Effects of olfactory bulb ablation and androgen on marking and agonistic behavior in male Mongolian gerbils (Meriones unguiculatus).

Male Mongolian gerbils, selected for high marking frequency, were paired with male opponents, and marking and fighting behavior were recorded. Animals then underwent castration, bilateral bulbectomy, unilateral bulbectomy, the combined operations, or a sham operation; and their behavior was again observed. All operated animals showed drastic reduction in both marking and aggressive encounters. Injections of testosterone propionate (TP) produced complete restoration of marking in castrates, but not in bilaterally or unilaterally bulbectomized animals or combined operates. The exhibition of aggression after injections of TP, however, was enhanced to supernormal levels in bulbectomized or bulbectomized-castrated animals. The results suggest the following: that removal of the olfactory bulbs may eliminate a critical neural input necessary for the normal expression of marking and agonistic; that although marking and fighting are influences by olfactory input and gonadal steroids, their regulatory mechanisms may not be identical; and that removal of the bulbs may sensitize a neural mechanism controlling aggression, thus potentiating its elicitation following administration of exogenous androgen.     

Pharmacological antagonism of mouse-killing behavior in the olfactory bulb lesion-induced killer rat

Representative agents from all of the major classes of drugs that have been reported to be selective antagonists of spontaneous mouse-killing behavior (i.e., antidepres-sants, antihistamines, anticholinergics, and stimulants) were tested for their ability to antagonize the mouse-killing response in rats that became killers following removal of the olfactory bulbs (O.B. lesion-induced killer rat) and in spontaneous killers. All of the drugs tested selectively antagonized the killing behavior of both spontaneous and lesion-induced mouse-killing rats. Several drugs (i.e., imipramine, amitriptyline, d-amphetamine, and chlorpheniramine) were found to be significantly less potent antagonists of mouse killing in the 0.6. lesioned rat as compared to spontaneous killers. Since all of the drugs that exhibited significant differences in activity between the two models have been shown to possess the ability to elevate norepinephrine levels at receptor sites in the brain, alterations in noradrenergic systems may account for the differences in sensitivity that were observed in this study. The possibility that there may be a common neural substrate for mouse killing in the two models is discussed.     

Effects of ethanol withdrawal on muricidal behavior

When naive rats of our colony were individually housed for 1 month with free access to laboratory chow and water as drinking fluid, 6% exhibited muricidal behavior. When naive rats of the same colony were similarly housed but received ethanol 20% in water as the sole source of drinking fluid (ll.5 g ethanol/kg/day), the percentage of killer rats was the same. However, when the rats were housed in similar conditions and submitted to a 1-day ethanol withdrawal, the percentage of muricidal rats increased to 25%. Ethanol intake in the same conditions as described above did not change muricidal behavior of spontaneous killers and did not induce killing behavior in nonkiller animals. GABA-mimetic agents administered IP blocked ethanol withdrawal-induced killing behavior as well as spontaneous muricidal activity.     

Interspecific aggression and reactivity in rats: Effects of selective raphe lesions and additional olfactory bulb ablation

Large depletion of brain 5 HT has been shown to induce mouse-killing behavior in the rat. Selective lesions of the raphe nuclei have been investigated in order to determine whether the various components of the 5 HT system exert some specific control over this aggressive behavior. Electrolytic lesions of the dorsal or the median raphe nucleus do not induce mouse killing, whereas combined lesions of these nuclei elicit this behavior in about 40% of naive rats. Consequently, it appears that serotonergic neurons originating in the dorsal and median raphe nuclei work synergistically in mediating inhibitory control over mouse-killing behavior. Loco-motor activity is increased in novel environments by each of the selective lesions and to a larger extent by combined raphe lesions; 24 hours activity in resting conditions is unchanged during the light period, and increased during the dark period of the daily cycle by the various lesions. As it has been shown previously that hyper-activity in response to novelty following raphe lesions is not directly related to the 5 HT decrease in the brain, it appears that interspecific aggression and motor responsiveness must not be dependent on the same neural substrate within the raphe nuclei. The raphe lesions do not facilitate the elicitation of mouse killing by further olfactory bulb ablations, in contrast to earlier results where bulbectomy facilitated the induction of this behavior by raphe lesions.     

Effects of olfactory bulb ablation on cardiac and ventilatory arousal responses and their habituation in the goldfish Carassius auratus

The effects of olfactory bulb ablation on the cardiac and ventilatory arousal responses to the onset of illumination and habituation of these responses were investigated in goldfish. Bulbectomy did not effect the magnitude of response on novel stimulus presentation. Normal, sham operated, and olfactory bulb-ablated animals showed similar rates of habituation. These results suggest that deficits in feeding and sexual behavior in goldfish are due to the loss of specific olfactory influences on lower brain centers and not due to a decrease in general responsiveness.     

Role of centrifugal projections to the olfactory bulb in olfactory processing

While there is evidence that feedback projections from cortical and neuromodulatory structures to the olfactory bulb are crucial for maintaining the oscillatory dynamics of olfactory bulb processing, it is not clear how changes in dynamics are related to odor perception. Using electrical lesions of the olfactory peduncle, sparing output from the olfactory bulb while decreasing feedback inputs to the olfactory bulb, we demonstrate here a role for feedback inputs to the olfactory bulb in the formation of odor-reward associations, but not for maintaining primary bulbar odor representations, as reflected by spontaneous odor discrimination.     

Bicuculline infusion into the accessory olfactory bulb facilitates the induction of maternal behavior in rats

The GABAA antagonist bicuculline, intracranially infused into the accessory olfactory bulb (AOB), facilitated the expression of maternal behavior (MB) in virgin Wistar female rats. Behavioral effects were observed 24 hours after infusion and were injection dependent. Pheromonal stimuli, generated by the pups, are thought to exert an inhibitory effect on vomeronasal nuclei involved in MB in virgin rats. The present study investigated the possibility that a decrement in AOB output, resulting from long-term compensatory synaptic changes to chronic bicuculline infusion, would facilitate the expression of MB. The implications of our findings for the mechanisms involved in the induction of MB and the maternal experience effect are discussed.     

pCREB in the neonate rat olfactory bulb is selectively and transiently increased by odor preference-conditioned training

Early olfactory preference learning in rat pups occurs when novel odors are paired with tactile stimulation, for example stroking. cAMP-triggered phosphorylation of cAMP response element binding protein (pCREB) has been implicated as a mediator of learning and memory changes in various animals (Frank and Greenberg 1994). In the present study we investigate whether CREB is phosphorylated in response to conditioned olfactory training as might be predicted given the proposed role of the phosphorylated protein in learning. On postnatal day 6, pups were trained for 10 min using a standard conditioned olfactory learning paradigm in which a conditioned stimulus, Odor, was either used alone or paired with an unconditioned stimulus, Stroking (using a fine brush to stroke the pup). In some instances stroking only was used. The pups were sacrificed at 0, 10, 30, or 60 min after the training. Using Western blot analysis, we observed that the majority of olfactory bulbs in conditioned pups (Odor + Stroking) had a greater increase in pCREB activation at 10 min after training than pups given nonlearning training (Odor only or Stroking only). The phosphorylated protein levels were low at 0 min and at 60 min after training. This is in keeping with the slightly delayed and short-lived activation period for this protein. The localization of pCREB increases within the olfactory bulb as seen by immunocytochemistry. Naive pups were not exposed to odor or training. There was a significantly higher level of label in mitral cell nuclei within the dorsolateral quadrant of the bulb of pups undergoing odor-stroke pairing. No significant differences were observed among nonlearning groups (Naive, Odor only, or Stroking only) or among any training groups in the granule or periglomerular cells of the dorsolateral region. The localized changes in the nuclear protein are consistent with studies showing localized changes in the bulb in response to a learned familiar odor. The present study demonstrates that selective increases in pCREB occur as an early step following pairing procedures that normally lead to the development of long-term olfactory memories in rat pups. These results support the hypothesized link between pCREB and memory formation.     

Effects of genetic vestibular defects on behavior related to spatial orientation and emotionality.

A large battery of behavioral tests was administered to normal mice and to mice with varying degrees of otoconial agenesis due to genes affecting vestibular development. Many significant differences were found, but a factor analysis revealed that the variance on the 11 best tests could be accounted for in terms of two underlying variables. Factor I, the more important of the two, was associated with activity, habituation, and spontaneous alternation. Factor II appeared to represent a fear of new stimuli or situations. In both cases factor scores were highly related to the degree of otoconial deficiency. One subgroup of mice with severe otoconial agenesis displayed hyperactivity and a total absence of either habituation or spontaneous alternation. In these animals, brain and body development were stunted, and the reactions to amphetamine and physostigmine were opposite to those seen in normal mice. The results support the idea that the static organs contribute importantly to spatial orientation and suggest that early-onset vestibular defects can result in profound alterations of emotionality.