Brain Neuroanatomical studies

The data presented in this chapter provide strong evidence, from both neurochemical and neuroanatomical studies, demonstrating that, following in vivo administration of a number of methylenedioxy-substituted amphetamine derivatives, there is widespread and long-lasting degeneration of serotonin neurons in brain, without any major or consistent effects on catecholamine neurons. A detailed examination of the parameters involved in the neurotoxic and neurodegencrative effects of MDMA on brain serotonin neurons indicates that ... 

Volumetric and morphological brain measurements are made with MRI. Modern MRI can produce detailed, high-contrast images of the entire brain in relatively short scan times with no invasive procedures or radioactivity. Thus, it is the modality of choice for detailed neuroanatomic studies in various neuropsychiatric disorders. Many groups have addressed the challenge of how to quantify subtle structural characteristics in the brain that appear to differ consistently between comparison groups. Methods such... 

Joseph, S.A. (1990) Immunoreactive adrenocorticotropin in rat brain a neuroanatomical study using antiserum generated against synthetic ACTH 1-39. Am. J. Anat. 158 533-548. 

The central distribution of THC was studied in the primate brain using positron emission tomography (Charlambous et al. 1991). The THC analog, (-)-18F-A8-THC, was administered intravenously to baboons. Neuroanatomical distribution in the baboon brain was comparable to prior autoradiographic studies, with binding evident in the basal ganglia, thalamus, and cerebellum. Clearance was rapid from these areas. 

A detailed description of the neuroanatomical structures involved in sleep is provided in the excellent reviews, of Jones (1989) and Hobson et al. (1998). Alertness and sleep are dependent on the activity of the brain as a whole, although different levels of consciousness are determined primarily by areas of the brain stem. Lesion and stimulation studies have been used to identify specific regions and delineate relevant neuronal systems (reviewed by Parkes, 1985). 

How representative are animal models to study the interaction between anxiety and neuropeptides Most importantly, the same circuits underlie both physiological and pathological anxiety in other words, pathological anxiety evolves from normal anxiety and fear (Rosen and Schulkin 1998). Furthermore, there are many neuroanatomical parallels in rodent and human anxiety, including neuropeptidergic circuits in hypothalamic and limbic brain areas. 

Neurotoxicity. Existing studies show that silver can be deposited in anatomically defined regions of the brain in both humans and animals following repeated oral exposure to silver. Other studies indicate that neuroanatomical changes can occur in young rats, and that the general activity level of... 

Olsen TS (1991) Outcome following occlusion of the middle cerebral artery. Acta Neurol Scand 83 254-258 Parvizi J, Damasio AR (2003) Neuroanatomical correlates of brainstem coma. Brain 126 1524-1536 Pedersen PM, Vinter K, Olsen TS (2004) Aphasia after stroke type, severity and prognosis. The Copenhagen aphasia study. Cerebrovasc Dis 17 35-43 Plum F (1972) Hyperpnea, hyperventilation, and brain dysfunction. Ann Intern Med 76 328 Plum F, Alvord EC (1964) Apneustic breathing in man. Arch Neurol 10 101-112... 

Mattiace LA, Baring MD, Manaye KF, Mihailoff GA, German DC (1989) Mesostriatal projections in BALB/c and CBA mice a quantitative retrograde neuroanatomical tracing study. Brain Res Bull 23 61-68. 

Nauta HJW, Pritz MB, Lasek RJ (1974) Afferents to the rat caudoputamen studied with horseradish peroxidase. An evaluation of a retrograde neuroanatomical research method. Brain Res 67 219-238. 

A variety of neuroanatomic differences have been observed in samples of autistic patients in comparison with controls. This topic has been reviewed in recent publications [43-45]. Magnetic resonance imaging (MRI) studies show that by 2-4 years of age, 90% of autistic children have an abnormal early brain overgrowth followed by abnormally slowed growth [45, 46]. The most common finding has been hyperplasia of cerebral gray matter and cerebral and cerebellar white matter in the early life of autistic patients [46]. 

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