Nerve cell maturation

Like other cells, a neuron has a nucleus with genetic DNA, although nerve cells cannot divide (replicate) after maturity, and a prominent nucleolus for ribosome synthesis. There are also mitochondria for energy supply as well as a smooth and a rough endoplasmic reticulum for lipid and protein synthesis, and a Golgi apparatus. These are all in a fluid cytosol (cytoplasm), containing enzymes for cell metabolism and NT synthesis and which is surrounded by a phospholipid plasma membrane, impermeable to ions and water-soluble substances. In order to cross the membrane, substances either have to be very lipid soluble or transported by special carrier proteins. It is also the site for NT receptors and the various ion channels important in the control of neuronal excitability. 

From a historical standpoint, no other cell type has attracted as much attention or caused as much controversy as the nerve cell. It is impossible in a single chapter to delineate comprehensively the extensive structural, topographical and functional variation achieved by this cell type. Consequently, despite an enormous literature, the neuron still defies precise definition, particularly with regard to function. It is known that the neuronal population usually is established shortly after birth, that mature neurons do not divide and that in humans there is a daily dropout of neurons amounting to approximately 20,000 cells. These facts alone make the neuron unique. 

Communication in the brain takes place between nerve cells or neurons. Psychoactive substances alter many aspects of communication between neurons, as will be discussed below. Neurons are highly speciahzed cells that exist in many shapes, sizes and varieties. However, they share the following basic structural regions cell body or soma, dendrites, axon, and terminal buttons. The cell body, or soma, is the metabolic centre of the neuron, and contains the nucleus and other structures that sustain the neuron. The nucleus plays a role in mature neurons, where it is used to synthesize proteins in response to a wide variety of stimuli (11, 17). 

Ulfig N, Nickel J, Bohl J. Monoclonal antibodies SMI311 and SMI312 as tools to investigate the maturation of nerve cells and axonal patterns in human fetal brain. Cell Tissue Res. 1998 291 433-443. 

We know that in the mature brain, neurotransmitters are released by nerve cell endings and act at synapses to mediate the interaction between nerve cells. There s now evidence that during the development of the prenatal brain, neurons can release transmitters before any connections are made, and that such released transmitters, acting as trophic factors, guide the formation of connections.17 Any environmental impact or mutation that affects the synthesis or release of neurotransmitters can be expected to have an effect on the development of the fetal brain. For example, during fetal development in Down syndrome, reductions apparently occur in the levels of various neurotransmitters. This may be one mechanism for the impaired brain development characteristic of this syndrome.18... 

The differentiated somatic cell of the integument (a keratinocyte) obeys proper biochemical orders (in the form of proto-oncoproteins with or without chemo-, cyto-, and lymphokines) to reverse its trajectory and become a stem cell, and then to re-differentiate into a nerve cell (Shinya Yamanaka s Nobel Prize, 2012). Improperly stimulated, it may become a basal cell carcinoma, or a squamous cell carcinoma. The ancient RNA/DNA complex will de-di ferentiate the mature somatic cell to its ancestral stage of existence. A fatal event mistakenly installed A process of re-juvenation inherently installed Is this a blind duty of the genomic retrotransposons for the maintenance of the living matter in whatever formation or shape (see in the text) ... 

The alterations in morphological organization of the brain resulting from hypothyroidism have been documented [10-13]. Numerous biochemical parameters are affected by altered thyroid states (for review see 14-16). Recent biochemical data on the effect of thyroid hormones on nerve cell differentiation indicate that they regulate microtubule assembly by changing the concentration and/or the activity of MAPS (tau fraction) [17]. The critical period of effectiveness of thyroid hormones in brain maturation raises a special problem. The correct organization of... 

At lower exposures, the effects of lead are more difficult to examine. It appears that data from recent studies on developing rats with low blood levels (up to 100/(g Pb/lOOml) appear to show effects of lead on maturing and differentiated nerve cell populations. The relevance of these changes to human subclinical lead intoxication is not clear. However, the overall correspondence in lead-poisoned man and rat would make further investigation in this area appear necessary. 

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