Expression of Fos and Jun Proteins Following Passive Avoidance Training in the Day-Old Chick

It has been shown previously that the immediate-early genes, c-fos and c-jun mRNA are induced in the 1-day-old chick forebrain after one-trial passive avoidance training in which chicks learn to avoid pecking at a bitter-tasting bead. Here, we have studied the expression of their proteins using antibodies to Fos and Jun. Western blotting disclosed two immunoreactive bands for the anti-Fos antibody (47 and 54 kD) and two immunoreactive bands for the anti-Jun antibody (39 and 54 kD). Two hours post-training there was an increase in the number of Fos-positive stained nuclei in right intermediate medial hyperstriatum ventrale (IMHV) (P<0.01), left IMHV (P<0.05), right lobus parolfactorius (LPO) (P<0.025) and left LPO (P<0.05) of birds trained on the bitter bead compared with controls that had pecked a water-coated bead. Staining for Jun protein was significantly greater in the right LPO of trained chicks (P<0.01). Other forebrain regions showed no increase over quiet control levels. The findings are discussed in the context of the cascade of events involved in passive avoidance memory consolidation in the day-old chick.     

Emotional memory formation is enhanced across sleep intervals with high amounts of rapid eye movement sleep

Recent studies indicated a selective activation during rapid eye movement (REM) sleep of the amygdala known to play a decisive role in the processing of emotional stimuli. This study compared memory retention of emotional versus neutral text material over intervals covering either early sleep known to be dominated by nonREM slow wave sleep (SWS) or late sleep, in which REM sleep is dominant. Two groups of men were tested across 3-h periods of early and late sleep (sleep group) or corresponding retention intervals filled with wakefulness (wake group). Sleep was recorded polysomnographically. Cortisol concentrations in saliva were monitored at acquisition and retrieval testing. As expected, the amount of REM sleep was about three times greater during late than during early retention sleep, whereas a reversed pattern was observed for SWS distribution (P<0.001). Sleep improved retention, compared with the effects of wake intervals (P<0.02). However, this effect was substantial only in the late night (P<0.005), during which retention was generally worse than during the early night (P<0.02). Late sleep particularly enhanced memory for emotional texts. This effect was highly significant in comparison with memory for neutral texts (P<0.01) and in comparison with memory after late and early wake intervals (P<0.001). Cortisol concentration differed between early and late retention intervals but not between sleep and wake conditions. Results are consonant with a supportive function of REM sleep predominating late sleep for the formation of emotional memory in humans.     

Chronic, severe hypertension does not impair spatial learning and memory in Sprague-Dawley rats

This study tested the hypothesis that long-term hypertension impairs spatial learning and memory in rats. In 6-wk-old Sprague-Dawley rats, chronic hypertension was induced by placing one of three sizes of stainless steel clips around the descending aorta (above the renal artery), resulting in a 20–80-mm Hg increase of arterial pressure in all arteries above the clip, that is, the upper trunk and head. Ten months later, the rats were tested for 5 d in a repeated-acquisition water maze task, and on the fifth day, they were tested in a probe trial; that is, there was no escape platform present. At the end of the testing period, the nonsurgical and sham control groups had similar final escape latencies (16±4 sec and 23±9 sec, respectively) that were not significantly different from those of the three hypertensive groups. Rats with mild hypertension (140–160 mm Hg) had a final escape latency of 25±6 sec, whereas severely hypertensive rats (170–199 mm Hg) had a final escape latency of 21±7 sec and extremely hypertensive rats (>200 Hg) had a final escape latency of 19±5 sec. All five groups also displayed a similar preference for the correct quadrant in the probe trial. Together, these data suggest that sustained, severe hypertension for over 10 mo is not sufficient to impair spatial learning and memory deficits in otherwise normal rats.     

Two Modulatory Inputs Exert Reciprocal Reinforcing Effects on Synaptic Input of Premotor Interneurons for Withdrawal in Terrestrial Snails

A cluster of serotonergic cells in the rostral part of pedal ganglia of the terrestrial snail Helix lucorum was shown previously to participate in modulation of withdrawal behavior, and to be necessary for elaboration of aversive withdrawal conditioning in intact snails. In the present experiments local extracellular stimulation of the serotonergic cells elicited a pairing-specific increase (difference between paired and explicitly unpaired sessions was significant, P<0.01) of synaptic responses in the premotor interneurons involved in withdrawal to paired nerve stimulation. Intracellular stimulation of only one Pd4 cell from the pedal group of serotonergic neurons increased (P<0.05) synaptic responses to contingent test nerve stimulation significantly in the same premotor interneurons for 2–3 hr.     

Reduced delayed-rectifier K+ current in the learning mutant rutabaga

In the Drosophila mutant rutabaga, short-term memory is deficient and intracellular cyclic adenosine monophosphate (cAMP) concentration is reduced. We characterized the delayed-rectifier potassium current (IK_DR) in rutabaga as compared with the wild-type. The conventional whole-cell patch-clamp technique was applied to cultured Drosophila neurons derived from embryonic neuroblasts. IK_DR was smaller in rutabaga (368±11 pA) than in wild-type (541±14 pA) neurons, measured in a Ca²⁺-free solution. IK_DR was clearly activated at ~0 mV in the two genotypes. IK_DR typically reached its peak within 10–20 msec after the start of the pulse (60 mV). There was no difference in inactivation of IK_DR for wild-type (14±3%) and rutabaga (19±3%). After application of 10 mM TEA, in wild-type, IK_DR was reduced by 46±5%, whereas in rutabaga, IK_DR was reduced by 28±3%. Our results suggest that IK_DR is carried by two different types of channels, one which is TEA-sensitive, whereas the other is TEA-insensitive. Apparently, the TEA-sensitive channel is less expressed in rutabaga neurons than in wild-type neurons. Conceivably, altered neuronal excitability in the rutabaga mutant could disrupt the processing of neural signals necessary for learning and memory.     

CA1 Long-Term Potentiation Is Diminished but Present in Hippocampal Slices from α-CaMKII Mutant Mice

Previous work has shown that mice missing the α-isoform of calcium–calmodulin-dependent protein kinase II (α-CaMKII) have a deficiency in CA1 hippocampal long-term potentiation (LTP). Follow-up studies on subsequent generations of these mutant mice in a novel inbred background by our laboratories have shown that whereas a deficiency in CA1 LTP is still present in α-CaMKII mutant mice, it is different both quantitatively and qualitatively from the deficiency first described. Mice of a mixed 129SvOla/SvJ;BALB/c;C57Bl/6 background derived from brother/sister mating of the α-CaMKII mutant line through multiple generations (>10) were produced by use of in vitro fertilization. Although LTP at 60 min post-tetanus was clearly deficient in these (−/−) α-CaMKII mice (42.6%, n=33) compared with (+/+) α-CaMKII control animals (81.7%, n=17), α-CaMKII mutant mice did show a significant level of LTP. The amount of LTP observed in α-CaMKII mutants was normally distributed, blocked by APV (2.7%, n=8), and did not correlate with age. Although this supports a role for α-CaMKII in CA1 LTP, it also suggests that a form of α-CaMKII-independent LTP is present in mice that could be dependent on another kinase, such as the β-isoform of CaMKII. A significant difference in input/output curves was also observed between (−/−) α-CaMKII and (+/+) α-CaMKII animals, suggesting that differences in synaptic transmission may be contributing to the LTP deficit in mutant mice. However, tetani of increasing frequency (50, 100, and 200 Hz) did not reveal a higher threshold for potentiation in (−/−) α-CaMKII mice compared with (+/+) α-CaMKII controls.     

Hippocampal Activations during Repetitive Learning and Recall of Geometric Patterns

Hippocampal activation is required for episodic memory. Encoding and retrieval of novel and memorable items have been related to different locations in the hippocampus; however, the data remain ambiguous. The application of a newly designed keyboard allowed investigation of brain activation during encoding and free immediate and delayed recall with functional magnetic resonance imaging (fMRI) in young healthy controls (n=12). Because of the repetitive learning and recall conditions, an individual learning gradient was used to contrast neural activity at different individual levels of novelty. During learning, subjects were asked to memorize 10 geometric patterns requiring the establishment of intra-item associations for memorization. After learning, subjects were asked to recall the items actively via the keyboard. Learning and recall were alternated five times. Delayed recall was scanned about 15 min after the fifth immediate recall condition without subjects having seen the items again. Left-sided anterior hippocampal activity was observed during conditions of initial learning as well as maximum recall. Neural activity during delayed recall did not reveal hippocampal responses and was characterized by a transition of neural activity from occipitoparietal regions to bilateral temporal cortices. We conclude that both lateralization and segregation depend on the specific relational characteristics of the stimuli requiring establishment of intra-item associations for encoding as well as retrieval. The absence of hippocampal activation during delayed recall together with the increase of lateral temporal involvement possibly corresponds with an emerging transition from episodic to long-term memory.     

SENSITIVITY OF CONDITIONAL-DISCRIMINATION PERFORMANCE TO WITHIN-SESSION VARIATION OF REINFORCER FREQUENCY

The present experiment developed a methodology for assessing sensitivity of conditional-discrimination performance to within-session variation of reinforcer frequency. Four pigeons responded under a multiple schedule of matching-to-sample components in which the ratio of reinforcers for correct S₁ and S₂ responses was varied across components within session. Initially, five components, each arranging a different reinforcer-frequency ratio (from 19 to 91), were presented randomly within a session. Under this condition, sensitivity to reinforcer frequency was low. Sensitivity failed to improve after extended exposure to this condition, and under a condition in which only three reinforcer-frequency ratios were varied within session. In a later condition, three reinforcer-frequency ratios were varied within session, but the reinforcer-frequency ratio in effect was differentially signaled within each component. Under this condition, values of sensitivity were similar to those traditionally obtained when reinforcer-frequency ratios for correct responses are varied across conditions. The effects of signaled vs. unsignaled reinforcer-frequency ratios were replicated in two subsequent conditions. The present procedure could provide a practical alternative to parametric variation of reinforcer frequency across conditions and may be useful in characterizing the effects of a variety of manipulations on steady-state sensitivity to reinforcer frequency.     

Effects of a delay-reinforcement procedure on performance under IRT>t schedules

Water-deprived rats were studied under a compound schedule that prescribed that responses terminating interresponse times (IRTs) greater than a fixed value t₁ (IRT > t₁ component schedule) initiated a delay of reinforcement interval t₂, at the end of which water was presented if the subject did not respond ( > t₂ component schedule). If the subject responded before the t₂ interval elapsed, the IRT > t₁ component schedule was re-initiated and water was not presented. The IRT > t₁ and > t₂ component schedules were not differentially correlated with distinctive stimuli. Rate of responding during the IRT > t₁ component decreased as a function of the value of t₂. The magnitude of the decreases in response rate appeared to be proportional to the subject's rate under the IRT > t schedule with no delay of reinforcement (t₂ = 0 sec). The effects were independent of the parameter value of the IRT > t₁ component schedule and of the rate of reinforcement. The results suggested that “efficiency” of performance under IRT > t schedules can be increased by appropriately arranging brief delays of reinforcement.     

Blueprints and Recipes: Gendered Metaphors for Genetic Medicine

In the face of documented difficulties in the public understanding of genetics, new metaphors have been suggested. The language of information coding and processing has become deeply entrenched in the public representation of genetics, and some critics have found fault in the blueprint metaphor, a variant of the dominant theme. They have offered the language of the recipe as a preferable metaphor. The metaphors of the blueprint and the recipe are compared in respect to their deterministic implications and other associations. The likelihood of the recipe metaphor framing cognition in more useful ways is called into question.     

Indeterminiertheit,Iterabilität und Intentionalität

In his recent paper Indeterminacy, empiricism, and the first person John R. Searle tries to refute Willard V. O. Quine's famous indeterminacy of translation thesis by arguing that this thesis is in fact areductio ad absurdum of Quine's own linguistic behaviorism. Searle accuses Quine of being (irrationally) antimentalistic and suggests that the absurdity of Quine's thesis might be avoided if a full-fledged intentionality were tolerated in the debate on meaning. — This anti-Quinean approach in some respects reminds of the improbable debate between Searle and Jacques Derrida ten years ago, when Derrida had split and deferred intentionality by showing that the essential iterability of signs inevitably infects every intentional act with an unremovable non-presence.In this paper it is argued that Searle's attacks on Quine and Derrida have both failed — and that there are structural similarities between these two failures which reveal some interesting parallels between Quine's and Derrida's philosophy.     

Nicotine Produces a Within-Subject Enhancement of Contextual Fear Conditioning in C57BL/6 Mice Independent of Sex

Nicotine enhances learning including contextual fear conditioning. The present study extends previous work on nicotine and conditioned fear to examine the nature of nicotine's enhancement of contextual fear conditioning and sex differences in contextual fear conditioning in C57BL/6 mice using a within-subjects design. Mice were trained by pairing of an auditory stimulus of 80 dB, 6 cps train of broad-band clicks conditioned stimulus (CS) with a 2 sec., 0.35 mA shock unconditioned stimulus (US). Twenty-four hours later mice were tested for freezing in the original context, and one hour later mice were retested in the same context. A 0.5 mg/kg dose of nicotine was given either for three conditions: (1) before training, testing, and retesting; (2) before training and retesting; and (3) before retesting only. The use of a within-subjects design allowed for testing if nicotine would produce state-dependent deficits in contextual fear conditioning. Nicotine did enhance contextual fear conditioning in the groups that received nicotine for both training and testing. Nicotine, however, did not alter freezing when given on training but not testing or testing but not training. No sex differences, however, existed for conditioning or for nicotine's effects on conditioning. These results suggest that nicotine enhanced acquisition and retrieval processes but did not produce state-dependent deficits when administered just for training or just for testing.     

Nicotine produces a within-subject enhancement of contextual fear conditioning in C57BL/6 mice independent of sex

Nicotine enhances learning including contextual fear conditioning. The present study extends previous work on nicotine and conditioned fear to examine the nature of nicotine’s enhancement of contextual fear conditioning and sex differences in contextual fear conditioning in C57BL/6 mice using a within-subjects design. Mice were trained by pairing of an auditory stimulus of 80 dB, 6 cps train of broad-band clicks conditioned stimulus (CS) with a 2 sec., 0.35 mA shock unconditioned stimulus (US). Twenty-four hours later mice were tested for freezing in the original context, and one hour later mice were retested in the same context. A 0.5 mg/kg dose of nicotine was given either for three conditions: (1) before training, testing, and retesting; (2) before training and retesting; and (3) before retesting only. The use of a within-subjects design allowed for testing if nicotine would produce state-dependent deficits in contextual fear conditioning. Nicotine did enhance contextual fear conditioning in the groups that received nicotine for both training and testing. Nicotine, however, did not alter freezing when given on training but not testing or testing but not training. No sex differences, however, existed for conditioning or for nicotine’s effects on conditioning. These results suggest that nicotine enhanced acquisition and retrieval processes but did not produc state-dependent deficits when administered just for training or just for testing.     

Decomposability of the Finitely Generated Free Hoop Residuation Algebra

In this paper we prove that, for n > 1, the n-generated free algebra in any locally finite subvariety of HoRA can be written in a unique nontrivial way as Ł₂ × A′, where A′ is a directly indecomposable algebra in . More precisely, we prove that the unique nontrivial pair of factor congruences of is given by the filters and , where the element is recursively defined from the term introduced by W. H. Cornish. As an additional result we obtain a characterization of minimal irreducible filters of in terms of its coatoms. Presented by Daniele Mundici     

Equivalents for a Quasivariety to be Generated by a Single Structure

We present some equivalent conditions for a quasivariety of structures to be generated by a single structure. The first such condition, called the embedding property was found by A.I. Mal′tsev in [6]. It says that if are nontrivial, then there exists such that A and B are embeddable into C. One of our equivalent conditions states that the set of quasi-identities valid in is closed under a certain Gentzen type rule which is due to J. Łoś and R. Suszko [5]. Presented by Jacek Malinowski     

Beta2 subunit containing acetylcholine receptors mediate nicotine withdrawal deficits in the acquisition of contextual fear conditioning

Acute nicotine enhances contextual fear conditioning, whereas withdrawal from chronic nicotine produces impairments. However, the nicotinic acetylcholine receptors (nAChR) that are involved in nicotine withdrawal deficits in contextual fear conditioning are unknown. The present study used genetic and pharmacological techniques to investigate the nAChR subtype(s) involved in the effects of nicotine withdrawal on contextual fear conditioning. beta2 or alpha 7 nAChR subunit knockout (KO) and corresponding wild-type (WT) mice were withdrawn from 12 days of chronic nicotine treatment (6.3mg/kg/day), and trained with 2 conditioned stimulus (CS; 85 dB white noise)--unconditioned stimulus (US; 0.57 mA footshock) pairings on day 13. On day 14, mice were tested for contextual and cued freezing. beta2 KO mice did not show nicotine withdrawal-related deficits in contextual fear conditioning, in contrast to WT mice and alpha 7 KO mice. A follow-up study investigated if nicotine withdrawal disrupts acquisition or recall of contextual fear conditioning. The high affinity nAChR antagonist dihydro-beta-erythroidine (DH beta E; 3mg/kg) was administered prior to training or testing to precipitate withdrawal in chronic nicotine-treated C57BL/6 mice. Deficits in contextual fear conditioning were observed in chronic nicotine-treated mice when DH beta E was administered prior to training, but not when administered at testing. These results indicate that beta2-containing nAChRs, such as the alpha 4 beta 2 receptor, mediate nicotine withdrawal deficits in contextual fear conditioning. In addition, nicotine withdrawal selectively affects acquisition but not recall or expression of the learned response.     

Three views of demonstrative reference

Three views of demonstrative reference are examined: contextual, intentional, and quasi-intentional. According to the first, such reference is determined entirely by certain publicly accessible features of the context. According to the second, speaker intentions are criterial in demonstrative reference. And according to the third, both contextual features and intentions come into play in the determination of demonstrative reference. The first two views (both of which enjoy current popularity) are rejected as implausible; the third (originally proposed by Kaplan in Dthat) is argued to be highly plausible.     

Nicotine enhances contextual fear conditioning in C57BL/6J mice at 1 and 7 days post-training

Nicotine has been demonstrated to enhance learning processes. The present experiments extend these results to examine the effects of nicotine on acquisition and consolidation of contextual and cued fear conditioning, and the duration of nicotine's enhancement of conditioned fear. C57BL/6 mice were trained with two pairings of an auditory CS and a foot shock US. Multiple doses of nicotine were given before or immediately after training and on testing day (0.0, 0.050, 0.125, 0.250, and 0.375 mg/kg, i.p). Freezing to both the context and auditory CS was measured 24h after training and again 1 week after training. Mice did not receive nicotine for the 1-week retest. Nicotine (0.125 and 0.250 mg/kg) given on both training and testing days enhanced freezing to the context at 24h. In addition, elevated freezing to the context was seen 1 week post-training in mice previously treated with 0.125 and 0.250 mg/kg nicotine. Thus, nicotine-treated mice did show elevated levels of freezing when retested 1 week later, even though no nicotine was administered at the 1-week retest. Mice that received nicotine on training day or testing day only and mice that received nicotine with mecamylamine, a nicotinic receptor antagonist, were not different from saline-treated mice. In addition, post-training administration of nicotine did not enhance fear conditioning. The present results indicate that nicotine enhancement of contextual fear conditioning depends on administration of nicotine on training and test days but results in a long-lasting enhancement of memories of contextual fear conditioning that remains in the absence of nicotine.