Anatomo-physiological variability of deep brain structures and stereo-neurosurgery of epilepsy.
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The transcription factor cAMP response element-binding protein (CREB) plays a critical role in plasticity processes underlying learning and memory. We investigated the phosphorylation of CREB in rat brain after forced swimming, a stressor known to impact on higher limbic and neocortical brain areas. As shown by immunohistochemistry, forced swimming increased phosphorylated CREB (P-CREB) levels in the dentate gyrus, all neocortical areas, the medial, lateral and basolateral nuclei of the amygdala, cerebellum but not in the hypothalamic paraventricular nucleus. Distinct differences in the P-CREB pattern were observed in the deeper vs. superficial layers of the neocortex. The response in P-CREB was stressor type-specific because exposure to either ether or a cold environment was ineffective. The forced swimming-induced changes in P-CREB levels showed a biphasic time-course: an early peak detected at 15 min was followed by a marked drop at 60 min; a second rise starting after 1-2 h, reached maximal values between 6 and 8 h, and remained elevated for at least 48 h. Examination of the neuroanatomical induction pattern of the CRE-inducible immediate early gene product c-fos revealed that it was only partly overlapping with that of P-CREB. Western analyses showed that only the 43-kDa CREB protein (an enhancer of CRE-containing promotors) was phosphorylated after forced swimming, while other members of the CREB/ATF family (CREM, ATF-1 and ATF-2) remained unaffected. The NF-kappaB pathway was not activated, indicating that forced swimming does not unspecifically evoke transcription factor activation. Thus, in contrast to physical stressors, such as ether or cold exposure, forced swimming, a stressor with a strong psychological component, elicits the recruitment of the CREB pathway in a widespread manner in the limbic system and neocortex; brain regions known to be implicated in various forms of (stress-related) learning and memory.
Haloperidol (1 mg/kg) was shown to increase significantly the dopamine (DA) turnover in n. accumbens and striatum and to a lesser degree in frontal cortex and hypothalamus of the rat brain; to decrease the noradrenaline content in hypothalamus. Sulpiride (50 mg/kg) slightly increased DA turnover in striatum and hypothalamus and lowered the serotonin (5-HT) content in frontal cortex. Carbidine (25 mg/kg) was found to increase DA turnover in frontal cortex, striatum and hypothalamus to a greater degree than haloperidol; 5-HT turnover was increased in all the cerebral regions. The results obtained indicated that the atypical neuroleptic drug carbidine exerts the predominant effect on the frontal cortex, the serotoninergic component being clearly pronounced.
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An accurate identification of cerebral structures is necessary to perform quantification of single photon emission computed tomography (SPECT). We have developed an anatomical localization system that accounts for individual brain shapes and sizes by using the Talairach proportional grid system. The locations of the commissural lines, which define the stereotactic coordinate system, are calculated from the external landmarks provided by the canthomeatal line. This is validated on MRI images. When applied to SPECT data, the use of a neuroanatomical atlas data along with the automaticity of the processing guarantees a high degree of objectivity and inter-observer reproducibility.
Clinical and neuropsychological investigations were performed using the Luriya method in 141 patients with arteriovenous malformations (AVM). These included 27 patients with AVM in different parts of the caudate nucleus, 34 with AVM in the thalamus, 39 with AVM in the hippocampal formation, and 41 with AVM in the cingulate gyrus. A total of 102 patients underwent surgery. Patients with AVM in various locations showed common memory impairments as well as individual features of memory disturbances depending on which structures were affected. The common feature was the development of an amnesiac symptom complex resembling Korsakov's syndrome. These lesions developed only in patients with combined damage to deep structures (preoperatively in patients with ventricular hemorrhages); with the exception of patients with AVM of the caudate nucleus, memory impairments were modality-non-specific; all patients showed impairment of auditory-speech memory at the late phase and of visual memory in terms of indirect recall. Memory impairments characteristic of lesions to individual structures were the presence of functional asymmetry of memory defects in available of the caudate nucleus and thalamus (if only speech problems were present) and constant inclusions and contaminations in patients with AVM of the cingulate gyrus. It is suggested that certain aspects of memory function may have been duplicated in different structures during evolution and that each structure makes its own contribution to overall memory function.
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First haloperidol administration is followed by the reorganization of evoked potentials in visual cortex. During haloperidol administration (10-12 days after the beginning) variations of evoked potentials is visual cortex and in subcortical structures uniform evoked potentials took place.
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