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Brain Res Brain Res Rev ; 45(1): 38-78, 2004 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-15063099


A deficiency in the noradrenergic system of the brain, originating largely from cells in the locus coeruleus (LC), is theorized to play a critical role in the progression of a family of neurodegenerative disorders that includes Parkinson's disease (PD) and Alzheimer's disease (AD). Consideration is given here to evidence that several neurodegenerative diseases and syndromes share common elements, including profound LC cell loss, and may in fact be different manifestations of a common pathophysiological process. Findings in animal models of PD indicate that the modification of LC-noradrenergic activity alters electrophysiological, neurochemical and behavioral indices of neurotransmission in the nigrostriatal dopaminergic system, and influences the response of this system to experimental lesions. In models related to AD, noradrenergic mechanisms appear to play important roles in modulating the activity of the basalocortical cholinergic system and its response to injury, and to modify cognitive functions including memory and attention. Mechanisms by which noradrenaline may protect or promote recovery from neural damage are reviewed, including effects on neuroplasticity, neurotrophic factors, neurogenesis, inflammation, cellular energy metabolism and excitotoxicity, and oxidative stress. Based on evidence for facilitatory effects on transmitter release, motor function, memory, neuroprotection and recovery of function after brain injury, a rationale for the potential of noradrenergic-based approaches, specifically alpha2-adrenoceptor antagonists, in the treatment of central neurodegenerative diseases is presented.

Locus Cerúleo , Modelos Neurológicos , Doenças Neurodegenerativas/metabolismo , Norepinefrina/fisiologia , Antagonistas de Receptores Adrenérgicos alfa 2 , Animais , Antioxidantes/uso terapêutico , Temperatura Corporal/efeitos dos fármacos , Lesões Encefálicas/fisiopatologia , Dopamina/metabolismo , Humanos , Inflamação/metabolismo , Locus Cerúleo/anatomia & histologia , Locus Cerúleo/fisiologia , Fatores de Crescimento Neural/fisiologia , Doenças Neurodegenerativas/classificação , Doenças Neurodegenerativas/tratamento farmacológico , Doenças Neurodegenerativas/etiologia , Plasticidade Neuronal/fisiologia , Norepinefrina/agonistas , Norepinefrina/antagonistas & inibidores , Norepinefrina/uso terapêutico , Recuperação de Função Fisiológica/efeitos dos fármacos , Recuperação de Função Fisiológica/fisiologia
Vis Neurosci ; 20(6): 687-701, 2003.
Artigo em Inglês | MEDLINE | ID: mdl-15088720


Lesion or inactivation of the superior colliculus (SC) of the cat results in an animal that fails to orient toward peripheral visual stimuli which normally evoke a brisk, reflexive orienting response. A failure to orient toward a visual stimulus could be the result of a sensory impairment (a failure to detect the visual stimulus) or a motor impairment (an inability to generate the orienting response). Either mechanism could explain the deficit observed during SC inactivation since neurons in the SC can carry visual sensory signals as well as motor commands involved in the generation of head and eye movements. We investigated the effects of SC inactivation in the cat in two ways. First, we tested cats in a visual detection task that required the animals to press a central, stationary foot pedal to indicate detection of a peripheral visual stimulus. Such a motor response does not involve any components of the orienting response and is unlikely to depend on SC motor commands. A deficit in this task would indicate that the SC plays an important role in the detection of visual targets even in a task that does not require visual orienting. Second, to further investigate the visual orienting deficit observed during SC inactivation and to make direct comparisons between detection and orienting performance, we tested cats in a standard perimetry paradigm. Performance in both tasks was tested following focal inactivation of the SC with microinjections of muscimol at various depths and rostral/caudal locations throughout the SC. Our results reveal a dramatic deficit in both the visual detection task and the visual orienting task following inactivation of the SC with muscimol.

Transtornos da Percepção/fisiopatologia , Colículos Superiores/fisiopatologia , Percepção Visual/fisiologia , Animais , Gatos , Agonistas GABAérgicos/farmacologia , Masculino , Muscimol/farmacologia , Colículos Superiores/efeitos dos fármacos