Dissertation Thesis (Ph.D.)--University of South Florida, 2007. / Includes vita. Includes bibliographical references (leaves 178-202). Also available online.

Thesis (Ph.D. in Neuroscience) -- University of Colorado, 2005. / Typescript. Includes bibliographical references (leaves 96-111). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;

Thesis (Ph. D.)--University of Washington, 2006. / Vita. Includes bibliographical references (leaves 48-60).

Although the processes used for temporarily storing and manipulating neural information have been extensively studied at the synaptic level far less attention has been given to the underlying cellular and molecular mechanisms that contribute to change in the intrinsic excitability of neurons. More importantly, how do these mechanisms of plasticity integrate with ongoing mechanisms of regulation of neural intrinsic excitability and, in turn, homeostasis of entire neural circuits? In this dissertation I describe the underlying mechanisms that contribute to persistent neural activity and, more globally, sensorimotor adaptation using weakly electric fish as my model system. Weakly electric fish have evolved a behavior adaptation known as the jamming avoidance response (JAR), and it is this adaptation that allows the organism to elevate its own electrical discharge in response to intraspecific interactions and subsequent distortions of the animal’s electric field. The elevation operates over a wide range and in vivo can last tens of hours upon cessation of a jamming stimulus. I demonstrate that the underlying mechanisms of the adaptation are mediated by calcium-dependent signaling in the pacemaker nucleus and that calcium-mediated phosphorylation plays an important role in the regulation of the long-term frequency elevation (LTFE). I demonstrate using an in vitro brain slice preparation from the weakly electric fish, Apteronotus leptorhynchus that the engram of memory formation depends on the cooperativity of calcium-dependent protein kinases and protein phosphatases. In addition, I show that the memory formation (in the form of LTFE) does not depend on the continued flux of calcium, but rather the phosphorylation events downstream of NMDA receptor activation. Moreover, I describe the differences in the expression of protein phosphatases and protein kinases as they relate to species-specific differences in sensorimotor adaptation. It is important to note that this is the first time that the cooperativity between different isoforms of protein kinase C (PKC) have been shown to play a role in graded long-term change in neuronal activity and, in turn, providing the neural basis of species-specific behavior. The neural adaptation of the electromotor system in weakly electric fish provides an excellent model system to study the underlying cellular and molecular events of vertebrate memory formation. / text

Os receptores canabinóides CB1 são abundantemente expressos nos núcleos da base (NB), sugerindo a participação do sistema canabinóide na Doença de Parkinson (DP). Os objetivos deste estudo foram investigar a localização do CB1 nos NB de ratos; avaliar o decurso temporal de sua expressão e de marcadores neuronais em modelo experimental da DP in vivo, e avaliar os efeitos do tratamento com compostos canabinóides em modelos experimentais da DP in vivo e in vitro. Nossos resultados mostraram que o CB1 é predominantemente expresso em neurônios GABAérgicos nos NB. A lesão dopaminérgica produziu mudanças temporais distintas da expressão do CB1 nas estruturas dos NB. O tratamento com o agonista canabinóide ACEA agravou à lesão dopaminérgica e o desempenho comportamental motor. Por outro lado, o tratamento com o antagonista AM 251, embora não tenha gerado diferenças neuroquímicas, gerou melhoras nos testes comportamentais. Por fim, em nosso modelo in vitro, o tratamento com inibidor de recaptação da anandamida AM 404 gerou uma discreta redução dos níveis de morte celular. / Cannabinoid receptors CB1 are abundantly expressed in the basal ganglia (BG), suggesting the involvement of the cannabinoid system in Parkinson\'s disease (PD). The objectives of this study were to investigate the location of CB1 in BG of rats; evaluate the time course expression of CB1 and neuronal markers in an experimental model of PD in vivo, and evaluate the effects of treatment with cannabinoids compounds in experimental models of PD in vivo and in vitro. Our results showed that CB1 is predominantly expressed in GABAergic neurons in BG. The dopamine lesion produced distinct temporal changes in the expression of CB1 in BG structures. Treatment with the cannabinoid agonist ACEA aggravated the dopaminergic lesion and the motor behavioral performance. Moreover, the treatment with the antagonist AM 251, although have not generated neurochemical changes,it promoted improvements in behavioral tests. Finally, in our in vitro model, the treatment with Anandamide transport inhibitor AM 404 led to a slight reduction in the levels of cell death.

INTRODUÇÃO: Lesões cerebrais isquêmicas ocorrem em índices bastante significativos, podendo levar a alterações cognitivas de graus variados, cujas repercussões clínicas podem ser de extrema gravidade para os pacientes acometidos. Para avaliar as conseqüências destas lesões nos aspectos funcionais, pode-se utilizar um dos componentes dos potenciais evocados auditivos relacionados a eventos, o Mismatch Negativity (MMN). OBJETIVOS: verificar se o MMN é capaz de detectar mudanças eletrofisiológicas em gerbils submetidos à isquemia cerebral e a hipotermia; verificar se o treinamento auditivo pode gerar mudanças eletrofisiológicas detectáveis pelo MMN, e comparar as latências do potencial com as células sobreviventes do hipocampo de gerbils submetidos à isquemia e a hipotermia. MÉTODOS: Estudo 1: 44 gerbils (Meriones Unguiculatus) adultos foram anestesiados com halotano e submetidos à isquemia cerebral através da oclusão bilateral das carótidas por sete minutos, e à captação do MMN. Os animais foram divididos nos grupos SHAM, HIPO, NORMO e HIPER, de acordo com a temperatura a que foram submetidos. Estudo 2: 28 gerbils foram submetidos a uma sessão de treinamento auditivo com duração de 300 segundos em caixa de esquiva com gerador de eletrochoque, e ao registro do MMN. Estudo 3: foi captado o MMN de 27 gerbils e, após terem sido sacrificados, foi realizada a quantificação de células sobreviventes da região CA1 do hipocampo através de cortes histológicos. RESULTADOS: Estudo 1: houve 100% de presença do MMN no grupo HIPO, não houve diferença estatisticamente significante entre os grupos SHAM e HIPO. Estudo 2: não houve diferença estatisticamente significante entre as latências do MMN antes e depois do treinamento auditivo. Estudo 3: observou-se maior número de células sobreviventes no hipocampo nos animais do grupo HIPO, e foi detectada baixa correlação entre o número de células sobreviventes e a latência do MMN. CONCLUSÕES: o MMN detectou as mudanças eletrofisiológicas geradas pelo efeito neuroprotetor da hipotermia, porém, o protocolo do treinamento auditivo utilizado neste estudo não gerou mudanças neurais nos animais que pudessem ser detectadas pelo MMN, e foi observada baixa correlação entre a latência do MMN e o número de células sobreviventes na região CA1 do hipocampo de gerbils submetidos à isquemia e a hipotermia. / INTRODUCTION: Significant ischemic cerebral lesions may result in cognitive disorders of varying degrees, with clinical repercussions that could be extremely severe for the affected patients. In order to evaluate the consequences of such lesions upon functional aspects, one of the components of event-related auditory evoked potentials, the Mismatch Negativity (MMN), may be used. AIM: to verify whether the MMN is able to identify electrophysiological changes in gerbils submitted to cerebral ischemia and hypothermia; to verify if auditory training may generate electrophysiological changes detectable by MMN, and to compare the potential\'s latencies with the surviving cells of the hippocampus of gerbils submitted to cerebral ischemia and hypothermia. METHODS: Study 1: 44 adult gerbils (Meriones Unguiculatus) were sedated with halothane and underwent cerebral ischemia through bilateral occlusion of the carotids for seven minutes, and the MMN was registered. Animals were divided in four groups, SHAM, HIPO, NORMO and HIPER, according to the temperature they were exposed. Study 2: 28 gerbils underwent a session of auditory training of 300 seconds in a passive shuttle box with an electroshock generator, and the MMN was registered. Study 3: the MMN of 27 gerbils were registered and after their scarifice, the amount of surviving cells in the CA1 region of the hippocampus was quantified through histological cuts. RESULTS: Study 1: the MMN was 100% present in the HIPO group, there was no significant statistical difference between groups SHAM and HIPO. Study 2: there was no significant statistical difference between the MMN latencies before and after the auditory training. Study 3: a greater number of surviving cells was observed in the hippocampus of animals from group HIPO, and a low correlation between the number of surviving cells and the MMN latency was detected. CONCLUSIONS: MMN detected electrophysiological changes generated by the neuroprotector effect of hypothermia, nevertheless the auditory training protocol used in this study did not generate neural changes in the animals that could be detected by MMN, and a low correlation between the MMN latency and the number of surviving cells in the CA1 region of the hippocampus of gerbils submitted to ischemia and hypothermia was observed.

Diversas evidências demonstram que as diferentes fases do sono agem de maneira complementar e diferencial na consolidação de memórias. No entanto os mecanismos celulares e moleculares dessa relação não estão estabelecidos. Foi postulado que a melhor maneira para se entender como o sono facilita o aprendizado é contrastando evidências experimentais obtidas em presença ou ausência de informação adquirida recentemente; e que a plasticidade sináptica dependente de atividade é o melhor correlato celular para o aprendizado e memória. Portanto, analisamos a expressão dos genes relacionados à plasticidade sináptica Arc, Bdnf, Camk4, Creb1, Egr1, Egr2, Fos, Nr4a1, Ppp2ca e Ppp2r2d durante o sono de ratos adultos expostos ou não a um ambiente enriquecido. Nove dos 10 genes avaliados (Arc, Bdnf, Creb1, Egr1, Egr2, Fos, Nr4a1, Ppp2ca e Ppp2r2d) mostraram aumento da expressão após a exposição. A expressão de Bdnf no hipocampo estava aumentada durante os estágios marcados pela dessincronização da atividade elétrica do cérebro (vigília e sono REM) sugerindo que Bdnf poderia ser um marcador da homeostase do sono. Pela primeira vez demonstramos que exposição ao ambiente enriquecido promoveu aumento na expressão de genes (Ppp2r2d, Ppp2r2ca) que codificam para a proteína fosfatase 2A (PP2A). Dado o papel dessa proteína na plasticidade sináptica dependente de atividade sugerimos que esse evento seja importante para as modificações na morfologia e atividade neuronal observados após a exposição a um ambiente enriquecido. Por fim, o nosso trabalho mostra que ocorre a reindução de genes relacionados à potencialização sináptica durante SREM (Egr1, Fos). E, pela primeira vez, demonstrou-se que um gene que codifica para uma proteína relacionada à depressão da atividade sináptica também está reinduzido (Ppp2r2d) no hipocampo. Esses resultados reforçam a necessidade de uma reativação na atividade cerebral durante o sono e, pela primeira vez, mostram-se evidências experimentais que a potencialização e depressão da plasticidade sináptica ocorrem concomitantemente durante o sono. / Independent lines of evidence show differential and complementary roles of slow wave sleep and REM sleep in memory consolidation. However molecular and cellular mechanisms governing this relation are not known. It was suggested that comparison of experimental evidences obtained in presence or absence of recently acquired information is necessary to investigate sleep-dependent memory consolidation. It is well known that the activity-dependent synaptic plasticity is the best cellular and molecular correlate of learning and memory. Therefore we carried out experiments analyzing expression of synaptic plasticity-related genes (Arc, Bdnf, Camk4, Creb1, Egr1, Egr2, Fos, Nr4a1, Ppp2ca e Ppp2r2d) during sleep in adult rats exposed or not to a novel experience. Expression of nine out of 10 analyzed genes (Arc, Bdnf, Creb1, Egr1, Egr2, Fos, Nr4a1, Ppp2ca e Ppp2r2d) was increased following novelty exposure. Bdnf expression was increased in hippocampus during vigilance states marked by desynchronized brain electrical activity (waking and REM sleep). Hence, suggesting that Bdnf has a role as a homeostatic marker of sleep need. Here, we showed for the first time that exposure to novelty induces expression of protein phosphatase 2A (PP2A) coding genes (Ppp2r2d, Ppp2r2ca) in the hippocampus. Given PP2A role in activity dependant synaptic activity and its association to cytoskeleton proteins this could account for changes in neural activity and morphology observed after exposure to novelty. Finally, we found reinduction of synaptic potentiation related genes during REM sleep (Egr1, Fos). Furthermore, we also found reinduction of Ppp2r2d, which is related to synaptic depression. These results suggest the need for neural circuit reactivation during sleep and, for the first time, we provide experimental evidences that the synaptic potentiation and depression occur concurrently during sleep.

Apart from CFRD, low cognitive skill index (CSI) was also found in CF patients and was attributed the lacking of vitamin E. Since it is known that insulin plays a role in the learning and memory, decreased plasma insulin level in CF patients is an alternative mechanism for impaired cognitive function. Although numerous studies have found that insulin can improve learning and memory, the mechanism of it is not well understood. In this study, we investigated the effect of insulin on the expression of hippocampal early-phase long-term potentiation (E-LTP) in the immature rats. Hippocampal brain slices were acutely prepared from 10-12 days and 2 months old rats and field excitatory postsynaptic potentials (tEPSCs) were recorded from CA1 region by a multi-electrode in vitro recording system. In the control group, the hippocampal slices of neonatal rats showed no increase in the magnitude of fEPSC after conventional high frequency stimulation (HFS). After pretreatment of the slices with 0.08ng/ml insulin for over one hour, there was no significant change in the magnitude of E-LTP. However, when the insulin concentration increased to 0.8ng/ml, a significant increase in the magnitude of E-LTP was observed. On the contrary, any doses of insulin failed to affect the magnitude of E-LTP of mature rats. These results suggested that insulin could dose-dependently facilitate the production of E-LTP in the hippocampus of infant rats. Application of AG-1024, an inhibitor of insulin receptor, largely abolished the insulin-dependent E-LTP in immature rats rather than adult rats, indicating the involvement of insulin signaling pathway in the insulin effect. On the other hand, increasing the concentration of glucose from 11mM to 22 or 33 mM did not facilitate the E-LTP and application of indinavir, a blocker of insulin-sensitive glucose transporter-4, did not inhibit the effect of insulin. Therefore, it is unlikely that the facilitory action of insulin on E-LTP is via an indirect effect on glucose homeostasis or utilization. Pretreatment with the MAPK pathway inhibitor PD98059 blocked insulin-mediated E-LTP facilitation. Furthermore, the tetanic stimulation induced a significant increase in the level of phosphorylated p42MAPK in the insulin-treated hippocampus than that in the control group. In conclusion, our results suggested that insulin could facilitate the production of hippocampal E-LTP in infant rats, which may play an important role in modulating the expression of LTP in the developing brain and perhaps is an underlying mechanism for the improving effect of insulin on learning and memory. Since insulin plays an important role in the developing brain, perhaps the deficiency of insulin effect resulted from CF patients induces the impairment of cognitive function. / Cystic fibrosis (CF), which is caused by the deficiency of cystic fibrosis transmembrne conductance regulator (CFTR), is the most common autosomal recessive systemic disease with an incidence of 1: 2500 in Caucasians. Cystic fibrosis-related diabetes (CFRD), as one of the complications of CF patients, is regarded as one of the leading co-morbidity in CF patients. The mechanism ofCFRD is attributed to the reduced number of islets due to pancreatic fibrosis caused by the loss of CFTR in pancreatic duct. However, the above mechanism failed to explain the dynamics of insulin secretion induced by glucose tolerance test (GTT) in some CF patients and therefore, we were forced to re-consider the mechanism for the pathogenesis of CFRD. Interestingly, the following facts imply that perhaps there is another mechanism for the onset of CFRD: decreased insulin secretion and decreased plasma HCO3 - concentration was observed in the metabolic acidosis disease, plasma HCO3- level increased accompanied by the elevation of plasma insulin after food intake and CFTR accounted for HCO3 - transport in many epithelial cells. These facts promoted us to hypothesize that the loss of HCO3--induced insulin secretion resulting from the deficiency of CFTR is an alternative mechanism for the onset of CFRD. Our results showed that HCO3- could induce insulin secretion of isolated islets from rats. Ca2+ imaging revealed that HCO3- dose-dependently induced an increase in intracellular Ca2+ ([Ca2+] i) in RIN-5F cells, an insulin-secreting cell line. Removal of extracellular Ca2+ or addition of nifedipine, the blocker of L-type Ca 2+ channel, decreased the effect of HCO3- significantly, indicating the activation of L-type Ca2+ channel during HCO3- stimulation. The inhibitory effect of BaCl2 implied the involvement of K+ channel. The results that HCO3--induced increase in [Ca 2+]i was reduced by PKA inhibitor and sAC blocker demonstrated that the pathway of sAC-cAMP-PKA-ATP-sentitive K+ channel (K ATP channel) was responsible for the effect of HCO3 -. The reduction of extracellular Cl- or the inhibitor of anion exchanger (AE) inhibited the [Ca2+]i increase induced by HCO3- significantly but the omission of external Na+ failed. The facts that CFTR blocker decreased the effect of HCO3- markedly and the expression of CFTR in RIN-5F cells revealed by western blotting suggested the CFTR-mediated HCO3- transport. These results suggested that HCO 3- could induce insulin secretion in a CFTR-dependent manner, which provided a new insight into the understanding of pathogenesis of CFRD and paved the way for the therapy of CFRD. / Zhao, Wenchao. / "November 2010." / Advisers: Chang Chan; Wing Ho Yung. / Source: Dissertation Abstracts International, Volume: 73-04, Section: B, page: . / Thesis (Ph.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 115-138). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [201-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

Introdução: O zumbido pode ser definido como a percepção consciente de um som ou ruído, sem a presença de estimulação acústica externa. Levando em consideração o prejuízo causado pelo zumbido, a falta de tratamentos definitivos e eficientes para todos os casos de zumbido, além da dificuldade de uso da Tinnitus Retraining Therapy - TRT, por ser onerosa e longa, fica evidente a necessidade da proposição de alternativas para reabilitação de pessoas com este problema. Sendo assim, a hipótese deste estudo é que o uso do treinamento auditivo formal pode causar uma reorganização plástica no sistema auditivo dos portadores de zumbido, promovendo uma melhora do sintoma, em virtude do fortalecimento das sinapses da via auditiva, bem como da sincronia de disparo dos neurônios envolvidos no processamento auditivo. Esta modificação seria observada por meio da avaliação comportamental, eletrofisiológica e por meio do questionário THI - Tinnitus Handcap Inventory. Objetivo: O objetivo do referido estudo foi verificar o efeito de um programa de treinamento auditivo formal em portadores de zumbido na percepção deste sintoma. Método: Participaram do estudo 13 indivíduos portadores de zumbido divididos em dois grupos randomizados, sendo seis no Grupo Estudo (GE) e sete no Grupo Controle (GC). Todos os indivíduos realizaram os seguintes procedimentos: anamnese; audiometria tonal e vocal; imitanciometria; avaliação eletrofisiológica da audição; acufenometria; aplicação do THI; avaliação do processamento auditivo reduzida (GIN - Gaps In Noise, Teste de Padrão de Frequência e Fala com Ruído). Após a avaliação dos indivíduos foram iniciados os treinamentos de acordo com cada grupo. O GE foi submetido ao treinamento auditivo formal, realizado em cabina acústica, por aproximadamente 40 minutos, em oito sessões, uma vez por semana, cujas atividades enfocavam principalmente habilidades auditivas temporais e de atenção auditiva. O GC foi submetido a oito sessões de treinamento visual de 40 minutos cada, realizadas uma vez por semana, com atividades como palavras cruzadas, caça palavras, jogo dos 7 erros e Sudoku. Para a análise estatística foram utilizados o teste pareado de Wilcoxon, técnica de modelos de medidas repetidas e modelos lineares múltiplos, com nível de significância de 0,05. Resultados: Na caracterização dos grupos, não foram observadas diferenças estatisticamente significantes para as variáveis gênero, idade, pitch e loudness do zumbido, bem como para os limiares auditivos na audiometria convencional e altas frequências. Foi realizada a comparação entre os grupos, pré e pós terapia auditiva e visual, dos testes eletrofisiológicos, comportamentais e THI. A análise dos dados, utilizando um ajuste do modelo de medidas repetidas para cada variável, mostrou que não houve diferenças estatisticamente significantes entre os grupos, quando comparadas as condições pré e pós treinamento, para nenhuma das avaliações realizadas. Conclusão: O presente estudo teve o objetivo de verificar o efeito de um programa de treinamento auditivo em portadores de zumbido, na percepção deste sintoma. Nossos achados não mostraram diferenças estatisticamente significantes entre os instantes pré e pós treinamento auditivo ou treinamento placebo, bem como entre os grupos (GC e GE), tanto para os achados eletrofisiológicos, quanto para a avaliação comportamental do processamento auditivo e para o THI / Introduction: Tinnitus may be defined as the conscious perception of sound or noise in the absence of external acoustic stimulation. Considering the damage caused by tinnitus, the lack of effective and efficient treatment for all cases of tinnitus and further the difficulty of using the Tinnitus Retraining Therapy - TRT, as it is costly and overlong, it is evident the need of proposing alternatives to rehabilitation of people with such problem. Thus, the hypothesis of the present study is that the formal auditory training may lead to reorganization in the auditory system of patients with tinnitus, promoting a decrease in the symptoms, due to the strengthening of synapses in the auditory pathway, and further a best synchronism of the fire neurons involved in auditory processing. This modification would be observed by assessing behavioral and electrophysiological through the THI questionnaire - Tinnitus handcap Inventory. Objective: The aim of this study was to investigate the effect of a formal auditory training program on patients with tinnitus perception of this symptom. Method: The study included 13 subjects with tinnitus who were divided into two randomized groups, six in the Study Group (SG) and seven in the control group (CG). All subjects performed the following procedures: interview; tonal and vocal audiometry, tympanometry, electrophysiological assessment of hearing; acuphenometry; application of THI; auditory processing assessment reduced (GIN - Gaps In Noise Test Pattern Frequency and Speech in Noise). After such procedures all subjects went through the auditory training according to each group. The experimental group was subjected to formal auditory training, performed in an acoustic cabin for aproximately 40 minutes in eight sessions, once a week; the activities were mainly focused on both temporal auditory skills and auditory attention. The CG underwent eight sessions of visual training that lasted 40 minutes each, held once a week, with activities such as crossword puzzles, word search puzzles, play Sudoku and the 7 mistakes. For statistical analysis we used the Wilcoxon matched pairs test, technical models for repeated measures and multiple linear models, with a significance level of 0.05. Results: In the characterization of the groups, there was found no statistically significant differences for the variables gender, age, pitch and loudness of tinnitus as well as hearing thresholds in conventional audiometry and high frequencies. Comparisons were performed between groups, pre and post auditory training and visual, electrophysiological testing, behavioral and THI. Data analysis, using the model of repeated measures for each variable, showed no statistically significant differences between groups when comparing the situations before and after training for any of the evaluations. Conclusion: The present study aimed to verify the effect of an auditory training program in patients with tinnitus, that is, in their perception of this symptom. Our findings showed no statistically significant differences before and after the auditory training and training placebo between the groups (CG and EG) and also for the electrophysiological findings, the behavioral assessment of auditory processing and THI

A l’heure actuelle, il reste largement à étudier comment le codage sensoriel des signaux vocaux de communication contribue à leur détection et à leur reconnaissance. Peu d’études se sont, en effet, penchées sur le codage des vocalisations au niveau des régions auditives en fonction de l’individu qui les produit et du degré de familiarité avec cet individu. Dans ce cadre, les oiseaux chanteurs sont un bon modèle parce qu’ils utilisent des vocalisations pour interagir et reconnaître leurs congénères et qu’ils possèdent, de plus, un ensemble de régions auditives. Parmi ces régions, le nidopallium caudomedian (NCM), une aire auditive analogue du cortex auditif secondaire chez les mammifères, est actuellement considérée comme une région spécialisée dans le traitement des vocalisations (chants et cris) de l’espèce : les neurones du NCM répondent plus fortement aux vocalisations de l’espèce qu’à celles d’une autre espèce. À partir de là, parce que chez le diamant mandarin, le cri de distance permet aux individus, mâles ou femelles, de reconnaître leur partenaire sexuel, nous avons cherché à savoir si, chez les femelles comme chez les mâles, les neurones du NCM montraient une discrimination dans leurs réponses auditives entre le cri d’individus connus (parmi lesquels figurait le partenaire sexuel) et ceux d’individus inconnus et si ces réponses reflétaient le degré de familiarité de ces vocalisations. Les enregistrements de l’activité des neurones du NCM, chez des diamants mandarins vigiles (grâce à un système de télémétrie) ou anesthésiés, lors de la présentation de cris de distance, ont révélé, chez les femelles vivant en couple et ayant été familiarisées avec un autre couple de diamants mandarins, une plus forte augmentation de l’activité lors de la diffusion des cris d’individus connus, mâles ou femelles, qu’aux cris d’individus inconnus. Une telle augmentation n’a pas été, en outre, observée chez des femelles contrôles qui n’avaient jamais entendu ces mêmes cris auparavant. De plus, ils ont indiqué que le nombre de neurones montrant un fort degré de sélectivité ainsi que la quantité d’information portée par les trains de potentiels d’action étaient plus importants chez les femelles vivant en couple que chez les femelles contrôles. En revanche, chez les mâles, bien que la plupart des neurones montrait des réponses lors de la diffusion des cris, aucune différence n’a été mise en évidence entre les cris d’individus connus et ceux d’inconnus. Nous avons alors cherché à savoir comment, d’un point de vue acoustique, les cris de distance étaient représentés au sein du NCM. En se basant sur une étude comportementale ayant déterminé quelles étaient les caractéristiques acoustiques qui contribuaient à la reconnaissance de ces cris, nous avons cherché à savoir si les neurones du NCM étaient sensibles à ces mêmes caractéristiques acoustiques. Les résultats ont montré que, chez les femelles, la suppression de la fréquence fondamentale et la modification du timbre du cri du partenaire sexuel ou du propre cri de l’oiseau provoquaient une forte diminution des réponses au sein du NCM alors que, chez les mâles, les réponses variaient selon le paramètre modifié et le type de cri présenté. Nos résultats suggèrent donc que, chez le diamant mandarin, le NCM est impliqué dans le codage du cri de distance. Cependant, ils mettent en évidence des différences dans ce codage entre les mâles et les femelles. Chez les femelles, ce codage permet de discriminer entre les cris d’individus connus et ceux d’individus inconnus alors que chez les mâles, son rôle reste à être déterminé. Chez les femelles, l’expérience sociale au travers de la mémorisation des signaux de communication des individus peut donc façonner les propriétés fonctionnelles des neurones d’une aire auditive secondaire. Ces propriétés pourraient donc continuellement subir des changements pour s'adapter à l’environnement social de l’individu. / How sensory signals are encoded in the brain and whether their behavioural relevance affects their encoding are central questions in sensory neuroscience. Studies have consistently shown that behavioural relevance can change the neural representation of sounds in the auditory system, but what occurs in the context of natural acoustic communication where significance could be acquired through social interaction remains to be explored. The zebra finch, a highly social songbird species that forms lifelong pair bonds and uses a vocalization, the distance call, to identify its mate offers an opportunity to address this issue. One auditory area in the songbird telencephalon, the caudo-medial nidopallium (NCM) that is considered as being analogous to the secondary mammalian auditory cortex, has recently emerged as part of the neural substrate for sensory representation of species-specific vocalizations: the activation of NCM neurons is greatest when birds are exposed to conspecific song, as compared to heterospecific song or artificial stimuli. This led us to investigate whether, in the zebra finch, NCM neurons could contribute to the discrimination among vocalizations that differ in their degree of familiarity: calls produced by the mate, by familiar individuals (males or females), or by unfamiliar individuals (males or females). In females, behaviourally relevant calls, i.e. the mate’s call and familiar calls, evoked responses of greater magnitude than unfamiliar calls. This distinction between responses was seen both in multiunit recordings from awake freely moving mated females (using a telemetric system) and in single unit recordings from anesthetized mated females. In contrast, control females that had not heard them previously displayed response of similar magnitude to call stimuli. In addition, more cells showed highly selective responses in mated than in control females suggesting that experience-dependent plasticity in call-evoked responses resulted in enhanced discrimination of auditory stimuli. In males, as in females, call playback evoked robust auditory responses. However, neurons in males did not appear capable of categorizing the calls of individuals (males or females) as ‘‘familiar’’ or ‘‘unfamiliar’’. Then, we investigated how calls are represented in the NCM of zebra finches by assessing whether certain call-specific acoustic cues drove NCM neurons to a greater degree than others. Behavioural studies had previously identified call-specific acoustic cues that are necessary to elicit a vocal response from male and female zebra finches. Single-unit recordings indicated that NCM neurons in females were particularly sensitive to call modifications in the spectral domain: suppressing the fundamental frequency of call stimuli or modifying the relative energy levels of harmonics in call caused a marked decrease in response magnitude of NCM neurons. In males, NCM neurons also appear to be sensitive to call modifications in the spectral domain, however changes in magnitude of responses (increase or decrease) depended on the acoustic cue that had been modified.Our results provide evidence that the NCM is a telencephalic auditory region that contributes to the processing of the distance call, in females as well in males. However, how the distance call is processed and represented in the NCM appears to differ between males and females. In females, the NCM could be involved in dicrimination between call stimuli whereas, in males, its functional role in call-processing remains to be determined. Our results also suggest that, in females, social experience with the call of individuals, by affecting the degree to which neurons discriminated between these calls, may shape the functional properties of neurons in a telencephalic auditory area. The functional properties of auditory neurons may therefore change continuously to adapt to the social environment.