection and discrimination tasks as on the corresponding acetate tests.

Acetates↗

Discrimination between the enantiomers of carvone and of terpinen-4-ol odorants in normal rats and those with lesions of the olfactory bulbs.

We assessed (1) whether the enantiomers of terpinen-4-ol, odorants that activate nearly identical areas of the olfactory bulb, are more difficult to discriminate than those of carvone, odorants that activate different areas of the olfactory bulb, and (2) whether olfactory bulb lesions that disrupt the pattern of bulbar activation produced by these enantiomers degraded the ability of rats to discriminate between them. In psychophysical tests, normal rats discriminated between the enantiomers of terpinen-4-ol and of carvone equally well. Surgical lesions that removed the majority of bulbar glomeruli activated by these odorants (as demonstrated in previous olfactory bulb studies using intrinsic optical imaging and 2-deoxyglucose) resulted in increased detection thresholds but few or no deficits in discriminating between suprathreshold concentrations of the enantiomers. These results fail to confirm predictions based on 2-deoxyglucose maps of bulbar activity that enantiomers of terpinen-4-ol should be more difficult to discriminate than those of carvone and that the ability to discriminate between enantiomers of an odorant are based on differences in patterns of bulbar activation revealed in such maps.

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Olfaction in olfactory bulbectomized rats.

Experimental rats had their right olfactory bulb removed on postnatal day 2 (P2) and their left olfactory bulb removed on P90. Control rats had one or both olfactory bulbs removed on P90. Before and after their adult-stage surgery, rats were trained using olfactometry and operant conditioning to detect and discriminate odors. Anterograde transport of horseradish peroxidase applied to the olfactory epithelium revealed numerous axons of olfactory sensory neurons in the right hemisphere of 27 experimental rats. These axons terminated in glomerular-like clusters within the frontal neocortex (n = 5) or anterior olfactory nucleus with some axons extending into the subventricular epithelium (n = 22). Seventeen of the experimental rats were able to detect a variety of odors and to discriminate between odors. Performance accuracy was related to the location and density of these anomalous inputs; experimental rats with inputs confined to frontal neocortex and those lacking any inputs to the forebrain were anosmic, as were adult-operated bilaterally bulbectomized rats. Our results provide strong support for the contention that, in the absence of the olfactory bulbs, olfactory connections to novel forebrain sites can support both odor detection and odor discrimination.

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Odors detected by mice deficient in cyclic nucleotide-gated channel subunit A2 stimulate the main olfactory system.

It is believed that odor transduction in the mammalian main olfactory system only involves the cAMP-signaling pathway. Here, we report on odor responsiveness in mice with a disrupted cyclic nucleotide-gated (CNG) channel subunit A2. Several odorants, including putative pheromones, can be detected and discriminated by these mice behaviorally. These odors elicit responses in the olfactory epithelium, main olfactory bulb, and olfactory (piriform) cortex of CNGA2 knock-out mice. In addition, responses to odors detected by CNGA2 knock-out mice are relatively insensitive to inhibitors of the cAMP pathway. These results provide strong evidence that cAMP-independent pathways in the main olfactory system of mammals participate in detecting a subset of odors.

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Zonal ablation of the olfactory sensory neuroepithelium of the mouse: effects on odorant detection.

Olfactory sensory neurons that express a specific odorant receptor, out of a thousand different, are unevenly distributed within, but restricted to one of four zones of the neuroepithelial sheet in the nasal cavity in the mouse. This zonal restriction of neurons expressing the same odorant receptor may have consequences, e.g. in case of localized injury. We found that the chemical dichlobenil can produce specific and permanent ablation of neurons in odorant receptor expression zone 1, while a higher dichlobenil dose causes reversible toxicity in neighboring zones. In behavior tests, mice lacking part of the olfactory epithelium had an increased detection threshold concentration of two-four orders of magnitude for some odorants but not others, resembling the phenomenon of specific hyposmia. This indicates that the broad tuning properties of single odorant receptors and their large number cannot fully compensate for loss of the receptor(s) with the highest sensitivity for a particular odorant.

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Olfactory discrimination of short chain fatty acids in rats with large bilateral lesions of the olfactory bulbs.

Rats trained preoperatively to discriminate between acetic acid and caproic acid and between acetic acid and propionic acid were tested for their memory of these tasks and ability to discriminate between these odorants and between the enantiomers of carvone after receiving large bilateral bulbar lesions that included most of the fatty acid responsive areas identified in prior physiological studies. Concentrations of acid odorants were varied to insure that discrimination was based on the qualitative difference between acids. Experimental rats performed somewhat poorer than controls on the memory test but had no significant deficits in performing the acid discrimination tasks or discriminating between the enantiomers of carvone. These results demonstrate that removal of most bulbar sites identified as responsive to fatty acids and the consequent disruption of patterned input to the bulb is largely without effect on discriminating odor qualities of structurally similar acids.

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Does intranasal application of zinc sulfate produce anosmia in the mouse? An olfactometric and anatomical study.

Mice pre-trained in an olfactometer were tested daily on odor detection and discrimination tasks after irrigation of their olfactory epithelium in each naris with 50 microl of 5% zinc sulfate or saline. Anterograde transport of a wheatgerm agglutinin-horseradish peroxidase (WGA-HRP) conjugate from the epithelium to the olfactory bulb was used to assess anatomical connectivity in these and in mice that were used only for histological analyses. One day after treatment, saline controls performed at high levels of accuracy in detecting vapor from solutions of 5-0.01% ethyl acetate and in an odor discrimination task but most ZnSO4-treated mice performed at chance for 5-30 days before showing recovery. Although dense WGA-HRP reaction product was found in the accessory olfactory bulb, there was little or no evidence for axonal transport to glomeruli of the main olfactory bulb in the first 4-8 days after treatment. These results demonstrate that intranasal application of ZnSO4 to mice produces a brief but essentially total disruption of functional connections from the olfactory epithelium to the main olfactory bulb and a corresponding transient anosmia.

Acetates↗

Odor discrimination and odor quality perception in rats with disruption of connections between the olfactory epithelium and olfactory bulbs.

Rats were trained using olfactometry and operant conditioning to discriminate among homologous fatty acids, homologous aldehydes, and a series of unrelated odors. Their memory for the positive and negative assignment of each odor (tested under extinction) was assessed before and after they had received selective lesions of the olfactory bulbs or injection of the olfactory epithelial toxin 3-methyl indole (3-MI). Response accuracy on the memory test provided a measure of the extent to which treatments altered the remembered perceptual quality of the odors. The degree of deafferentation of the bulb by treatment with 3-MI was assessed using anterograde transport of horseradish peroxidase applied to the olfactory epithelium. Rats treated with 3-MI had a detectable reaction product only in varying numbers of glomeruli on the lateral and, in some cases, posterior medial walls of the olfactory bulb. Bulbar lesions destroyed the dorsal and dorsomedial bulbar areas that have been identified in optical and electrophysiological studies as showing responses to fatty acids. Rats with bulbar lesions had good to near perfect retention on their post-treatment memory test on all odor pairs, as did 3-MI-treated rats that still had substantial input to glomeruli on the lateral or posterior medial wall of the bulb. 3-MI-treated rats with substantially fewer afferent connections had severe retention deficits, particularly for the aldehyde and fatty acid odors, but this loss was secondary to deficits in the ability to discriminate among these odors. The results indicate that input to bulbar areas that are activated by a series of homologous odors may not be essential for odor discrimination and that deafferentation of the majority of bulbar glomeruli may be primarily without effect on odor quality perception as assessed by the memory test. These outcomes point to a much higher degree of redundancy within the olfactory bulb than that envisioned by current combinatorial or odotopic hypotheses of odor quality coding or, alternatively, to mechanisms of odor coding used in the awake behaving animal that have not yet been elucidated.

Afferent Pathways↗

Cognitive deficits in docosahexaenoic acid-deficient rats.

This study investigated the influence of brain docosahexaenoic acid (DHA) deficiency on simple and complex olfactory-based learning and memory in 2nd generation (F2) adult male rats. Rats raised and maintained on either an n-3-adequate or an n-3-deficient diet were tested for acquisition of an olfactory learning set and an olfactory memory task, and for motivation to obtain a water reward. Despite a 76% decrease in brain DHA, n-3-deficient rats were able to acquire most simple 2-odor discrimination tasks but were deficient in the acquisition of a 20-problem olfactory learning set. This deficit could not be attributed to changes in sensory capacity but, instead, appeared to represent a deficit in higher order learning.

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