A common mechanism in verb and noun naming deficits in Alzheimer's patients.

We tested the ability of Alzheimer's patients and elderly controls to name living and non-living nouns, and manner and instrument verbs. Patients' error patterns and relative performance with different categories showed evidence of graceful degradation for both nouns and verbs, with particular domain-specific impairments for living nouns and instrument verbs. Our results support feature-based, semantic representations for nouns and verbs and support the role of inter-correlated features in noun impairment, and the role of noun knowledge in instrument verb impairment.

Role of pregnancy and parturition in induction of maternal behavior in prairie voles (Microtus ochrogaster).

In prairie voles (Microtus ochrogaster), most virgin females are infanticidal. To determine the onset of maternal responsiveness, female prairie voles were tested for maternal behavior as virgins and at different times throughout pregnancy. Female voles that were infanticidal as virgins by and large remained infanticidal throughout pregnancy. In contrast, about 30% of voles that were maternal as virgins became infanticidal during pregnancy. To test whether events associated with parturition facilitate the onset of maternal behavior, females had their litters delivered by Caesarean section within a day of expected delivery or were allowed to give birth naturally with sham surgery occurring shortly before or after birth. Females that gave birth naturally were fully maternal and did not attack unrelated pups, but females subjected to artificial delivery remained infanticidal. This suggests that events closely related to parturition are crucial for full development of maternal behavior in female prairie voles.

Intraoral cheek fistulae: a refined technique.

Taste reactivity testing (TRT), which entails infusing a solution into the oral cavity of subjects, is used across a wide range of studies. For laboratories inexperienced in the conventional technique of implanting cheek fistulae, the surgery can be problematic for both the subjects and the experimenter. We have proposed a refined method for fistulae implantation that is less invasive, thereby reducing the pain and distress of the animals. Using this refined technique, we were able to replicate the findings of previous TRT studies, namely that a high dose of lithium chloride produces an increase in aversive and a decrease in ingestive orofacial and somatic responses. Using indices of health, we demonstrate that unlike animals with the conventional method of fistulae implantation, subjects that receive the refined technique regain their pre-surgery body weights rapidly and show no physical signs of discomfort. Additional advantages of the refined technique are discussed.

High doses of vasopressin delay the onset of extinction and strengthen acquisition of LiCl-induced conditioned taste avoidance.

When low doses of vasopressin are given 50 min after pairing sucrose consumption with a high dose of LiCl, extinction of the LiCl-induced conditioned taste avoidance is accelerated. These low doses of vasopressin do not themselves induce conditioned taste avoidance when paired with sucrose consumption. Predicated on previous studies administering two avoidance-inducing agents after sucrose consumption, studies were designed to determine whether high doses of vasopressin capable of inducing conditioned taste avoidance would (1) delay rather than accelerate extinction of a conditioned taste avoidance induced by a high dose of LiCl and (2) strengthen acquisition of a conditioned taste avoidance induced by a low dose of LiCl. The results of three studies showed that doses of 9 and 18 microg/kg of vasopressin induced a conditioned taste avoidance when injected 50 min after sucrose consumption, delayed the onset of extinction when injected 50 min after pairing sucrose consumption with a high dose of LiCl, and strengthened acquisition of a conditioned taste avoidance when injected 50 min after pairing sucrose consumption with a low dose of LiCl. Taken together, these data suggest that the delay in onset of extinction is due to a strengthening of acquisition. It has been suggested that vasopressin is a mnemonic neuropeptide that delays extinction of learned tasks. However, for conditioned taste avoidance, the evidence for the effects of low doses of vasopressin on extinction do not support this hypothesis and the evidence for high doses of vasopressin can be accounted for by the avoidance-inducing properties of vasopressin.

The role of histamine in estradiol-induced conditioned consumption reductions.

Conditioned consumption reductions (CCRs) develop toward novel taste stimuli as a consequence of associating those tastes with certain physiological changes. Few studies have focused on the neurochemical basis of this learned behavior. The purpose of these experiments was to reexamine the role of histamine in CCRs elicited by estradiol. Previous studies have suggested that histamine mediates CCRs induced by radiation, centrifugal rotation, and estradiol. However, because the animals were trained in a drug state, but tested in a nondrug state, it is possible that state-dependent learning confounded the results of these studies. The following series of experiments was performed to test this possibility for estradiol-induced CCRs. Implementing our own methodologies in Experiment 1, we demonstrated that an estradiol-induced CCR was blocked by treatment with the histamine 1 receptor blocker, chlorpheniramine maleate, before sucrose consumption during acquisition. In Experiment 2, identical states were maintained during acquisition and extinction by administering chlorpheniramine prior to sucrose exposure during both phases. The results indicated that chlorpheniramine blocked the estradiol-induced CCR. However, circumventing state-dependency in Experiment 3 by administering chlorpheniramine following exposure to sucrose during acquisition augmented the estradiol CCR. Taken together, the results of these experiments suggest that the ability of chlorpheniramine to abolish estradiol-induced CCRs is not due to state-dependency or to the antihistaminergic properties of chlorpheniramine. It is proposed that the results of all of the experiments can be accounted for by the aversive properties of chlorpheniramine.

Peripheral vasopressin accelerates extinction of conditioned taste avoidance.

Both peripheral and central administration of vasopressin improves retention and delays extinction when given before or after acquisition of shock avoidance learning. For conditioned taste avoidance, however, vasopressin prolongs extinction when injected peripherally before acquisition tests and accelerates extinction when infused intracerebroventricularly after acquisition. The following experiments were designed to determine whether this inconsistency is based on the route of administration or timing of vasopressin treatment. Because acquisition of conditioned taste avoidance is strengthened when an agent that is capable of inducing avoidance is administered after LiCl injection, it was determined in experiment 1 that a 6 microg/kg dose of vasopressin did not induce conditioned taste avoidance when administered 50 min after consumption of a sucrose solution. In experiment 2, it was determined that this dose of vasopressin accelerated extinction of a LiCl-induced conditioned taste avoidance when given 50 min after LiCl injection. These results suggest that the inconsistency is not based on route of administration. In experiment 3, it was determined that there was a tendency for animals to show prolonged extinction when vasopressin was administered 20 min before access to a sucrose solution. All of the results taken together suggest that the differential effects of vasopressin on extinction are due to the timing of administration. It was suggested that vasopressin accelerates extinction when given after acquisition by reducing the effectiveness of LiCl and it prolongs extinction when given before acquisition by altering neural responsiveness in areas mediating conditioned taste avoidance.

Exposure to estradiol before but not during acquisition of LiCl-induced conditioned taste avoidance accelerates extinction.

Estradiol accelerates extinction of LiCl-induced conditioned taste avoidance when it is present continuously before and during acquisition. We have suggested that the effect of estradiol on extinction is due to its illness-associated, rather than learning-associated, properties. If this were the case, then one would expect estradiol to act before but not during acquisition. This expectation is based on previous work showing attenuation of learned taste avoidance when rats are given distal preexposure (greater than 24 h before conditioning) or proximal preexposure (less than 24 h before conditioning) to the illness-inducing agent LiCl before acquisition of a LiCl-induced conditioned taste avoidance. In three separate experiments, estradiol was administered during three different time periods via subcutaneous implantation of a 10-mm estradiol-filled capsule. In each experiment, the extinction of estradiol-treated females was compared to that of females implanted with empty capsules. In the first experiment, female rats were given distal exposure to estradiol before acquisition. Capsules were implanted 11 days before acquisition and were removed 2 days before acquisition. In the second experiment, female rats were given proximal exposure to estradiol before acquisition. Capsules were implanted 2.5 h before LiCl was paired with a sucrose solution and were removed 16.5 h later. In the third experiment, female rats were given exposure to estradiol during acquisition. Capsules were implanted at the same time as LiCl administration and were removed 18 h later. The only estradiol-treated females to show accelerated extinction were those given distal preexposure to estradiol in Experiment 1. These data do not support a learning-associated hypothesis and only partially support an illness-associated hypothesis. The failure to find accelerated extinction following proximal preexposure may reflect an inappropriate choice of the parameters used in the experiment or a difference in the stimulus properties of LiCl and estradiol that allow each to serve as conditioning and preexposure agents in conditioned taste avoidance paradigms [corrected].

Central infusion of vasopressin in male rats accelerates extinction of conditioned taste avoidance induced by LiCl.

In shock avoidance tasks, extinction is prolonged when vasopressin is infused into the lateral ventricle after an acquisition session. Experiments were performed to determine whether a dose of vasopressin that does not induce conditioned taste avoidance (CTA) could prolong extinction of a LiCl-induced CTA when it is infused into the lateral ventricle of Sprague-Dawley male rats after acquisition. The first experiment was designed to determine whether infusion of vasopressin into the lateral ventricle would induce a CTA. Consumption of a sucrose solution was paired with infusion of vasopressin or saline, and even after two pairings, none of the vasopressin-treated rats showed decreases in sucrose consumption. Therefore, in the second experiment, this same dose of vasopressin was infused into the lateral ventricle 50 min after consumption of a sucrose solution was paired with an injection of LiCl. Vasopressin increased the rate of extinction of the LiCl-induced CTA. These results are the opposite of what has been found after peripheral administration of vasopressin before acquisition and/or extinction of a LiCl-induced CTA. Possible reasons for the difference in the direction of the effect on extinction include differential effects of vasopressin depending on the route of administration, the timing of injection, and the presence of aversive effects produced by the neuropeptide.