Behavioral and Neural Biology
ISSN : 0163-1047
Published by: Elsevier BV (10.1016)
Total articles ≅ 1,531
Latest articles in this journal
Behavioral and Neural Biology, Volume 62; https://doi.org/10.1016/s0163-1047(05)80014-7
Behavioral and Neural Biology, Volume 62, pp 237-243; https://doi.org/10.1016/s0163-1047(05)80022-6
Post-training intraperitoneal administration of α-D[+]-glucose (10–300 mg/kg) facilitated 24-h retention, in male Swiss mice, of a one-trial step-through inhibitory avoidance task. The dose-response curve was an inverted U. Glucose did not increase the retention latencies of mice that had not received a footshock during training. The effect of glucose (30 mg/kg, ip) on retention was time-dependent, which suggests that the drug facilitated memory storage. The memory facilitation induced by glucose (30 mg/kg, ip) was prevented by atropine (0.5 mg/kg, ip) administered after training, but 10 min prior to glucose treatment. In contrast, neither methylatropine (0.5 mg/kg, ip), a peripherally acting muscarinic receptor blocker, nor mecamylamine (5 mg/kg, ip) or hexamethonium (5 mg/kg, ip), two cholinergic nicotinic receptor antagonists, prevented the effects of post-training glucose on retention. Low subeffective doses of the central acting anticholinesterase physostigmine (35 μg/kg, ip), administered immediately after training, and glucose (10 mg/kg, ip), given 10 min after training, acted synergistically to improve retention. The effects of glucose (10 mg/kg, ip) were not influenced by the peripherally acting anticholinesterase neostigmine (35 μg/kg, ip). Considered together, these findings suggest that the memory facilitation induced by post-training administration of glucose could result from an enhancement of brain acetylcholine synthesis and/or its release that, in turn, might modulate the activity of muscarinic cholinergic mechanisms that are critically involved in memory storage.
Behavioral and Neural Biology, Volume 62, pp 244-252; https://doi.org/10.1016/s0163-1047(05)80023-8
The effects of various levels of hypobaric hypoxia, exposure to reduced atmospheric pressure, on spatial memory in rats were examined. Hypobaric hypoxia simulates high altitude conditions where substantial deficits in human cognitive performance occur. However, few studies have measured cognitive changes in animals during exposure to this type of hypoxia. Male Fischer 344 rats were tested in the learning set version of the Morris water maze, a test known to assess spatial memory. Rats were tested at 2 and 6 hours while exposed to a range of simulated altitudes: sea level, 5500 m, 5950 m, and 6400 m. Altitude exposures at 5950 or 6400 m decreased both reference and working memory performance, as demonstrated by latency, distance, and speed measures, in an elevation-dependent fashion. During sea level testing on the day following hypobaric exposure, decrements in reference memory were still observed on all dependent measures, but only speed was impaired on the working memory task. These results agree with human studies that demonstrate elevation-dependent impairments in spatial memory performance during exposure to hypobaric hypoxia. The deficits may be attributable to changes in hippocampal cholinergic function.
Behavioral and Neural Biology, Volume 62, pp 265-272; https://doi.org/10.1016/s0163-1047(05)80027-5
Behavioral and Neural Biology, Volume 62, pp 178-189; https://doi.org/10.1016/s0163-1047(05)80016-0
Complex relational processes underlying place navigation learning were analyzed by minimizing the relational elements available to rats. The animals navigated in a standard water maze in darkness using controlled remote visual cues (back-lit shapes in opaque buckets aimed at the pool to keep the background dark) while being tracked by an infrared camera and computer. Learning was similar with 2 (AB) or 4 (ABCD) cues and as good as in a fully lit room with many cues (asymptotic escape time t=5–7 s). The ABCD-trained rats were not impaired by removal of any 2 cues (t=7). For AB-trained rats, adding 2 new cues (ABEF) or replacing AB with EF (EF) caused small (t=11) or big disruption (t=20), respectively. By block 2, both groups (ABEF, EF) returned to asymptotic performance. But testing the ABEF rats on block 2 with only EF indicated that EF was learned (t=12) but not as well as when only EF was present (t=5). Thus transfer from a redundant to a minimal cue condition is immediate and easier than vice versa. Theoretical implications are discussed.
Behavioral and Neural Biology, Volume 62, pp 201-209; https://doi.org/10.1016/s0163-1047(05)80018-4
Depending on dose and task requirements, ethanol can have either a facilitative or an impairing influence on learning. Some explanations for this dichotomy have considered ethanol's suppression of behavioral variability and processing of incidental stimuli (e.g., context). The present study examined the effect of ethanol on context and conditioned stimulus (CS) learning in the preweanling rat. To assess state-dependent effects, a drug dissociation design was used. Learning to both context and CS were analyzed within each dose of ethanol (0, 1.2, 1.6, or 2.0 g/kg) and a trend analysis was conducted to determine dose-response relationships as a function of train-test state. The 1.2 g/kg dose of ethanol did not affect conditioning to either the context or the CS. A 1.6 g/kg dose tended to disrupt context, but not CS, conditioning. The influence of 2.0 g/kg ethanol depended on train-test conditions. Ethanol administration prior to training resulted in the stronger impairment of CS learning while context conditioning was most disrupted if ethanol was given only prior to testing. The results suggest that ethanol selectively attenuates processing of stimuli, possibly dependent on relative saliency at the time of testing.
Behavioral and Neural Biology, Volume 62, pp 210-223; https://doi.org/10.1016/s0163-1047(05)80019-6
Stimulus-induced arousal (sensitization) of a component of appetitive behavior in honeybees, the proboscis extension reflex (PER), was used to investigate different aspects of nonassociative memory. The sensitizing stimulus (sucrose solution) was applied to one antenna, as a compound to antenna and proboscis, and to the proboscis. Stimulus duration was either 1 or 3 s. Sensitization was evaluated by monitoring PER toward an odor before (pretest) and after (test) application of the sensitizing stimulus. All responses were quantified by recording from muscle M17 which represents the motor program of PER. Data were analyzed by determining (1) the response probability to the odor and (2) the response strength by determing the number of M17-spikes and the percentage of licking bees per trial. The analysis of the response probability led to two main results: the proportion of animals responding to the test odor depended on stimulus site, and, dependent on stimulus site, a longer application of the sensitizing stimulus resulted in different sensitization rates. The strength of the sensitized response, however, did not correspond to the probability, with which it was elicited, but rather to the strength of the response to the sensitizing stimulus itself. Furthermore, the three groups were not equally affected by the short and long stimulation. The analysis of the proportion of animals licking during test confirmed the data obtained using the number of muscle spikes as a measure of response strength. These results suggest an internal evaluation of the sensitizing stimulus depending on its quality and intensity. The differential affects after antennal and proboscis stimulation may be realized via an arousal system which has two independent functions, a permissive one modulating response probability and one modulating response strength. The permissive function of arousal may be regulated via an intervening inhibitory system whose activation critically depends on the functional significance of the arousing stimulus. The content of this short-term form of memory may be interpreted as an expectation for food which is regulated according to experienced consequences.
Behavioral and Neural Biology, Volume 62, pp 230-236; https://doi.org/10.1016/s0163-1047(05)80021-4
Gonadectomized male and female Sprague-Dawley rats, given estradiol (E2) via sc Silastic capsules that generated proestrus levels of hormones, were tested for spatial memory performance on an 8-arm radial maze. Performance of males, with or without E2, exceeded that of females, with or without E2, for choice accuracy parameters over 20 trials. In addition, males reached criterion earlier than females (6 vs 11 trials). There were no significant effects of E2 on performance of either sex. When a 1-h delay was instituted between the 4th and 5th choices, the performance of males remained better than that of the females, and E2 administration was associated with a small, but significant, improvement in performance of the males but not the females. E2 administration to 25-month-old males also did not affect performance in regular trials, but performance was enhanced in trials with delays of 1–3 h after the 4th choice. These results show that estradiol can influence spatial memory performance and suggest that E2 may be beneficial for age and/or disease-related memory impairments.
Behavioral and Neural Biology, Volume 62, pp 253-258; https://doi.org/10.1016/s0163-1047(05)80024-x
This experiment investigated the effect of intraseptal administration of the GABAergic antagonist bicuculline methiodide on benzodiazepine-induced amnesia. Male Sprague-Dawley rats were implanted with cannula aimed at the medial septal area and allowed to recover for 1 week. Ten minutes prior to training in a continuous multiple trial inhibitory avoidance task, buffer solution or bicuculline methiodide (56 or 100 pmol/0.5 μl) was injected into the medial septal area. This infusion was immediately followed by systemic (ip) administration of saline or midazolam (1.5 or 3.0 mg/kg). In comparison with saline controls, animals given the higher dose of midazolam (3.0 mg/kg), required more trials to reach acquisition criterion (remaining in the starting chamber for 100 s). This midazolam-induced acquisition deficit was blocked by an intraseptal infusion of bicuculline methiodide (100 pmol). On a 48-h retention test the performance of animals given either dose of midazolam was significantly impaired relative to vehicle controls: Furthermore, although intraseptal infusion of bicuculline methiodide prior to systemic injection of midazolam blocked the midazolam-induced acquisition impairment, bicuculline did not block the midazolam-induced retention impairment. These results suggest that although the medial septal area may be involved in midazolam-induced acquisition deficits, this area is not a critical site of action for benzodiazepine-induced effects on inhibitory avoidance retention.