Behavioral and neural biology最新文献

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.

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.

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.

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.

It is well-established that administration of moderate doses of the adrenal catecholamines epinephrine or norepinephrine shortly after training results in the enhancement of later retention performance in laboratory animals. these substances, released endogenously as a result of arousal, are thought to modulate memory processes by stimulating peripheral receptors that send neural messages to the brain, thus altering the memory storage process. The applicability of this hypothesis to the modulation of memory processes in humans was tested in this experiment by using elderly subjects who were chronically taking beta-receptor antagonist medications to control hypertension. A moderate level of muscle-tension-induced arousal was produced by having subjects squeeze a hand dynamometer during the initial storage and recall of highlighted words in short 200-word paragraphs. Twenty young normal individuals, 22 normotensive elderly subjects, 21 elderly subjects taking either calcium-channel blockers or angiotensin-converting enzyme inhibitors to control hypertension, and 21 elderly subjects taking beta-blocker antihypertensive medications served as subjects. The young subjects, normal elderly subjects, and those taking non-beta-blocker medications all showed enhanced long-term recognition performance as a result of the arousal manipulation. However, those subjecs chronically taking beta-receptor-antagonist medications showed no enhancement of memory. These findings provide support for the hypothesis that physiological arousal is an important modulator of memory and that adrenal catecholamine, systems are likely to mediate this effect. Further, this study indicates that elderly individuals taking beta-blocker medications may be less able to benefit from the normal memory modulating effects of arousal. Finally, these findings suggest that similar mechanisms modulate both declarative verbal memory in humans and conditioned avoidance learning in laboratory animals.

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.

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.