Convergent evidence suggests that the perirhinal cortex (PRC) is involved in perception, in addition to long-term memory, by representing higher-order object feature conjunctions. Recent functional magnetic resonance imaging (fMRI) investigations have shown greater PRC activity during the processing of objects with a higher versus lower degree of features in common, but notably, these studies have been limited to examining only two levels of feature overlap. To address this, we scanned neurologically healthy participants with fMRI during a 1-back working memory task for objects that possessed a very low, low, medium or high degree of feature overlap. Somewhat consistent with previous findings, trends towards greater PRC activity for high versus medium feature overlap objects, and for semantically identical compared to semantically different objects were observed. However, other aspects of our data, including diminished PRC activity during medium versus low feature overlap objects, are difficult to interpret and require further investigation.

Convergent evidence suggests that the perirhinal cortex (PRC) is involved in perception, in addition to long-term memory, by representing higher-order object feature conjunctions. Recent functional magnetic resonance imaging (fMRI) investigations have shown greater PRC activity during the processing of objects with a higher versus lower degree of features in common, but notably, these studies have been limited to examining only two levels of feature overlap. To address this, we scanned neurologically healthy participants with fMRI during a 1-back working memory task for objects that possessed a very low, low, medium or high degree of feature overlap. Somewhat consistent with previous findings, trends towards greater PRC activity for high versus medium feature overlap objects, and for semantically identical compared to semantically different objects were observed. However, other aspects of our data, including diminished PRC activity during medium versus low feature overlap objects, are difficult to interpret and require further investigation.

<p>Memories are not veridical representations of the environment. Rather, an individual's goals can influence how the surrounding environment is represented in long-term memory. The present dissertation aims to delineate the influence of reward and punishment motivation on human declarative memory encoding and its underlying neural circuitry. Chapter 1 provides a theoretical framework for investigating motivation's influence on declarative memory. This chapter will review the animal and human literatures on declarative memory encoding, reward and punishment motivation, and motivation's influence on learning and memory. Chapter 2 presents a study examining the behavioral effects of reward and punishment motivation on declarative memory encoding. Chapter 3 presents a study examining the neural circuitry underlying punishment-motivated declarative encoding using functional magnetic resonance imaging (fMRI), and compares these findings to previous studies of reward-motivated declarative encoding. Chapter 4 presents a study examining the influence of reward and punishment motivation on neural sensitivity to and declarative memory for unexpected events encountered during goal pursuit using fMRI. Finally, Chapter 5 synthesizes these results and proposes a model of how and why motivational valence has distinct influences on declarative memory encoding. Results indicated that behaviorally, reward motivation resulted in more enriched representations of the environment compared to punishment motivation. Neurally, these motivational states engaged distinct neuromodulatory systems and medial temporal lobe (MTL) targets during encoding. Specifically, results indicated that reward motivation supports interactions between the ventral tegmental area and the hippocampus, whereas, punishment motivation supports interactions between the amygdala and parahippocampal cortex. Together, these findings suggest that reward and punishment engage distinct systems of encoding and result in the storage of qualitatively different representations of the environment into long-term memory.</p> / Dissertation

Some authors have argued that the primary function of the posterior parietal cortex is to control visual attention and awareness, whereas others have argued that the posterior parietal cortex is specialized for controlling actions. The purpose of the present thesis was to examine the influence of prism adaptation – a visuomotor adaptation technique – on visual attention deficits in patients with lesions of parietal cortex. Lesions to dorsal regions of the posterior parietal cortex lead to optic ataxia – a disorder in which visually guided reaching is disrupted. In contrast lesions to ventral (i.e. inferior) regions of the posterior parietal cortex of the right hemisphere lead to spatial neglect – a disorder in which patients are unaware of people or objects in contralesional (left) space. Chapter 1 presents an overview of the organization of the posterior parietal cortex, as well as an introduction to the disorders of spatial neglect and optic ataxia and the use of prism adaptation as a treatment for spatial neglect. Chapter 2 examined the influence of prism adaptation on attentional deficits in patients with right brain damage. Results demonstrated that prism adaptation reduced both the disengage deficit and the rightward attentional bias, two of the classic attentional deficits in neglect. Chapter 3 investigated the role of the dorsal posterior parietal cortex in controlling both reflexive and voluntary attention in two patients with optic ataxia. Lesions to the dorsal posterior parietal cortex led to both a disengage deficit and a rightward attentional bias, similar to patients with neglect, even though neither of the patients had any clinical symptoms of neglect. Contrary to previous work these results indicated that dorsal portions of the posterior parietal cortex – a region not commonly damaged in neglect – are important for controlling the orienting and reorienting of both reflexive and voluntary attention. Furthermore, these results indicated that optic ataxia is not purely a visuomotor disorder that is independent of any perceptual or attentional deficits as was previously assumed. Based on the results of Chapters 2 and 3 it was hypothesized that the beneficial effects of prism adaptation on attention may operate via the superior parietal lobe, a region which is typically undamaged in neglect, and is known to be important for controlling attention and action. Chapter 4 provided support for this hypothesis by demonstrating that a patient with lesions to the superior parietal lobe, who had the same attentional deficits as the right brain damaged patients tested in Chapter 2, failed to demonstrate any beneficial effects of prism adaptation on his attentional performance. Specifically, prism adaptation had no influence on his disengage deficit or his rightward attentional bias. Therefore, these data provide direct evidence that the beneficial effects of prisms on attention rely, at least in part, on the superior parietal lobe. Finally, Chapter 5 concludes with a summary of the research findings from the present thesis, and puts forward a new theory to conceptualize the mechanisms underlying the beneficial effects of prisms in patients with neglect.

Some authors have argued that the primary function of the posterior parietal cortex is to control visual attention and awareness, whereas others have argued that the posterior parietal cortex is specialized for controlling actions. The purpose of the present thesis was to examine the influence of prism adaptation – a visuomotor adaptation technique – on visual attention deficits in patients with lesions of parietal cortex. Lesions to dorsal regions of the posterior parietal cortex lead to optic ataxia – a disorder in which visually guided reaching is disrupted. In contrast lesions to ventral (i.e. inferior) regions of the posterior parietal cortex of the right hemisphere lead to spatial neglect – a disorder in which patients are unaware of people or objects in contralesional (left) space. Chapter 1 presents an overview of the organization of the posterior parietal cortex, as well as an introduction to the disorders of spatial neglect and optic ataxia and the use of prism adaptation as a treatment for spatial neglect. Chapter 2 examined the influence of prism adaptation on attentional deficits in patients with right brain damage. Results demonstrated that prism adaptation reduced both the disengage deficit and the rightward attentional bias, two of the classic attentional deficits in neglect. Chapter 3 investigated the role of the dorsal posterior parietal cortex in controlling both reflexive and voluntary attention in two patients with optic ataxia. Lesions to the dorsal posterior parietal cortex led to both a disengage deficit and a rightward attentional bias, similar to patients with neglect, even though neither of the patients had any clinical symptoms of neglect. Contrary to previous work these results indicated that dorsal portions of the posterior parietal cortex – a region not commonly damaged in neglect – are important for controlling the orienting and reorienting of both reflexive and voluntary attention. Furthermore, these results indicated that optic ataxia is not purely a visuomotor disorder that is independent of any perceptual or attentional deficits as was previously assumed. Based on the results of Chapters 2 and 3 it was hypothesized that the beneficial effects of prism adaptation on attention may operate via the superior parietal lobe, a region which is typically undamaged in neglect, and is known to be important for controlling attention and action. Chapter 4 provided support for this hypothesis by demonstrating that a patient with lesions to the superior parietal lobe, who had the same attentional deficits as the right brain damaged patients tested in Chapter 2, failed to demonstrate any beneficial effects of prism adaptation on his attentional performance. Specifically, prism adaptation had no influence on his disengage deficit or his rightward attentional bias. Therefore, these data provide direct evidence that the beneficial effects of prisms on attention rely, at least in part, on the superior parietal lobe. Finally, Chapter 5 concludes with a summary of the research findings from the present thesis, and puts forward a new theory to conceptualize the mechanisms underlying the beneficial effects of prisms in patients with neglect.

Cyclin-dependent kinase-5 (Cdk5) was identified as a serine/threonine kinase that plays an important role in neuronal development. Association with one of the neuronal activators, p35 or p39, is required for Cdk5 to elicit its diverse effects in the nervous system, such as neurite outgrowth. In addition to these, increasing evidence suggests that Cdk5 also plays an important role in cocaine addiction, neurotransmitter release, NMDA receptor phosphorylation. This thesis is divided into three parts which deals with the effects of Cdk5 inhibitor¡Ðroscovitine on the morphine tolerance development, acute inflammatory pain, and pilocarpine-induced seizure respectively. The first part explored the effect of Cdk5 inhibitior¡Ðroscovitine on the morphine antinociceptive tolerance development. Delta FosB activation is involved in morphine tolerance. Cyclin-dependent kinase- 5 (Cdk5) is found to be the downstream target of delta FosB. We examined the effects of the potent selective Cdk5 inhibitor¡Ðroscovitine on the development of antinociceptive tolerance of morphine. Tolerance was induced by continuous infusion of morphine 5 &#x00B5;g/hr intrathecally (i.t.) for 5 days. The effect of co-administration of roscovitine 1 &#x00B5;g/hr i.t. for 5 days was also examined. Roscovitine co-administration enhanced the antinociceptive effect of morphine in morphine tolerant rats. It also shift the morphine antinociceptive dose¡Ðresponse curve to the left during morphine tolerance induction, and reduced the increase in the ED50 of morphine two-fold. Collectively, these findings suggest Cdk5 modulation may be involved in the development of morphine tolerance and its inhibitor will enhance antinociceptive effect. The second part discussed the roscovitine effect on acute inflammatory pain. Formalin injected into the rat hind paw will evoke flinching (consisting of an elevation and shrinking back of the injected paw), a reliable parameter of pain behavior. The nociceptive response to formalin occurs in a biphasic pattern: there isan initial acute period (phase 1), and after a short period of remission, phase 2 begins and consists of a longer period (1 hour) of sustained activity. The initial response was initially attributed to a direct algogenic effect of formalin, whereas phase 2 was associated with the central sensitization. In this study, the Cdk5 inhibitor¡Ðroscovitine was injected intrathecally to elucidate the mechanism of Cdk5 activation during formalin-induced hyperalgesia. The 50 ul of 5% formalin solution was used as the noxious stimulant. The rats were injected with 0, 50, 100, and 200ug roscovitine intrathecally thirty minutes before hind paw formalin injection. Intrathecal 200ug roscovitine injection attenuates the phase I flinch response. And intrathecal 50, 100, and 200ug roscovitine injection suppress phase II flinch response effectively. Roscovitine administration could effectively suppress the formalin-induced flinch behavior. This implies the activation of Cdk5 plays an important role in the sensitization after nociceptive stimulation. The third part focus on the roscovitine effect on the pilocarpine induced seizure. Pilocarpine temporal lobe epilepsy model is widely used. Chronic electroconvulsive therapy could upregulate Cdk5 activity. Cdk5 inhibitor¡Ðroscovitine could suppress NMDA induced long-term potentiation in hippocampal slice. Intracerebroventricular injection of 100£gg roscovitine 30 min before pilocarpine-induced epilepsy could significantly decrease the seizure-induced mortality ( 11% in roscovitine group VS 77% in control group). The escape latency, spatial memory impairment, in the pilocarpine-induced seizure group is significant longer than the roscovitine pretreatment group in the Morris water maze test after one month (p¡Õ0.05). It is concluded Cdk5 may play an important in the pathogenesis of epilepsy. Therefore, Cdk5 inhibition may become another way for the epilepsy treatment.

The purpose of this study was to investigate the association between extracellular basal hippocampal glutamate levels and cognitive function in epileptic patients. We used the zero-flow microdialysis method to measure the extracellular concentrations of glutamate in the epileptogenic and non-epileptogenic hippocampus of 23 awake epileptic patients during the interictal period. All patients underwent extensive neuropsychological testing to assess cognitive functioning prior to probe implantation. Basal glutamate levels in the epileptogenic hippocampus were significantly higher than the non-epileptogenic hippocampus (mean, 11.96 micromolar (µM) versus 2.92 µM, respectively). Elevated basal glutamate levels in the epileptogenic hippocampus correlated with decreased scores on the Verbal Selective Reminding Test (V-SRT) (R[exponent]2 = 0.36, p = 0.0244). When controlling for MRI-detected hippocampal atrophy within epileptogenic regions, elevated basal glutamate levels within atrophic hippocampus correlated with decreased cognitive functioning measured by both the V-SRT (R[exponent]2 = 0.7764, p = 0.0204) and Performance Intelligence Quotient (PIQ) (R[exponent]2 = 0.7324, p = 0.0297), but not within non-atrophic hippocampus (V-SRT: R2 = 0.1013, p = 0.4424; PIQ: R[exponent]2 = 0.2303, p = 0.2288). These data suggest that elevated basal glutamate levels in the epileptogenic hippocampus may be implicated in the pathogenesis of hippocampal atrophy and may contribute to impaired cognitive functioning involving verbal memory and visual-spatial skills in patients with temporal lobe epilepsy.

Reproduction de : Thèse d'exercice : Médecine : Nancy 1 : 2005. / Titre provenant de l'écran-titre.

Recognition of speech at the receiver end generally gets degraded in distant talking atmospheres of laptops, teleconfereing, video conferences and in hands free telephony, where the quality of speech gets contaminated and severely disturbed because of the additive noises. To make useful and effective, the exact speech signals has to be extracted from the noise signals and the user has to be given the clean speech. In such conditions the convenience of microphone array has been preferred as a means of civilizing the quality of arrested signals. A consequential growth in laptop technology and microphone array processing have made possible to improve intelligibility of speech while communication. So this contention target on reducing the additive noises from the original speech, beside design and use of different algorithms. In this thesis a multi-channel microphone array with its speech enhancement of signals to Wiener Beamformar and Generalized side lobe canceller (GSC) are used for Laptops in a noisy environment. Systems prescribed above were implemented, processed and evaluated on a computer using Mat lab considering SNR, SNRI as the main objective of quality measures. Systems were tested with two speech signals, among which one is Main speech signal and other is considered as Noise along with another random noise, sampling them at 16 KHz .Three Different source originations were taken into consideration with different input SNR’s of 0dB, 5dB, 10dB, 15dB, 20dB, 25dB. Simulation Results showed that Noise is been attenuated to a great extent. But Variations in SNR and SNRI has been observed, because of the different point origination of signals in the respective feilds.Variation in SNR and SNRI is been observed when the distance between the main speech originating point and microphone is too long compared to the noise signals. This states that origination of signals plays a huge role in maintaining the speech quality at the receiver end. / D.No 4-22, Gandla street, papanaidupeta-517526 chittoor district,Andhra pradesh India naveenkumarthupalli@gmail.com

Abnormally slow processing of language may be a factor contributing to the poor verbal memory seen in many patients with lesions of the anterior temporal region in the left hemisphere. This possibility was examined by comparing the performance of 12 patients with left temporal-lobe resections (LT), 10 patients with similar lesions in the right hemisphere (RT) and 13 normal control (NC) subjects on a lexical-decision task, a sentence-plausibility-judgement task, and a story-recall task. Stimuli were presented aurally, and, in the latter two tasks, at 5 different speech rates ranging from 125 words per minute (wpm) to 325 wpm. Recall of stories by LT subjects was not abnormally sensitive to the effect of increasing rate, although it was inferior to that by NC subjects at all speeds. LT patients presented aurally but not visually (Frisk and Milner, 1991), suggesting that the left anterior temporal region plays a special role in the processing of speech sounds.