Role of fear in mediating shuttle escape learning deficit produced by inescapable shock

The relation between the shuttlebox escape deficit produced by prior inescapable shock (IS) and fear during shuttlebox testing as assessed by freezing was investigated in rats. IS rats learned to escape poorly and were more fearful than either escapably shocked subjects or controls, both before and after receiving shock in the shuttlebox. However, fear and poor escape performance did not covary with the manipulation of variables designed to modulate the amount of fear and the occurrence of the escape deficit. A 72-hr interval between IS and testing eliminated the escape deficit but did not reduce preshock freezing. Diazepam before testing reduced both preshock and postshock fear in the shuttlebox but had no effect on the escape deficit. Naltrexone had no effect on fear but eliminated the escape deficit. This independence of outcomes suggests that the shuttlebox escape deficit is not caused by high levels of fear in IS subjects.     

How to study the kinetic depth effect experimentally

Sperling, Landy, Dosher, and Perkins (1989) proposed an objective 3D shape identification task with 2D artifactual cues removed and with full feedback (FB) to the subjects to measure KDE and to circumvent algorithmically equivalent KDE-alternative computations and artifactual non-KDE processing. (1) The 2D velocity flow-field was necessary and sufficient for true KDE. (2) Only the first-order (Fourier-based) perceptual motion system could solve our task because the second-order (rectifying) system could not simultaneously process more than two locations. (3) To ensure first-order motion processing, KDE tasks must require simultaneous processing at more than two locations. (4) Practice with FB is essential to measure ultimate capacity (aptitude) and, thereby, to enable comparisons with ideal observers. Experiments without FB measure ecological achievement--the ability of subjects to extrapolate their past experience to the current stimuli.     

Cholinergic-dopaminergic interactions in cognitive performance

Both acetylcholinergic (ACh) and dopaminergic (DA) systems have been found to be crucial for the maintenance of accurate cognitive performance. In a series of studies examining those aspects of cognitive function revealed by the radial-arm maze, we have found that these two neurotransmitter systems interact in a complex fashion. Choice accuracy deficits in the radial-arm maze can be induced by blockade of either muscarinic- or nicotinic-ACh receptors. The choice accuracy deficit induced by blockade of muscarinic receptors with scopolamine can be reversed by the DA receptor blocker, haloperidol. The specific DA D1 blocker SCH 23390 also has this effect, whereas the specific D2 blocker raclopride does not, implying that it is D1 blockade that is critical for reversing the scopolamine effect. On the other hand, the choice accuracy deficit induced by nicotinic blockade with mecamylamine is potentiated by haloperidol. This effect is also seen with the D2 antagonist raclopride, but not with the D1 antagonist SCH 23390, implying that it is the D2 receptor which is important for the potentiation of the mecamylamine effect. The relevance of the D2 receptor for nicotinic actions on cognitive function is emphasized by the finding that the selective D2 agonist LY 171555 reverses the choice accuracy deficit caused by mecamylamine. Nicotinic and muscarinic blockade are synergistic in the deficit they produce. Antagonist doses subthreshold when given alone produce a pronounced impairment when given together. This latter deficit can be reversed by the D2 agonist LY 171555. These studies have outlined the complex nature of ACh-DA interactions with regard to cognitive function. Possible neural circuits for these interactions are discussed. The effectiveness of these selective DA treatments in reversing cognitive deficits due to ACh underactivation suggests a novel approach to treating cognitive dysfunction in syndromes such as Alzheimer's disease.     

Ethanol-mediated taste aversions and state-dependency in preweanling (16-day-old) rats

Requirements for conditioning of an ethanol-mediated taste aversion in 16-day-old rat pups were examined. Experiment 1 demonstrated that preweanling rats are capable of acquiring, in two trials, an aversion to a 15% sucrose solution when followed by intragastric intubation of a 1.2 g/kg dose of 17% v/v ethanol, but not when followed by a 0.4 g/kg dose. Comparison was with control animals given sucrose followed by an equivalent volume isocaloric Half and Half. When the 0.4 g/kg dose of ethanol preceded sucrose presentation by 30 min (Experiment 2), the aversion was learned, suggesting that the effective delay between the sucrose and the critical consequences of the ethanol had been too long with the former procedure. Expression of the sucrose aversion required, however, the reinstatement of the context of intoxication--state-dependent retention. Finally, the results of Experiment 3B indicated that, in addition to the association between the sucrose and the aversive consequences of alcohol intoxication, the orosensory cues resulting from alcohol's direct elimination, via such processes as respiration and salivation, became associated with the appetitive properties of the sucrose. This was evidenced by a conditioned increase in preference for ethanol odor. Possible age-related differences in the ability to associate stimuli with alcohol's unconditioned consequences, and in state dependency are discussed.     

Glucose and physostigmine effects on morphine- and amphetamine-induced increases in locomotor activity in mice

Recent findings indicate that glucose antagonizes several behavioral effects of cholinergic antagonists and augments those of cholinergic agonists. For example, scopolamine elicits increased locomotor activity, an action which is attenuated by glucose and by combined treatment with glucose and physostigmine at doses which are individually without effect. Opiate and catecholamine agonists, such as morphine and amphetamine, also elicit hyperactivity. The present study examined interactions of glucose and physostigmine with morphine- and amphetamine-induced hyperactivity. Mice received saline, morphine (10 mg/kg), or amphetamine (1 mg/kg) 50 min prior to testing, followed by saline, physostigmine (0.01, 0.05, 0.1, or 0.2 mg/kg), or glucose (10, 50, 100, or 500 mg/kg) administered 20 min prior to activity testing in an open field. Physostigmine significantly attenuated both morphine- and amphetamine-induced increases in activity, but higher doses were required to attenuate the effects of amphetamine. Like physostigmine, glucose significantly attenuated morphine-induced activity levels, but unlike physostigmine, glucose did not attenuate amphetamine-induced activity. Thus, the behavioral effects of morphine were more susceptible to modification by physostigmine and glucose than were the effects of amphetamine. The attenuation of morphine-induced hyperactivity demonstrates a similarity between glucose and cholinergic agonists, and also indicates that glucose may inhibit, directly or indirectly, opiate functions. More generally, these findings add to the evidence that circulating glucose levels selectively influence a growing list of behavioral and neurobiological functions.     

Rule abstraction, item memory, and chunking in rat serial-pattern tracking

Two studies used a stimulus tracking paradigm to test whether rats are sensitive to the rule-based formal properties of structured serial patterns. Hooded rats tracked 16-element patterns of flashing lights by pressing levers under an array of 6 indicator lights. In Experiment 1, rats tracked a pattern similar to one previously used with human subjects and yielded remarkably similar results. More errors and response omissions occurred at boundaries of structural "chunks" than within chunks, and errors often reflected anticipation of the next chunk or extrapolation of the preceding chunk. In Experiment 2, temporal "phrasing" cues encouraged different groups to encode a pattern as a series of either "runs" or "trills." Differential placement of pauses induced rats to encode different rule-based representations of the pattern. Results indicate that under appropriate conditions rats may encode a representation of formal structure when they learn organized response patterns.     

Performance objectives in the stance phase of human pathological walking

Permanent disruption of aspects of a highly learned skill such as walking force adaptations to occur to the movement. Firstly the body must determine what factors will guide the formation of the new walking pattern, and secondly that new movement pattern must be learned. Frequently the questionable assumption is made that the performance objectives of the new skill are the same as the original. This work used non-linear optimal control and multiple segment simulation to evaluate the ability of several possible objective functions to predict pathological walking patterns. These predictions were then also compared to the results from normal walking. Preliminary results indicate the performance objectives of pathological gaits may be quite different from those of normals. Some support was also provided for the existence of simultaneous multiple performance objectives in complex movements.     

Risk perceptions and participation in colorectal cancer screening

Compared individuals at high versus average risk for colorectal cancer (CRC) with respect to factors they cited as affecting their risk of developing CRC. We also examined the relationship of these risk-factor perceptions to perceived susceptibility and participation in a CRC screening test. All individuals in the high-risk group were informed that, as a sibling of someone with CRC, they were more likely to get this cancer themselves. We found minimal differences among siblings with respect to perceived susceptibility. Further, although high-risk siblings were more likely to participate in screening, only 20.2% cited heredity as a risk-increasing factor, and, among these siblings, there was no relationship between screening participation and the citation of any specific risk factors, including heredity. These findings demonstrate the need for more research examining how high-risk individuals process risk-relevant information and the effect of this information on health behavior.     

How far can attraction-caused misalignment account for the Morinaga misalignment effect?

Summary When a line (the pointer) is collinear with a dot, the addition of a second line (the induction line) contiguous with the dot or near it may cause the pointer to appear to be collinear with a point further along or nearer to the induction line. The geometrical relations upon which this effect, which we call attraction-caused misalignment, depends have been studied with the Obonai and Wundt-Loeb (Hotopf, 1981; Hotopf & Brown, 1988) figures. Drawing upon the studies of misalignment in the Morinaga figure carried out by Restle (1976), Day, Bellamy, and Norman (1983), and Day and Kasperczyk (1985), as well as upon two new experiments, we show that misalignment in the Morinaga figure is also attraction-caused misalignment, as previously defined. We conclude with a discussion of a number of theories that aim at accounting for attraction misalignment.