Cognition and metacognition at extreme altitudes on Mount Everest

The FACTRETRIEVAL2 test battery, which assesses both retrieval of general information from memory and metacognition about that retrieval, was administered to people before and after a recent expedition to Mount Everest and at extreme altitudes above 6,400 m (higher than any mountain in North America or Europe). The major findings were as follows: First, the same extreme altitudes already known to impair learning did not affect either accuracy or latency of retrieval, and this robustness of retrieval occurred for both recall and forced-choice recognition. Second, extreme altitude did affect metacognition: The climbers showed a decline in their feeling of knowing both while at extreme altitude and after returning to Kathmandu (i.e., both an effect and an aftereffect of extreme altitude). Third, extreme altitude had different effects than alcohol intoxication (previously assessed by Nelson. McSpadden, Fromme, & Marlatt, 1986). Alcohol intoxication affected retrieval without affecting metacognition, whereas extreme altitude affected metacognition without affecting retrieval; this different pattern for extreme altitude versus alcohol intoxication implies that (a) hypoxia does not always yield the same outcome as alcohol intoxication and (b) neither retrieval nor metacognition is strictly more sensitive than the other for detecting changes in independent variables.     

Evolutionary psychology,biology, and cultural evolution

Evolutionary approaches to behavior, so far from indicating that human behavioral patterns must be universal and wired, actually provide us with good reasons for expecting cultural diversity and good tools for showing how it might develop. Even gender-role related behavior may be very plastic. Highly macho male behavior may be an adaptation to dangerous ecological and economic constraints. Similarly, homicide rates differ massively from culture to culture and may be under the control of specificable ecological and economic constraints.Adapted from a symposium talk given at the annual meeting of the Society for Experimental Social Psychology, October 13, 1990, Buffalo, New York. David Buss, Nancy Cantor, and Claude Steele made helpful comments on earlier versions of this paper.     

The ontogeny of hemispheric specialization: some old hypotheses revisited

This paper re-examines two hypotheses on the ontogeny of hemispheric specialization that long ago fell into disfavor in neuropsychology. It is argued that these hypotheses, equipotentiality and progressive lateralization, may have suffered from misinterpretation that fostered premature acceptance of the developmental invariance view of hemispheric specialization. An alternative view is presented that incorporates both hypotheses within a neurodevelopmental context using anatomical (postmortem) and childhood aphasia data.     

Predicate-argument structure as a link between linguistic and nonlinguistic representations

We present a study wherein a severe Broca's aphasic patient was trained to learn symbols representing both pure transitive and dative predicates--predicates differing in argument structure--in a visually based artificial language (c-ViC). We found a decrease in performance when two symbols, rather than one, were used to depict these "verbs." However, this decrease in performance was more pronounced for symbols representing pure transitive verbs--those that allow only one argument structure--than for symbols representing dative verbs--those that allow two different argument structures. Also, dative "verbs" yielded better performance when they were inserted in more complex, three-argument "sentences" than when they were inserted in two-argument "sentences." The opposite pattern was found for pure transitives. These results are discussed in terms of our claim that argument structure serves as a point of connection between linguistic information and non-linguistic visual information and in terms of the possibility that argument structure entries are shaped by the form in which visual information is parsed.     

Range and regression, loudness scales, and loudness processing: toward a context-bound psychophysics

How does context affect basic processes of sensory integration and the implicit psychophysical scales that underlie those processes? Five experiments examined how stimulus range and response regression determine characteristics of (a) psychophysical scales for loudness and (b) 3 kinds of intensity summation: binaural loudness summation, summation of loudness between tones widely spaced in frequency, and temporal loudness summation. Context affected the overt loudness scales in that smaller power-function exponents characterized larger versus smaller range of stimulation and characterized magnitude estimation versus magnitude production. More important, however, context simultaneously affected the degree of loudness integration as measured in terms of matching stimulus levels. Thus, stimulus range and scaling procedure influence not only overt response scales, but measures of underlying intensity processing.     

Benzodiazepine receptor ligand influences on acquisition: suggestion of an endogenous modulatory mechanism mediated by benzodiazepine receptors

In rats, pretraining ip administration of the central benzodiazepine receptor antagonist, flumazenil (5.0 mg/kg), or of the inverse agonist, n-butyl-beta-carboline-3-carboxylate (BCCB) (0.2 or 0.5 mg/kg), facilitated retention of a step-down inhibitory avoidance task; the central agonists, clonazepam and diazepam (0.4 or 1.0 mg/kg), had an opposite effect, and the peripheral agonist, 4'-chlordiazepam (1.25 or 6.25 mg/kg), was without effect. Pre- but not post-training flumazenil (2.0 mg/kg) blocked the effect of BCCB (0.5 mg/kg), clonazepam (1.0 mg/kg), or diazepam (1.0 mg/kg) given also pretraining. The post-training administration of all of these drugs had no effect on retention of the avoidance task. Flumazenil (5.0 mg/kg) and BCCB (0.5 mg/kg), given before training, enhanced retention test performance of habituation to a buzzer but not of habituation to an open field. In the three tasks studied, none of the drugs used had any appreciable effect on training session parameters. These results suggest that there is an endogenous mechanism mediated by benzodiazepine agonists, sensitive to inverse agonists, that normally down-regulates acquisition of certain behaviors; this mechanism becomes activated only when the tasks involve or occur with a certain degree of stress or anxiety (i.e., inhibitory avoidance or habituation to the buzzer) and not in less stressful or anxiogenic tasks (i.e., habituation to an open field).     

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.