Neuronal maturity

Rivera, C, Voipio, J, Payne, JA, Ruusuvuori, E, Lahtinen, H, Lamsa, K, Pirvola, U, Saarma, M and Kaila, K (1999) The K+/CU co-transporter KCC2 renders GABA hyperpolarizing during neuronal maturation. Nature 397 251-255. 

The mechanism which operates to select the functional member of an allele pair during neuronal maturation is not known for vomeronasal... 

Clanis H. and Key B. (2001). Expression of glycoproteins in the vomero-nasal organ reveals a novel spatiotemporal pattern of sensory neurone maturation. J Neurobiol 46, 113-125. 

Preclinical studies have shown that prenatal exposure to nicotine reduces brain weight, decreases cortical thickness, and produces abnormalities of pyramidal neuron maturation (Lee, 1998). Reduction in CNS markers of catecholamine activity, such as tyrosine hydroxylase activity, have been observed however, these appear to normalize by adolescence (Levitt, 1998). 

Changes in brain structure can occur in many different ways. For instance, neuronal death or disruptions in neuronal maturation (see also section 3.2), differentiation (see also section 3.7), migration, synaptic formation, glial and neurochemical development (see also section 3.4), can all have effects on brain structure. 

Dawson, H. N., Ferreira, A., Eyster, M. V., Ghoshal, N., Binder, L. L, Vitek, M. P. (2001). Inhibition of neuronal maturation in primary hippocampal neurons from tau deficient mice. J. Cell Sci. 114, 1179-1187. 

During development, programmed cell death is a common norm in developing neurons. However, the intrinsic pro-apoptotic pathw ays are obliterated as neurons mature. Thus, mere withdraw al of trophic factors does not suffice in inducing their death. Additionally, a genuine apoptotic signal is required for onset of self-suicide process in neurons. Specific gene-products undertake the apoptotic task in different types of neurons and different stimuli may induce distinct apoptotic pathw ays in them (Pettmann and Henderson, 1998). 

As the neurons mature, the neurite processes (axons and dendrites) will increase in length and complexity. Normally one of the neurites grows more rapidly in length and acquires axonal characteristics, while the remaining extensions elongate slower and becomes dendrites [84], The connections between cells are formed in far greater numbers than necessary during development and these are later slowly reduced to the required level. However, little is known about the molecular processes behind this phenomenon. 

To achieve neuronal mature function, the neurons must communicate by forming cell-cell connections through synapses. In rats this process occurs over the first three weeks postnatally [85] and in humans through adolescence [86]. Neurons generally have thousands of synapses and retain their ability to form new synapses throughout life. 

Many of the therapeutic uses of L-tryptophan are directed toward its effect on neurotransmission. Actually, diet itself clearly influences neurotransmission. This can best be illustrated in grossly undernourished children. Investigations have reported that starvation can impair neuronal maturation and can have lasting effects upon intellectual and behavior performance. When gross malnutrition does not exist, subtle changes in diet may modulate brain function. L-tryptophan, as well as tyrosine and choline, in the diet are precursors for neuronal synthesis of serotonin, dopamine, and norepinephrine, and acetycholine, respectively. Thus, L-tryptophan may be useful under certain circumstances as a drug in treatment of humans.121 On the other hand, in states of undernutrition, L-tryptophan therapy in itself is not curative, while proper nutrition may be the therapy of choice. 

Azmitia, E.C. and de Kloet, E. (1987) ACTH neuropeptide stimulation of serotonergic neuronal maturation in tissue culture modulation by hippocampal cells. Prog. Brain Res. 72 311-318. 

There is evidence that the concentration of normal metabolites in the brain varies according to the patients age (van der Knaap et al., 1990 Kreis et al, 1993). This variation is more noticeable during the first three years of life, but may be seen up to 16 years of age (van der Knaap et al, 1990). The most striking variation is an increase in the NAA/Cr ratio and a decrease in the Cho/Cr ratio as the brain matures (Figure 65.1). These changes may reflect neuronal maturation and an increase in the number of axons, dendrites and synapses. 

Moreover, since myelin induces neuronal maturation, the decrease in protein synthesis may also impact neurons/ axons. Therefore, the observed global decrease in protein synthesis detected in PKU mouse brain (Smith and Kang, 2000) may not be surprising. 

T-Protein present in neurons stabilizes microtubules. This operation is controlled by kinases. Within the neurodegenerative diseases, it is necessary to mention two of these enzymes in the context of natural substances. GSK-3p plays a key role in T2DM and AD. CDK5 is involved in the processes of neuronal maturation and migration, or more precisely neuronal structuring during brain development. It is a very active topic and therefore there is great interest in the substances, which may affect their activity. 

Separation of Drug Carrier from DDV was Neuronal Maturation-Dependent... 

Different stages of spinal cell culture growth were used to evaluate the efficacy of separation of drug carrier from DDV. Confocal image analysis revealed that about 20, 32 and 40% of the drug carrier component separated from DDV and diffused into the cytosol from endosomes in 1, 2 and 3 weeks culture, respectively (Fig. 4, Dl, D2 and 4, D3 table 1). These results indicated that the separation of the drug carrier from DDV is neuronal maturation-dependent. Furthermore, the separations of DDV components occur in a time-dependent manner. 

Samat HB (2013) Clinical neuropathology practice guide 5-2013 markers of neuronal maturation. Clin Neuropathol 32 340-369... 

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