Neuronal Changes

Examination of cell number by DNA analysis shows no change for the whole brain after 30 d high Pb exposureAt 60 d of age, however, there was an increase in whole brain DNA, which the authors interpreted as diffuse gliosis in Pb-intoxicated animals. Lead does produce a 10-20% reduction in the DNA of the cerebellum in 3-week-old rat pups exposed to encephalopathic levels of Pb. This suggests that postnataUy dividing cells of the cerebellum are sensitive to the effects of Pb, and that there may be an ultimate reduction in the number of cells in this brain area. Such a reduction in cerebellar DNA is not found sifter low doses of Pb.  

Neither Pentschew smd Garro nor Krigman et al. were able to find any morphologiced evidence of a significant amount of cortical necrosis after developmented Pb exposure in the encephalopathic range. 

Peripheral nervous system axonal degeneration has been a consistent finding following Pb exposure in humans/ rhesus monkeys/ and guinea pigs. Lead exposure in developing animals results in a reduction in the diameter of rat pyramidal tract axons. Similar findings of reduced axonal size were observed in the optic nerves of Pb-exposed mice.  

A morphometric examination of the hippocampal mossy fiber system (the axons of the hippocampal dentate granule cells) following Pb exposure during development was carried out by Alfano et al. The development of this axonal system is of particular interest since this pathway sequesters the largest amount of Pb in the normal brain, and forms a major internal circuit in the hippocampus. The authors report that high Pb exposure causes reductions in the development of this pathway, even in the absence of any differences in brain weights. 

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Wagner, G.C. Lucot, J.B. Schuster, C.R. and Seiden, L.S. Alpha-methyltyrosine attenuates and reserpine increases methampheta-mine-induced neuronal changes. Brain Res 270 285-288, 1983. 

Grivel, J., Cvetkovic, V., Bayer, L. el al. (2005). The wake-promoting hypocretin/orexin neurons change their response to noradrenaline after sleep deprivation. J. Neurosci 25, 4127-30. 

Information transfer between two nerves in the brain occurs at synaptic junctions, across which chemical messengers (neurotransmitters) diffuse. The neurotransmitter binds to a receptor on the postsynaptic neurone, changing its membrane potential. If the membrane potential decreases, this either initiates an action potential or increases the likelihood that a further depolarisation, from stimulation by another nerve, will initiate an action potential. Such a neurotransmitter is described as excitatory. In contrast, if it increases the membrane potential, it reduces the likelihood of initiation of an action potential, such a... 

FIGURE 12-38. Another current therapeutic approach to preventing the neuronal destruction in Alzheimer s disease is also based on the molecular neurobiology of beta amyloid formation but emphasizes the involvement of APO-E binding protein in this process. If the synthesis of good APO-E could be ensured or the synthesis of bad APO-E prevented, possibly amyloid would not accumulate in the neuron. Changing the deposition of beta amyloid would hopefully prevent the progressive course of Alzheimer s disease. 

This was yet one more effort to find an MDMA-like substitute by the miniscule manipulation of the MDMA molecule. Perhaps a small molecular change might leave the particular magic of the MDMA action alone, but eliminate the serotonin neuron problem in test animals. Maybe the serotonin neuron change is essential for MDMA to have the action it has. Who can tell ... 

The discovery of toxin-induced parkinsonism in drug addicts led to the idea that idiopathic Parkinson disease may occur when susceptible individuals are exposed to some environmental toxin.14 Exposure to such a toxin through industrial waste or certain herbicides may begin the neuronal changes that ultimately result in Parkinson disease. A specific environmental factor, however, has not been identified yet. 

The cause of Parkinson disease remains unknown. However, the neuronal changes that produce the symptoms associated with this movement disorder... 

Biggio, F., Gorini, G., Caria, S., Murru, L., Mostallino, M. C., Sanna, E., and Follesa, P. (2006). Plastic neuronal changes in GABA(A) receptor gene expression induced by progesterone metabolites In vitro molecular and functional studies. Pharmacol. Biochem. Behav. 84, 545-554. 

Bartus RT, Dean RL, Cavanaugh K, Eveleth D, Carriero DL, Lynch G (1995) Time-related neuronal changes following middle cerebral artery occlusion Implications for therapeutic intervention and the role of calpain. J Cereb Blood Flow Metab 15 969-979... 

Ingham CA, Hood SH, Arbuthnott GW (1989) Spine density on neostriatal neurones changes with 6-hydroxydopamine lesions and with age. Brain Res 505 334-338. 

Uylings, H.B., de Brabander, J.M. (2002). Neuronal changes in normal human aging and Alzheimer s disease. Brain Cogn. 49 268-76. 

Cece R, Petruccioli MG, Cavaletti G, Barajon I, Tredici G. An ultrastructural study of neuronal changes in dorsal root ganglia (DRG) of rats after chronic cisplatin administrations. Histol. 41. Histopathol. 1995 10 837-845. 

Is it possible to localize memory No. This is because having a memory is a psychological property of a person, or an animal, as a whole. In other words, as brains do not have memories, one cannot localize them in the brain. However, maybe one can localize those neuronal changes necessary and sufficient for a particular change in behaviour Thus, the trick is to not try to localize a psychological process ( memory ), but the substrate of its behaviour corollary (the memory trace ). 

The leading idea of this monograph is the view that in a species capable of acquiring drives the function of the cortical neurons changes in response to training in three consecutive phases. Each of these represents a characteristic form of behavior, as follows ... 

This means that whenever a drive is acquired, chains of ICRs are fixed in the brain thus, groups of telencephalic neurons change irreversibly through practice, training or exercise, as described in Sect. 3.4.2 at the same time, groups of neurons responsible for emotions are inevitably coupled to the integral whole that can be ecphorized later at any time in the future. 

Kwai, K., Nitecka, L., Ruetzler, C.A., Nagashima, G., Joo, F., Mies, G., Nowak, T. S., Saito, N., Lohr, J. M., and Klatzo, I., Global cerebral ischemia associated with cardiac arrest in the rat. I. Dynamics of early neuronal changes, J. Cereb. Blood Flow Metab., 12, 238, 1992. 

Chen, J-C. Schnepper, P.W. To, A. and Volicer, L. Neuronal changes in the rat brain after intraventricular administration of tryptamine-4,5- dione. Neuropharmacology 31 215-219, 1992. 

Zigmond, R., Hyatt-Sachs, H., Baldwin, C., Qu, X., Sun, Y., McKeon, T., Schreiber, R. and Vaidyanathan, U. (1992) Phenotypic plasticity in adult sympathetic neurons changes in neuropeptide expression in organ culture. Proc. Natl. Acad. Sci. USA 89 1507-1511. 

Maybe the serotonin neuron change is essential for MDMA to have the action it has. Who can tell ... 

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