bluuebunny/crossref_metadata_2025_split huggingface dataset:
Determination of individual stimulus–response curves in the visual cortex
Authors: Hagenbeek Rogier E. , Rombouts Serge A.R.B. , van Dijk Bob W. , Barkhof Frederik 
Published: October 2002

AbstractActivation in the visual cortex is typically studied using group average changes in an on–off paradigm for a single flicker frequency. We used functional magnetic resonance imaging (fMRI) to characterize the stimulus–response curve in the visual cortex as a function of flicker frequency in individual subjects, using LED goggles with 17 frequency steps between 0 and 30 Hz. Ten healthy young individuals were studied on two different occasions (mean interval; 22 days). In all but one subject, a third‐order polynomial curve could be fitted to the data. From the response curve we calculated the peak response (the frequency where the response amplitude was maximal), the percentage change (relative difference) of the response amplitudes between 8 Hz and the peak frequency, and the average slope of response (towards the peak). On both occasions we could determine a peak response for each subject with small within‐subject variability. The average absolute difference in peak response between both sessions was 1.37 Hz (range, 0.2–4.3 Hz), indicating that the peak frequency is rather stable for a given individual. In conclusion, our study illustrates the ability of fMRI to examine the stimulus–response curve in individual subjects in the visual cortex. Based on our findings, the peak response and the slope of response seem highly reproducible within subjects. A similar analysis of the stimulus–response curve may be applicable to other types of stimuli. Hum. Brain Mapping 17:245–251, 2002. © 2002 Wiley‐Liss, Inc.
Medial temporal lobe activation during context‐dependent relational processes in episodic retrieval: An fMRI study
Authors: Tsukiura Takashi , Fujii Toshikatsu , Takahashi Toshimitsu , Xiao Ruiting , Sugiura Motoaki , Okuda Jiro , Iijima Toshio , Yamadori Atsushi 
Published: October 2002

AbstractPrevious studies have reported that the medial temporal lobe (MTL) structures contribute to the processing of relations among multiple stimuli in episodic encoding. There have been few studies, however, on the episodic retrieval requiring processing of relations among multiple components that was involved in our events. We used functional magnetic resonance imaging (fMRI) to investigate neural activities during the retrieval of relations within an organized episode and the recognition of an episodic component. Healthy, normal participants memorized 50 four‐scene comic strips before fMRI scanning. In the retrieval phase with fMRI scanning, participants were engaged in three tasks: a visual identification (VI) task, a story recall (SR) task, and a picture recognition (PRe) task. In the VI task, participants were asked to judge whether they could identify at least one female character in the two scenes presented vertically. In the SR task, participants were shown the first and last scenes from strips memorized previously and asked to judge whether or not the two scenes were from the same strip. In the PRe task, participants were shown two scenes and asked to judge whether they both belonged to the memorized scenes. The two contrasts of SR with VI and PRe with VI demonstrated some commonly activated areas, such as the bilateral middle frontal gyrus and cerebellum. More importantly, the SR task differentially activated the bilateral parahippocampal gyrus, whereas the PRe task differentially activated right prefrontal areas, including the inferior frontal and precentral gyri. The results suggest that the activity of the MTL structures may be strongly associated with episodic memory retrieval requiring context‐dependent relational processing. Hum. Brain Mapping 17:203–213, 2002. © 2002 Wiley‐Liss, Inc.
Monitoring eye movements during fMRI tasks with echo planar images
Authors: Tregellas Jason R. , Tanabe Jody L. , Miller David E. , Freedman Robert 
Published: October 2002

AbstractVerifying task compliance during functional magnetic resonance imaging (fMRI) experiments is an essential component of experimental design. To date, studies of oculomotor tasks such as smooth pursuit eye movements have either measured task performance outside the magnet and assumed similar performance during functional neuroimaging, or have used MR‐compatible eye movement recording devices, which can be costly and technically difficult to use. We describe a simple method to visualize and quantify eye movements during an imaging experiment using the gradient echo images. We demonstrate that local eye movements will influence whole‐head motion correction procedures, resulting in inaccurate movement parameters and potentially lowering the sensitivity to detect activations. Hum. Brain Mapping 17:238–244, 2002. © 2002 Wiley‐Liss, Inc.
Novelty detection and repetition suppression in a passive picture viewing task: A possible approach for the evaluation of neuropsychiatric disorders
Authors: Jessen Frank , Manka Christoph , Scheef Lukas , Granath Dirk‐Oliver , Schild Hans H. , Heun Reinhard 
Published: October 2002

AbstractThe applicability of functional magnetic resonance imaging (fMRI) in patients with Alzheimer's disease (AD) or schizophrenia is frequently limited by cognitive impairment, which prevents the adequate execution of complex tasks. An experimental design that puts only minor demands on the patients' cognitive ability but engages disease‐relevant brain structures would be of benefit. Novelty detection and repetition suppression are two basic components of memory that might be used to investigate specific brain areas under these conditions. Novelty detection has been related to hippocampal activation increases. Stimulus repetition related activation decreases (suppression) have been observed in the extrastriate cortex and have been related to perceptual priming. Both processes have been examined primarily in neuroimaging studies with complex cognitive tasks. We used event‐related fMRI to investigate novelty‐ and repetition‐related effects in an attended but passive picture‐viewing task in healthy subjects. The differential activation, detected in the novel vs. repeated contrast, was located in the bilateral anterior hippocampus and in bilateral occipital and inferior‐temporal areas. The hippocampal activation is of interest because medial temporal lobe lesions are key features in AD and schizophrenia. The repetition‐related activation decreases in the extrastriate areas are of potential value in investigating the conflicting results regarding perceptual priming impairment in both disorders. Our results indicate that activation of disease‐relevant brain regions under passive task conditions is possible. This might increase the utility of functional imaging in cognitively impaired patients. Hum. Brain Mapping 17:231–237, 2002. © 2002 Wiley‐Liss, Inc.
Activity‐induced changes of spine morphology
Authors: Nikonenko Irina , Jourdain Pascal , Alberi Stefano , Toni Nicolas , Muller Dominique 
Published: October 2002

AbstractSpine morphology has been shown in recent years to exhibit a high degree of plasticity. In developing tissue such as organotypic slice cultures, shape changes in spines as well as reorganization of the postsynaptic density (PSD) occur within minutes. Furthermore, several studies have shown that these and other changes can be induced by or are dependent on synaptic activation. Formation of filopodia, enlargement of spines, formation of spines with perforated PSDs, appearance of new spines, and formation of specific types of synapses such as multiple synapse boutons (MSBs), in which two spines contact the same terminal, have all been reported to be induced in an activity‐dependent manner. The common denominator of most of these different processes is that they are calcium and NMDA receptor dependent. Their time course, however, may vary. Some appear quite rapidly after stimulation (e.g., filopodia, perforated synapses), while others are clearly more delayed (e.g., formation of spines, appearance of MSBs). How these different structural changes relate to each other, as well as their functional significance, have therefore become intriguing issues. The characteristics of these different types of morphological changes are reviewed, with a discussion of the possibility that structural plasticity contributes to changes in synaptic efficacy. Hippocampus 2002;12:585–591. © 2002 Wiley‐Liss, Inc.
A large sustained Ca2+ elevation occurs in unstimulated spines during the LTP pairing protocol but does not change synaptic strength
Authors: Conti Rossella , Lisman John 
Published: October 2002

AbstractSynapses in the CA1 region of the hippocampus undergo bidirectional synaptic modification in response to different patterns of activity. Postsynaptic Ca2+ elevation can trigger either synaptic strengthening or weakening, depending on the properties of the local Ca2+ signal. During the pairing protocol for long‐term potentiation (LTP) induction, the cell is depolarized under voltage‐clamp and is given low‐frequency synaptic stimulation. As an initial step toward understanding the Ca2+ dynamics during this process, we used confocal microscopy to study the Ca2+ signals in spines evoked by the depolarization itself. This depolarization activates voltage‐dependent Ca2+ channels (VDCC), but whether these channels inactivate rapidly or remain functional throughout the long depolarizations used in the pairing protocol remains unknown. Cells were depolarized to 0 mV for 2–3 min. This depolarization led to a large initial elevation of Ca2+ in spines that never decayed back to resting levels. The maintained signal was close to the Kd of the low‐affinity (5 μM) Ca2+ dye, Magnesium Green. We attempted to determine the functional role of this elevation, using the Ca2+‐channel blocker D‐890. The addition of D‐890 in the internal solution produced a nearly complete abolition of the Ca2+ elevation during depolarization. Under these conditions, the NMDA conductance was normal, but LTP was almost completely blocked. This might suggest the importance of VDCC in LTP; however, we found that high concentrations of D‐890 can directly inhibit calmodulin protein kinase II (CaMKII), an enzyme required for LTP induction. Thus, whereas D‐890 is a useful tool for blocking postsynaptic VDCC, it cannot be used to study the contribution of these channels to plasticity. We conclude that the activation of VDCC produces a large and persistent elevation of Ca2+ in all spines, but does not produce either LTP or long‐term depression (LTD) in the absence of synaptic stimulation. The possible reasons for this are discussed. Hippocampus 2002;12:667–679. © 2002 Wiley‐Liss, Inc.
Learning and memory of cue–reward association meaning by modifications of synaptic efficacy in dentate gyrus and piriform cortex
Authors: Truchet B. , Chaillan F.A. , Soumireu‐Mourat B. , Roman F.S. 
Published: October 2002

AbstractThis article begins with a review of recent experiments investigating the synaptic efficacy changes occurring in rat dentate gyrus and piriform cortex during an associative olfactory task. In all these experiments, animals were trained to discriminate among an artificial cue, a patterned electrical stimulation distributed to the lateral olfactory tract associated with a water reward, and a natural odor associated with a flash of light. Monosynaptic field potential responses evoked by single electrical stimuli to the lateral olfactory tract were recorded in the ipsilateral piriform cortex before and just after each training session. Monosynaptic field and polysynaptic field potentials evoked by single electrical stimuli applied respectively to the lateral perforant pathway and lateral olfactory tract were also recorded in ipsilateral dentate gyrus. The results showed an increase in synaptic efficacy subsequent to the first training session in the dentate gyrus network when compared with piriform cortex at the later stage of the learning. The early increase of monosynaptic response in the dentate gyrus was observed immediately after the first learning session but disappeared 24 h later. Inversely, a synaptic depression developed across sessions, becoming significant at the onset of the last (fifth) session. The polysynaptic potential recorded in this structure increased substantially when rats began to discriminate the learning cues, usually after the second or third learning session. Then, from the third to the fifth session, an LTP like‐phenomenon appeared in piriform cortex when rats perfectly mastered the associations. Experiments using high‐frequency stimulation to prevent changes in gyrus dentatus indicated that the onset of the observed depression was necessary for the learning of the olfactory associations. The fact that hippocampal and cortical neuronal networks exhibited different timing in synaptic efficacy changes could physiologically explain learning and memory processes. Hippocampus 2002;12:600–608. © 2002 Wiley‐Liss, Inc.
Hippocampal function during behaviorally silent associative learning: Dissociation of memory storage and expression
Authors: Talk Andrew C. , Gandhi Chetan C. , Matzel Louis D. 
Published: October 2002

AbstractIn laboratory studies, the assessment of memory is typically associated with overt behavioral responses. Thus, it has been difficult to determine whether the enhancement of hippocampal sensory‐evoked potentials that often accompany memory formation are the neurophysiological manifestation of a memory “trace” or are a secondary product of the behavioral expression of the memory. We addressed this issue by examining changes in evoked hippocampal field potentials during sensory preconditioning, a form of behaviorally silent relational learning that requires an intact hippocampus for execution. Rats were exposed to presentations of a white noise (S1) that terminated with a tone (S2). These pairings of ostensibly “neutral” stimuli supported no change in the behavior elicited by the noise. However, if the tone was subsequently paired with mild footshock (US), suppression of ongoing licking behavior (indicative of fear) was elicited by the noise, indicating that the animal had associated the noise with tone (S1‐S2), and had represented the noise‐tone‐shock (S1‐S2‐US) relationship. Pre‐training neurotoxic lesions of the hippocampus had no effect on conditioned suppression to tone after tone‐shock (S2‐US) pairings, but disrupted the expression of continued suppression to noise (S1) after tone‐shock pairings. In a second experiment, sensory‐evoked field potentials in the dorsal hippocampus were recorded with extracellular electrodes. No changes in the hippocampal response evoked by white noise were observed after pairings of noise and tone, i.e., no evidence for a memory trace could be detected. In contrast, after tone was paired with footshock, two short‐latency negative potentials within the noise‐evoked field response increased in amplitude, a response often presumed to reflect a neurophysiological correlate of memory storage. In total, these results suggest that although the hippocampus critically contributes to the processing of a behaviorally silent associative memory, there may be no role for changes in the amplitude of hippocampal sensory‐evoked field potentials in storing representations of the relationships between sensory experiences. Hippocampus 2002;12:648–656. © 2002 Wiley‐Liss, Inc.
Long‐term potentiation as a substrate for memory: Evidence from studies of amygdaloid plasticity and Pavlovian fear conditioning
Authors: Goosens Ki A. , Maren Stephen 
Published: October 2002

AbstractRecent reports have raised concerns about the ability of long‐term potentiation (LTP) to account for associative learning and memory. In this paper, we review the many mechanistic similarities between one form of associative learning, Pavlovian fear conditioning, and amygdaloid LTP. We then address many of the criticisms levied against LTP within the framework of fear conditioning. We believe that many of the apparent discrepancies between LTP and behavior can be generally accounted for by a failure to appreciate that learned behavior is supported by multiple synapses in an extensive network of brain structures. We conclude that LTP remains a viable substrate for memory. Hippocampus 2002;12:592–599. © 2002 Wiley‐Liss, Inc.
Regulated transcription of the immediate‐early gene Zif268: Mechanisms and gene dosage‐dependent function in synaptic plasticity and memory formation
Authors: Bozon Bruno , Davis Sabrina , Laroche Serge 
Published: October 2002

AbstractThe immediate‐early gene Zif268 is a member of the Egr family of inducible transcription factors. Data from gene expression studies have suggested that this gene may play a critical role in initial triggering of the genetic machinery that has long been considered a necessary mechanism for maintenance of the later phases of LTP and also for the consolidation or stabilization of long‐lasting memories. Until recently, however, the data supporting this assumption have been based primarily on circumstantial evidence, with no direct evidence to suggest that Zif268 is required for long‐lasting synaptic plasticity and memory. In this report, we review our own data using Zif268 mutant mice; we show that although the early phase of dentate gyrus LTP is normal in these mice, the later phases are not present, and the ability of the mice to maintain learned information over a 24‐h period is deficient. In addition, we present new information showing a task‐dependent gene dosage effect in Zif268 heterozygous mice. We show that spatial learning is particularly sensitive to reduced levels of Zif268, as one‐half of the complement of Zif268 in heterozygous mice is insufficient to maintain spatial long‐term memories. Hippocampus 2002;12:570–577. © 2002 Wiley‐Liss, Inc.
Hippocampal LTP and memory in mouse strains: Is there evidence for a causal relationship?
Authors: Gerlai Robert 
Published: October 2002

AbstractThe mechanisms underlying memory are under intense investigation. One of the most promising candidates at the cellular level is long‐term potentiation (LTP). Numerous pharmacological and molecular genetic manipulations have led to alteration in both LTP and memory. However, the causal relationship between these phenotypical changes is debated. The problem of causality can be addressed in numerous ways. One suggestion is to investigate natural variation in both LTP and memory performance in mouse strains. If variation in synaptic and behavioral phenomena is found, correlation between these traits may be investigated. The advantages and disadvantages of this approach are discussed. An empirical example using four mouse strains is also presented to highlight some general problems. The following arguments are made. First, multiple electrophysiological and behavioral paradigms with idiosyncratic condition characteristics should be conducted to avoid false‐positive findings due to alterations unrelated to memory and its mechanisms. Multiple stimulation and memory protocols may also allow one to study the complexity and multiplicity of processes. Second, analysis of a large number of mouse strains may be needed to avoid false interpretation of results due to spurious gene associations and/or linkage disequilibrium. Third, quantitative genetic analysis using, for example, diallele crosses, may be employed to properly investigate biologically meaningful, i.e., genetic, effects. It is concluded that with the use of additional methods (e.g., QTL analysis, gene expression arrays, and biochemical analysis) providing converging evidence, analysis of mouse strains will be instrumental in addressing the question regarding the role LTP may play in memory. Hippocampus 2002;12:657–666. © 2002 Wiley‐Liss, Inc.
Synaptic reentry reinforcement based network model for long‐term memory consolidation
Authors: Wittenberg Gayle M. , Sullivan Megan R. , Tsien Joe Z. 
Published: October 2002

AbstractThe conversion of newly formed declarative memories into long‐term memories is known to be dependent on the hippocampus. Recent experiments suggest that memory consolidation requires reactivation of the NMDA receptor in CA1 during the initial week(s) after training. This led to the hypothesis that the repeated post‐learning reinforcement of synaptic modifications, termed synaptic reentry reinforcement (SRR), is essential for long‐term memory consolidation and storage. Based on experimental observations, we have built a computational model to further illustrate and explore the effect of the SRR process on the formation of long‐term memory. We show that SRR is capable of strengthening and maintaining memory traces despite inherent variability in the system due to such processes as the turnover of synaptic receptors and their associated signaling and structural proteins. Furthermore, we demonstrate that new rounds of synaptic modification triggered by memory reactivation, either during conscious recall or sleep, could lead to the selective consolidation of a subset of memory traces. Finally, we show why the SRR process in the hippocampus is required during the initial post‐training weeks for synaptic reinforcement based memory consolidation in the cortex. Hippocampus 2002;12:637–647. © 2002 Wiley‐Liss, Inc.
Neurogenesis may relate to some but not all types of hippocampal‐dependent learning
Authors: Shors Tracey J. , Townsend David A. , Zhao Mingrui , Kozorovitskiy Yevgenia , Gould Elizabeth 
Published: October 2002

AbstractThe hippocampal formation generates new neurons throughout adulthood. Recent studies indicate that these cells possess the morphology and physiological properties of more established neurons. However, the function of adult generated neurons is still a matter of debate. We previously demonstrated that certain forms of associative learning can enhance the survival of new neurons and a reduction in neurogenesis coincides with impaired learning of the hippocampal‐dependent task of trace eyeblink conditioning. Using the toxin methylazoxymethanol acetate (MAM) for proliferating cells, we tested whether reduction of neurogenesis affected learning and performance associated with different hippocampal dependent tasks: spatial navigation learning in a Morris water maze, fear responses to context and an explicit cue after training with a trace fear paradigm. We also examined exploratory behavior in an elevated plus maze. Rats were injected with MAM (7 mg/kg) or saline for 14 days, concurrent with BrdU, to label new neurons on days 10, 12, and 14. After treatment, groups of rats were tested in the various tasks. A significant reduction in new neurons in the adult hippocampus was associated with impaired performance in some tasks, but not with others. Specifically, treatment with the antimitotic agent reduced the amount of fear acquired after exposure to a trace fear conditioning paradigm but did not affect contextual fear conditioning or spatial navigation learning in the Morris water maze. Nor did MAM treatment affect exploration in the elevated plus maze. These results combined with previous ones suggest that neurogenesis may be associated with the formation of some but not all types of hippocampal‐dependent memories. Hippocampus 2002;12:578–584. © 2002 Wiley‐Liss, Inc.