The ability of various chemicals to elicit olfactory beta-waves in the pyriform cortex of meadow voles (Microtus pennsylvanicus) and laboratory rats (Rattus norvegicus).

Previous research has shown that, in freely moving laboratory rats, the odors of benzyl alcohol, camphor, carvacrol, isopentenyl methyl sulfide, 2-propylthietane, salicylaldehyde, trimethylthiazoline, and xylene (plus other compounds) elicit high amplitude bursts of roughly 20-Hz waves (beta-waves) in the olfactory bulb and pyriform cortex. Since all these compounds are effective antifeedants in a variety of small herbivores, a more extensive test of the effect of the odor of a variety of antifeedants on pyriform cortex activity in meadow voles (Microtus pennsylvanicus) was undertaken. A beta-wave response was reliably elicited in the vole pyriform cortex by the odors of isopentenyl methyl sulfide (a component of fox odor), 2-propyl thietane (a component of stoat odor), and xylene but not by the odors of 29 other compounds. The results indicate: (a) that there are clear interspecific differences in the olfactory reactions of the pyriform cortex and (b) that not all antifeedants elicit beta-waves in the pyriform cortex.

Effects of cyclazocine and scopolamine on swim-to-platform performance in rats.

DL-Cyclazocine (0.5-2.0 mg/kg, i.p.) produced no impairment in rats' acquisition and retention of the behavior of swimming to a large visible platform in a water tank. However, cyclazocine produced a significant enhancement or potentiation of the impairment in swim-to-platform behavior produced by scopolamine. Since cyclazocine has previously been shown to abolish serotonin-dependent electrocortical activation (enabling it, in combination with central muscarinic blockade, to block all cortical activation), the results lend further support to the hypothesis that blockade of electrocortical activation produces dementia rather than sleep or coma as was previously believed.

Pyriform cortex beta-waves: odor-specific sensitization following repeated olfactory stimulation.

The first exposure to the odors of carbon tetrachloride, isopentenyl methyl sulfide, methyl ethyl ketone, 2-propylthietane, salicylaldehyde, toluene, 2,4,5-trimethyl thiazoline, or xylene elicits a weakly developed 20 Hz wave response (beta-waves) in central olfactory structures in the rat. Repeated presentations of these odors produces a gradual enhancement or sensitization of olfactory beta-waves over 5-10 trials given in 1-3 min. The odors of 2-aminoacetophenone and 2-hydroxyacetophenone produce sensitization after an average of 15-17 presentations. The sensitized beta-wave response to the odors of 2-propylthietane and xylene persists for at least 5 days and probably much longer. Sensitization to one odor transfers partially or not at all to other novel odors even though repeated presentation of the new odor also produces sensitization. Since the initial negative response of the olfactory mucosa (presumably due to receptor depolarization) is not enhanced by repeated olfactory stimulation, it is presumed that the altered responsivity is due to synaptic changes in central olfactory structures such as the olfactory bulb or pyriform cortex. Finally, data are presented to show that behavioral antifeedant activity by an odorant does not invariably mean that the odorant has the ability to elicit an olfactory beta-wave response.

Fast wave activity in the rat rhinencephalon: elicitation by the odors of phytochemicals, organic solvents, and a rodent predator.

Recent research has shown that bursts of approximately 20 Hz fast waves are elicited in rhinencephalic cortex in rats by the odors of a number of different organic solvents and of components of the secretions of predators such as the weasel and the fox. We now show that a number of phytochemicals (benzyl alcohol, carvacrol, eucalyptol, and salicylaldehyde) will elicit fast wave bursts of about 20 Hz in the rat pyriform cortex. Additional organic solvents (carbon tetrachloride, chloroform, diethyl ether, 1, 2-dimethoxyethane, n-heptane, mesitylene, methylcyclohexane, and commercial gasoline and kerosene, but not N,N-dimethylformamide or dimethyl sulfoxide) and another component of fox secretions (isopentenylmethyl sulfide) were also effective. Many of these compounds will also elicit fast wave bursts of about 20 Hz in the dentate gyrus. The effectiveness of benzyl alcohol, camphor, carvacrol, eucalyptol, isopentenylmethyl sulfide, 2-propylthietane, salicylaldehyde, toluene, and trimethylthiazoline (all of which elicit rhinencephalic fast waves in rats) in suppressing feeding in various small herbivores suggests that the recording of odor-induced rhinencephalic fast waves may provide an easy means of identifying new antifeedants. We found no evidence that the bursts of 20-Hz activity seen in the rat rhinencephalon were kindling-induced seizure-like reactions of the olfactory brain to the vapors of toxic chemicals.

Oscillatory fast wave activity in the rat pyriform cortex: relations to olfaction and behavior.

Bursts of rhythmical fast waves (> 1 mV, peak frequency approximately 16 Hz; mean frequency approximately 20 Hz) are elicited in the olfactory bulb and pyriform cortex in waking or urethane-anesthetized rats (1.25 g/kg, i.p.) by olfactory stimulation with organic solvents (xylene, toluene, methyl methacrylate, oil of turpentine) or components of anal gland secretions of rat predators (2-propylthietane, weasel; trimethyl thiazoline, red fox). These waves are specifically related to olfaction since they: (a) are blocked when the nares are sealed; (b) are not elicited by non-olfactory stimuli; (c) are unrelated to concurrent motor activity; and (d) can only be elicited in anesthetized-tracheotomized rats when an odorous airstream is drawn through the nasal passages. Pyriform fast waves appear to be somewhat specific to the odors of organic solvents and predators as other strong odors (ammonia, caproic and butyric acids, cadaverine) are ineffective. During natural sleep or after treatment with scopolamine hydrobromide, low voltage pyriform background activity is replaced by larger amplitude, irregular 1-20 Hz waves. The scopolamine-induced waves are not blocked by spontaneous motor activity. We suggest that the pyriform cortex, like the archicortex and the neocortex, receives a cholinergic activating input.