Brain parietal

Decreased numbers of dendritic spines and malformed spines in brain parietal cortex were observed at postnatal day 30 in rat pups whose mothers were administered 256-480 mg lead/kg/day as lead acetate in drinking water during gestation and lactation (Murray et al. 1978). PbB levels were not reported. 

Camkkl Brain (parietal cortex, hippocampus, brainstem, mesencephalon and thalamus, caudate-putamen and cerebellum) Thymus, spleen, many other tissues (Tokumitsu et al., 1995 Anderson et al., 1998 Sakagami et al., 2000 Vinet et al., 2003)... 

Compared to the Category Test, SSP and SRT results show a relatively mixed performance profile. This profile is indicative of temporal lobe impairment and may explain the idiosyncratic character of PCP-induced brain dysfunction. Other HRB subtest data suggest that parietal lobe-mediated functions are less influenced by PCP abuse, since approximately 30 percent of this sample had error-free performances on a test sensitive to finger agnosia. 

Named for the bones of the cranium under which they lie, the lobes are conspicuously defined by prominent sulci of the cortex, which have a relatively constant position in human brains. Each lobe is specialized for different activities (see Figure 6.3). Located in the anterior portions of the hemispheres, the frontal lobes are responsible for voluntary motor activity, speaking ability, and higher intellectual activities. The parietal lobes, which are posterior to the frontal lobes, process and integrate sensory information. The occipital lobes, located in the posterior-most aspects of the cerebrum, process visual information, and the temporal lobes, located laterally, process auditory information. 

Textbooks on neuroscience often describe the location and function of hundreds of individual brain regions (see references above). However, for current purposes these will be kept to a minimum (Figure 2.1). Anatomically, the brain can be subdivided into the forebrain containing the telencephalon and diencephalon, the midbrain or mesencephalon and the hindbrain (metencephalon and myelencephalon). The telencephalon includes the left and right cerebral hemispheres encompassed by the cerebral cortex (neocortex). Cortex is a translation of the word bark and is so-called because its surface, made up of numerous sulci (grooves or invaginations) and gyri (raised areas), is on the outer surface of the brain like the bark of a tree. Each hemisphere is divided into four lobes, named from the front (rostral) to back (caudal) of the brain frontal, temporal, parietal and occipital. 

FIGURE 1-1 Coronal section of the human brain at the thalamic level stained by the Heidenhain technique for myelin. Gray matter stains faintly, all myelinated regions are black. The thalamus ( ) lies beneath the lateral ventricles and is separated at this level by the beginning of the third ventricle. The roof of the lateral ventricles is formed by the corpus callosum (small arrows). Ammon s horns are shown by the large arrows. Note the outline of gyri and sulci at the surface of the cerebral hemispheres, sectioned here near the junction of the frontal and parietal cortices. 

LTP has been shown in many parts of the brain but it has been most extensively studied in the hippocampus, a phy-logenetically old part of the cerebral cortex that in humans is embedded in the temporal horn and in rats and rabbits lies beneath the parietal and temporal neocortex (Fig. 15-3A). The hippocampus is essential for (declarative) memory formation in rats the role of hippocampus in acquisition of spatial information has been studied in... 

Brain SPECT of AD patients typically shows bilateral posterior temporal and parietal hypoperfusion. The areas of reduced perfusion are secondary to the reduced brain metabolism in areas of neuronal depletion. This scintigraphic pattern of bilateral decreased posterior parietal-temporal perfusion has a predictive value of greater than 80% for AD [63], The sensitivity and specificity of brain SPECT for the diagnosis of AD are 86% and 96%, respectively [127],... 

The effect of LSD on cerebral blood flow was studied in the rat (Goldman et al. 1975). An intravenous injection of LSD increased blood flow to frontal and parietal cortex within 10 minutes, and to the cerebellum within 20 minutes. Increases (significant or nonsignificant) were evidenced in all brain areas assessed, except for the hippocampus, where a minor, nonsignificant reduction was noted. 

Kumari et al, (2003) 12 2 mg nicotine, subcutaneously N-Back Nicotine improved accuracy in all N-back conditions and reduced response times during the more demanding conditions of the task. Irrespective of drug condition, frontal and parietal regions were activated with increasing memory load. Nicotine, however, increased brain activation in the anterior cingulate (0-back, 1-back, 2-back), superior frontal (1-back, 2-back), and left superior parietal cortex (1-back, 2-back, 3-back), in the 3-back condition, nicotine reduced activation in the right superior parietal cortex. 

Distributional analysis of reaction times revealed that nicotine decreased the validity effect more in the high than in the low validity cue condition. Nicotine reduced orienting-related activation in the right parietal brain regions (TPJ), This effect occurred only in the condition with the high valid cues. Conversely the low valid cue condition increased neural activation in the right parietal regions. 

As we move forward, it will prove helpful to get some basic aspects of the human nervous system in place. An enormous amount of work has gone into making associations between brain anatomy and function. Starting with the three main parts of the brain, we know that the cerebrum is the seat of consciousness. It is divided into two hemispheres, which are linked by the corpus callosum. In a very general sense, the left hemisphere is associated with intellectual and the right hemisphere with emotional responses. Within the cerebrum, one can associate a number of brain areas (the prefrontal, frontal, temporal, parietal, and occipital lobes, for example) with functions including vision and hearing. One can make crude maps in which function is mapped onto brain structure. 

The basal rate of proton secretion is around 10% of maximal but the perception of food (smell, taste, sight or even just the thought of it) increases secretion. This is the cephalic effect of food. Nervons signals from the brain canse release of acetylcholine, histamine and gastrin to stimnlate acid secretion from the parietal cells. When food actnally reaches the stomach, distension, proteins, peptides and amino acids farther stimulate the release of gastrin. 

Gastric secretion. Stimulation of gastric acid production by vagal impulses involves an M-cholinoceptor subtype (M -receptor), probably associated with enterochromaffin cells. Pirenzepine (p. 106) displays a preferential affinity for this receptor subtype. Remarkably, the HCl-secreting parietal cells possess only Ma-receptors. Mi-receptors have also been demonstrated in the brain however, these cannot be reached by pirenzepine because its lipophilicity is too low to permit penetration of the blood-brain barrier. Pirenzepine was formerly used in the treatment of gastric and duodenal ulcers (p. 166). 

Histamine (B). Histamine is stored in basophils and tissue mast cells. It plays a role in inflammatory and allergic reactions (p. 72, 326) and produces bronchoconstriction, increased intestinal peristalsis, and dilation and increased permeability of small blood vessels. In the gastric mucosa, it is released from enterochromaffin-like cells and stimulates acid secretion by the parietal cells. In the CNS, it acts as a neuromodulator. Two receptor subtypes (G-pro-tein-coupled), H and H2. are of therapeutic importance both mediate vascular responses. Prejunctional H3 receptors exist in brain and the periphery. 

Figure 5. Positron emission tomography shows the brain areas activated and deactivated during REM sleep when compared to waking. In the forebrain, more activated areas are principally limbic structures, while the posterior cingulate cortex, part of the prefrontal and parietal cortex, are deactivated. Modified from Hobson et al. (1998). Reprinted from NeuroReport with permission.

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