Mouse killing in rats induced by lesions of the medial hypothalamus or medial accumbens: short-term preoperative exposure to a mouse does not suppress the killing

Rats were either exposed or not exposed to a mouse in their living cage for a 48-hr period. At the end of this time a bilateral lesion was made in the medial accumbens region or in the medial hypothalamus. When tested 2 days postoperatively, the killing frequency among rats that had been exposed to mice preoperatively was not significantly lower than that of rats that were not preoperatively exposed. The ineffectiveness of preoperative experience in suppressing the mouse killing induced by medial accumbens and medial hypothalamic lesions is similar to that found previously with dorsal-median raphe lesions and olfactory bulb lesions and is in contrast to the ease with which preoperative experience prevents mouse killing induced by septal lesions and serotonergic lesions induced by 5,7-dihydroxytryptamine.     

Calcium signaling in mitral cell dendrites of olfactory bulbs of neonatal rats and mice during olfactory nerve Stimulation and beta-adrenoceptor activation

Synapses formed by the olfactory nerve (ON) provide the source of excitatory synaptic input onto mitral cells (MC) in the olfactory bulb. These synapses, which relay odor-specific inputs, are confined to the distally tufted single primary dendrites of MCs, the first stage of central olfactory processing. beta-adrenergic modulation of electrical and chemical signaling at these synapses may be involved in early odor preference learning. To investigate this possibility, we combined electrophysiological recordings with calcium imaging in olfactory bulb slices prepared from neonatal rats and mice. Activation of ON-MC synapses induced postsynaptic potentials, which were associated with large postsynaptic calcium transients. Neither electrical nor calcium responses were affected by beta-adrenergic agonists or antagonist. Immunocytochemical analysis of MCs and their tufted dendrites revealed clear immunoreactivity with antibodies against alpha1A (Cav2.1, P/Q-type) and alpha1B (Cav2.2, N-type), but not against alpha1C (Cav1.2, L-type) or alpha1D (Cav1.3, L-type) calcium channel subunits. Moreover, nimodipine, a blocker of L-type calcium channels, had no effect on either electrical or calcium signaling at ON-MC synapses. In contrast to previous evidence, we concluded that in neonatal rats and mice (P5-P8), mitral cells do not express significant amounts of L-type calcium channels, the calcium channel type that is often targeted by beta-adrenergic modulation. The absence of beta-adrenergic modulation on either electrical or calcium signaling at ON-MC synapses of neonatal rats and mice excludes the involvement of this mechanism in early odor preference learning.     

Separate neural sites for d-amphetamine suppression of mouse killing and feeding behavior in rats

The present study was conducted to investigate several possible neural sites for d-amphetamine's effect on mouse killing and feeding behaviors. d-Amphetamine (10, 20, and 30 μg) injected into each lateral ventricle, suppressed mouse kiling, food, and water intake in a dose-dependent manner. Bilateral adminstration of d-amphetamine (20 μg) into the central amygdaloid nucleus abolished mouse killing behavior but did not affect feeding and drinking. By contrast, bilateral amphetamine injections into the substantia nigra, or into the ventral region of the caudate nucleus, did not suppress mouse killing behavior, but significantly decreased food and water intake. The lateral hypothalamus was sensitive to d-amphetamine injections, which suppressed mouse killing and food intake as well as water intake. d-Amphetamine injections into the nucleus accumbens produced inconsistent effects on mouse killing and feeding. Our observations suggest a differentiation of the neural sites that mediate feeding from those underlying mouse killing behavior.     

Suppression of mouse killing and apomorphine-induced social aggression in rats by local anesthesia of the mystacial vibrissae.

Local anesthesia of the facial epidermis can effect a substantial decrease in shock-elicited fighting of paired rats. The present experiments constitute methodological extensions to mouse killing and spontaneous drug-induced social aggression. In the first experiment, known mouse-killing rats were given bilateral lidocaine or placebo injections administered under ether anesthesia. Attack and kill latencies were significantly longer under lidocaine than under placebo; all subjects killed under placebo, whereas a third of all subjects failed to kill on the initial lidocaine test. On subsequent lidocaine testing, latencies decreased and nonkilling rats killed. In a second experiment intense apomorphine-induced conspecific fighting of rats preselected for aggressiveness was markedly reduced following lidocaine anesthesia. The comparative results of both experiments are interpreted in reference to theoretical assertions regarding the import of sensory information in stimulus-bound attack and the typology of central aggression systems.     

Mouse killing by rats: Suppression by electrical stimulation ventral to the anterior septum

Killing of mice was suppressed in 18 out of 24 rats by electrical stimulation of the region ventral to the anterior septum lying between the vertical arm of the diagonal band of Broca and the rostral limb of the anterior commissure. The mean effective minimum stimulation intensity was 8.2 uA (60 HZ, RMS). Stimulation of the cingulate cortex did not suppress mouse killing (mean stimulus intensity: 38.7 uA). Electrical recordings revealed after discharge in response to the stimulation in only one animal. At the stimulation intensity which suppressed mouse killing, there was no significant suppression of eating in 6 of 9 animals tested. These results are consistent with other evidence implicating the region ventral to the anterior septum in the modulation of mouse killing in the rat.     

Effects of transections to the vomeronasal nerves or to the main olfactory bulbs on the initiation and long-term retention of maternal behavior in primiparous rats.

While the onset of maternal behavior at parturition is mediated by hormones, the maintenance of maternal behavior during the first few postpartum weeks depends on experiences acquired while the dam interacts with pups (Rosenblatt, 1990). In fact, if female rats are permitted as little as 2 h or maternal experience within 36 h after Cesarean delivery, they exhibit heightened maternal behavior during maternal induction tests 10 days later; in contrast, dams separated from young at the time of Cesarean delivery and not permitted a maternal experience fail to respond maternally in tests 10 days later (Orpen & Fleming, 1987). In this study we investigated the role of chemosensory input through the vomeronasal and main olfactory systems in this maternal experience effect. Six groups of primiparous females were tested for maternal behavior to foster pups presented 9-10 days after Cesarean delivery: three groups were permitted to interact with pups for a 2-h period 36 h after Cesarean delivery; and three groups were separated from pups until testing and were given no maternal experience. Within each experience condition, one group sustained bilateral section of the vomeronasal nerves, one sustained bilateral coronal cuts through the midsection of the main olfactory bulbs, and one group sustained small medial olfactory bulb cuts. The results showed that animals sustaining vomeronasal or olfactory transections, regardless of experience condition, exhibited significantly reduced latencies to maternal behavior in maternal induction tests. However, these chemosensory disruptions did not prevent an additional facilitation of maternal behavior produced by a prior maternal experience.     

A specific role for the human amygdala in olfactory memory

The medial temporal lobe is known to play a role in the processing of olfaction and memory. The specific contribution of the human amygdala to memory for odors has not been addressed, however. The role of this region in memory for odors was assessed in patients with unilateral amygdala damage due to temporal lobectomy (n = 20; 11 left, 9 right), one patient with selective bilateral amygdala damage, and in 20 age-matched normal controls. Fifteen odors were presented, followed 1 h later by an odor-name matching test and an odor-odor recognition test. Signal detection analyses showed that both unilateral groups were impaired in their memory for matching odors with names, these patients were not significantly impaired on odor-odor recognition. Bilateral amygdala damage resulted in severe impairment in both odor-name matching as well as in odor-odor recognition memory. Importantly, none of the patients were impaired on an auditory verbal learning task, suggesting that these findings reflect a specific impairment in olfactory memory, and not merely a more general memory deficit. Taken together, the data provide neuropsychological evidence that the human amygdala is essential for olfactory memory.     

The development of olfactory preferences for artificial odors briefly experienced by the precocial spiny mouse young

Groups of pups, aged 2, 4, 6, 12, 16, and 18 days of the precocial murid rodent spiny mouse (Acomys cahirinus), were each exposed for 1.5 h to one of the experimental odors, cinnamon or cumin, present in the surrounding environment. The odors were not contingent upon home-cage odors or any other reinforcers. This simple exposure produced a strong preference for the exposed odor in multichoice preference tests carried out 48 h after the exposure in pups from groups aged 2 through 16 days. Older pups exposed to cinnamon or cumin at Day 18 did not show a significant preference for the familiar odor. Both experimental odors used were found to be neutral for control experimentally naive pups within a tested age span. These results point at a stimulus familiarity, rather than associative learning in the development of olfactory preferences in young spiny mouse pups.     

The rate of scent marking by male rats and consequent olfactory preferences of female rats

An experiment is reported designed to test the hypothesis that female rats might discriminate between males that differed in the quantity of odor deposited by scent marking. Male odor donors were selected by prior screening for high or low rates of scent marking in an open arena. Females were then tested to determine whether they showed any preference for males that marked at a high rate. It was found that female rats did discriminate, but that they preferred to remain near males selected for low rates of scent marking.     

Cross-modal self-recognition: the role of visual, auditory, and olfactory primes

Three priming experiments were conducted to determine how information about the self from different sensory modalities/cognitive domains affects self-face recognition. Being exposed to your body odor, seeing your name, and hearing your name all facilitated self-face recognition in a reaction time task. No similar cross-modal facilitation was found among stimuli from familiar or novel individuals. The finding of a left-hand advantage for self-face recognition was replicated when no primes were presented. These data, along with other recent results suggest the brain processes/represents information about the self in highly integrated ways.     

Effects of some physiological and pharmacological manipulations on shock- facilitated mouse killing by onychomys leucogaster (Northern grasshopper mouse)

Onychomys leucogaster (northern grasshopper mice) were induced to kill mice with response-contingent shock, and the effects of several physiological, pharmacological, and endocrinological variables were assessed. Lesions of the septum facilitated mouse killing, while lesions of the amygdala abolished spontaneous mouse killing and delayed shock-facilitated killing. Chlorpromazine (2.5–5 mg/kg) and chlordiazepoxide (5–10 mg/kg) facilitated mouse killing on postdrug trials but did not affect killing when the animals were drugged. Adrenalectomy, castration, and castration adrenalectomy did not alter the frequency of kill nor were sex-related differences in killing noted. These results were compared to those found by others studying the effects of lesions and drugs on mouse killing by rats.     

Noradrenergic control of odor recognition in a nonassociative olfactory learning task in the mouse

The present study examined the influence of pharmacological modulations of the locus coeruleus noradrenergic system on odor recognition in the mouse. Mice exposed to a nonrewarded olfactory stimulation (training) were able to memorize this odor and to discriminate it from a new odor in a recall test performed 15 min later. At longer delays (30 or 60 min), the familiar odor was no longer retained, and both stimuli were perceived as new ones. Following a post-training injection of the alpha(2)-adrenoceptor antagonist dexefaroxan, the familiar odor was still remembered 30 min after training. In contrast, both the alpha(2)-adrenoceptor agonist UK 14304 and the noradrenergic neurotoxin DSP-4 prevented the recognition of the familiar odor 15 min after the first exposure. Noradrenaline release in the olfactory bulb, assessed by measurement of the extracellular noradrenaline metabolite normetanephrine, was increased by 62% following dexefaroxan injection, and was decreased by 38%-44% after treatment with UK 14304 and DSP-4. Performance of mice in the recall test was reduced by a post-training injection of the beta-adrenoceptor antagonist propranolol or the alpha(1)-antagonist prazosin, thus implicating a role for beta- and alpha(1)-adrenoceptors in the facilitating effects of noradrenaline on short-term olfactory recognition in this model.     

Discrimination by olfactory cues in albino rats reflecting familiarity and relatedness among conspecifics

The present investigation sought to determine whether albino rat pups could discriminate among familiar siblings, nonfamiliar siblings, familiar nonsiblings (foster littermates), and nonfamiliar nonsiblings (unrelated agemates) using only olfactory cues. Pairing all possible combinations of familiarity and kinship variables (six), the odors were presented in paired combinations to each of twelve experimental subjects. Results from dependent t tests indicated that the albino rat pups could discriminate between the following pairs of odors using only the olfactory sensory modality: (a) familial siblings and nonfamiliar siblings, (t = 3.41, p = .006); (b) familiar siblings and nonfamiliar nonsiblings, (t = 9.62, p = .001); (c) nonfamiliar siblings and nonfamiliar nonsiblings, (t = 3.15, p = .009); and (d) familiar nonsiblings and nonfamiliar nonsiblings (t = 2.58, p = .026).