Biased responding: a case series demonstrating a relationship between somatic symptoms and impaired recognition memory performance for traumatic brain injured individuals.

Biased responding on the Sternberg Recognition Memory Test was observed in four patients with traumatic brain injury. None of these individuals met the Diagnostic and Statistical Manual's (DSM-IV) criteria for malingering. Individual recognition memory scores were high shortly after injury, declined to chance or below at the 6- and 12-month evaluations, and then showed substantial recovery by the 24-month evaluation. Recall memory performance actually declined slightly across this same 2-year period. Recognition memory scores were related to the extent to which the patients endorsed somatic items on the Hamilton Rating Scale for Depression (HAM-D). Poor performance was associated with high somatic scores. The relationship between memory and somatic scores on the HAM-D in this case series suggests that unconscious processes can influence memory performance and, because of this, that clinicians should not use such performance as a primary indicator of malingering. More importantly, biased responding and actual memory deficits may coexist. This is indicated in the current cases by the failure of recall memory to improve during the 2 years these patients were followed.

Post-traumatic amnesia after closed head injury: a review of the literature and some suggestions for further research.

Post-traumatic amnesia (PTA) is a transient sequela of closed head injury (CHI). The term PTA has been in clinical use for over half a century, and generally refers to the subacute phase of recovery immediately after unconsciousness following CHI. The duration of PTA predicts functional outcome after CHI, but its pathophysiological mechanism is not known. This paper compares current methods of determining the duration of PTA, summarizes reports on neuropsychological deficits in PTA, reviews available data that allow inferences about its mechanism, and suggests methods for further exploration of its pathophysiology.

Effects of long-term restricted feeding on radial maze performance by aged rats.

Rats were fed every other day (EOD) from 3-21 months of age prior to training in an 8-arm radial maze with retention intervals of 0, 1 or 5 hr imposed between the fourth and fifth choices. Their performance was compared to that of another aged group fed ad lib throughout life prior to radial maze training and to 3 month old controls. Rats fed ad lib until training adapted to the maze more slowly than young controls and were impaired in acquiring accurate spatial memory. EOD feeding eliminated age-related differences in the initial rate of adaptation to the radial maze but had no effect on the development of accurate spatial memory at any of the retention intervals. These results indicate that differences in deprivation history are probably not responsible for previous findings that radial maze training early in life prevents the appearance of age-related deficits in accurate spatial memory.

Cholinergic agonists suppress play fighting in juvenile rats.

Previous research has suggested that acetylcholine might activate play fighting in juvenile rats through its actions on central muscarinic receptors. To test this hypothesis we evaluated the effects on play fighting by the muscarinic agonists pilocarpine and arecoline given alone or in combination with the muscarinic antagonists scopolamine or methylscopolamine. Scopolamine, but not methylscopolamine which penetrates the brain poorly, suppressed play as indexed by frequency of pinning. Pilocarpine and arecoline also suppressed pinning at higher doses. Concurrent treatment with various agonist-antagonist dose combinations produced additive rather than counteractive effects. These data do not support the supposition that central muscarinic circuits are involved in the activation of play fighting.

Preserved spatial memory in old rats survives 10 months without training.

Aged rats with extensive prior training on the radial maze retain the capacity for accurate spatial working memory (WM) for at least 3 months without practice. To investigate the temporal limits of this influence of prior experience we compared the reacquisition of spatial WM by a group of experienced 21.5-month-old rats to the original acquisition by naive 3-month-old rats. The aged rats had received 225 radial maze tests between 3 and 11 months of age. Despite 10 months without practice the old rats rapidly reacquired critical performance. Their reacquisition was markedly superior to original learning by the young rats, even when delays as long as 5 h were imposed between the rats' fourth and fifth choices during the daily tests in the eight-arm maze. Additional tests showed that neither young nor old rats employed a response strategy to maintain accurate spatial WM performance. Experience clearly confers long-lived protection against the otherwise deleterious effects of aging on spatial WM, but the mechanism by which this influence arises is unknown.

Blindness and play fighting in juvenile rats.

Play behavior of blinded and sighted juvenile rats was measured using the brief paired-encounter procedure. Dyads of sighted-sighted, blind-blind, or sighted-blind rats were observed in a large or small chamber on alternate days for ages 28 through 43 days. Blinded rats played as frequently as sighted rats regardless of pair composition or chamber size. Vision is not essential for initiating or maintaining play fighting.

Spatial memory in rats: electroconvulsive shock selectively disrupts working memory but spares reference memory.

In two experiments rats were trained until they displayed highly accurate spatial memories when a 4-h delay was imposed between the to-be-remembered event (TBRE) and the retention test in a 12-arm radial maze. If the procedure tested only working memory (WM) electronvulsive shock (ECS) 2 h after the TBRE produced amnesia but ECS immediately after the TBRE was ineffective. If the testing procedure also involved a reference memory (RM) component, ECS degraded WM regardless of whether it was given 0 or 2 h after the TBRE. RM was not affected. With either training procedure administering ECS 2 h before the TBRE was ineffective. Thus, in the radial maze truly old spatial RM was immune to disruption by ECS while more recent WM was vulnerable. Possible explanations of the data are presented.

Scopolamine degrades spatial working memory but spares spatial reference memory: dissimilarity of anticholinergic effect and restriction of distal visual cues.

The influence of the centrally active anticholinergic, scopolamine hydrobromide, on working and reference memory was studied in rats tested in a 12-arm radial maze. Both 0.25 and 0.5 mg/kg doses of the drug increased the number of working memory (WM) errors but had no effect on reference memory (RM) errors. A lower dose (0.125 mg/kg) was ineffective, as was the peripherally active anticholinergic, scopolamine methylbromide (0.5 mg/kg). Some of the behavioral effects of anticholinergics on spatial memory are mimicked by blindness or eliminating distal visual cues. If distal visual cues were more important for maintaining accurate WM than for RM, the selective effect of scopolamine on WM could be easily explained. But surrounding the maze with a curtain to eliminate extramaze cues increased RM errors without significantly increasing WM errors. Thus, the selective effect of anticholinergies on spatial memory in the radial maze is qualitatively different from the effect of restricting distal visual cues and must arise from some other action of the drug.

Preservation of accurate spatial memory in aged rats.

Male rats were tested in an 8 arm radial maze from 6-26 months of age with 5 hr delay imposed between choices 4 and 5. At 26 months their spatial memory was more accurate than when they were first tested at 6 months and also more accurate than that exhibited by another 5 month old group tested concurrently. However, these old rats acquired a noval spatial habit more slowly than the younger animals. In a subsequent study, we compared the acquisition of accurate spatial memory by rats that were 3 or 21.5 months old at the start of training. Older rats adapted to the maze more slowly and required more sessions to achieve criterion with no delay imposed during the test. There was no reliable difference in acquisition when a 1 hr delay was imposed between choices 4 and 5, but the old rats learned more slowly with a 5 hr delay. On memory tests after criterion performance had been achieved, the older rats performed as well as the younger animals at all delay intervals. Aged rats are deficient in acquiring the skills required for accurate spatial memory, but once acquired these skills do not deteriorate. The possibility that other "memory" deficits associated with aging might be alleviated by overtraining is discussed.

Amphetamine disrupts both working and reference memories of rats trained in a radial maze.

To assess the effects of amphetamine on working and reference memory rats were trained on a 12-arm radial maze with six arms baited and six arms unbaited until stable performance was achieved. Administration of 2.0 mg/kg d-amphetamine sulfate increased both working and reference memory errors, but only if a 5-min delay was imposed after three successful choices. With no delay this dose had no reliable effect on either working or reference memory. Lower doses (0.5 or 1.0 mg/kg) were ineffective even when a delay was imposed during the test. We suggest that amphetamine heightens arousal, which disrupts accurate retention when the rat's attention to the relevant cues is interrupted, as during a brief delay. Alternative explanations are discussed.

Spatial memory over long retention intervals: nonmemorial factors are not necessary for accurate performance on the radial-arm maze by rats.

A. Markowska, O. Buresová, and J. Bures (1983, Behavioral and Neural Biology, 38, 97-112) argued that the apparent persistence of accurate spatial working memory over delays of several hours arises from the formation of response strategies and the use of olfactory stimuli that develop with extended training at long delays. To test this explanation rats with extensive prior training at long delays were forced to enter the first four arms in a random order. On test days, the maze was rotated 180 degrees during the 2-h retention interval to determine whether the rats were using intramaze or extramaze (i.e., spatial) cues to guide their choices. On both rotation and control days, postdelay choices were spatially guided, averaging over 90% correct. Accurate spatial working memory at long delays is a reproducible phenomenon and does not appear to result from nonmemorial artifacts.

Episodic long-term memory in the rat: effects of hippocampal stimulation.

Rats with electrodes implanted in dorsal hippocampus were trained to perform a delayed spatial matching-to-sample task on a radial arm maze. Subseizure level electrical stimulation of the dorsal hippocampus applied during the study phase disrupted retention of a specific arm when tested at a 20-min delay but had no effects at 1- and 12-min delays. There were no state-dependent or proactive effects of stimulation. Subseizure level stimulation of the hippocampus immediately after the study phase resulted in normal retention. In contrast, seizure level stimulation of the hippocampus applied either during or immediately after the study phase disrupted retention at all three (1, 12, 20 min) retention delays. The data support the interpretation that the hippocampus is involved in the encoding of critical information (spatiotemporal attributes) in long-term working memory, but not short-term memory.

Short-term memory: the role of d-amphetamine.

d-Amphetamine injections produce a dose-dependent disruption of performance within a discrete delayed alternation and a spatial delayed matching-to-sample task. Since d-amphetamine in the doses used had no deleterious effects on discrimination performance (no delay condition), it is suggested that d-amphetamine disrupts neuronal activity representing short-term memory. The data provide support for an independence model of short- and long-term memory.

Short-term memory: the role of the midbrain reticular formation.

Low-intensity electrical stimulation of the midbrain reticular formation (MRF) in rats disrupted retention in a discrete-trail delayed alternation task independent of temporal locus of application of the stimulation. The stimulation did not appear to disrupt a motor set, have rewarding or aversive consequences, alter arousal level significantly, or affect encoding or retrieval processes. It is suggested that MRF stimulation might alter delayed alternation performance via neural and behavioral mechanisms associated with the maintenance of activated memory traces over short periods of time.