The disturbances in SHR do not appear to be restricted to a single neurotransmitter system. Differences between SHR and WKY suggest that the fundamental defect in SHR affects several, functionally distinct, neurotransmitter pathways. The disturbances of SHR can possibly be attributed to defects in two major second messenger systems, namely, impaired cyclic adeno-sine monophosphate (cAMP) formation (8) and impaired calcium influx into cells (58).
Horn et al. (59) showed that synaptic plasma membranes prepared from SHR cerebrum have lower Ca2+ adenosine triphosphatase activity than WKY. This implies that Ca2+ is removed at a slower rate from SHR cytoplasm than WKY; hence the concentration gradient that drives Ca2+ into the cell is not as steep in SHR as in WKY. A lower Ca2+ concentration gradient may account for the decreased Ca2+ uptake observed in cerebral cortex slices of SHR compared to WKY (58). Decreased Ca2+ influx could impair W-methyl-D-aspaitate receptor function (58). Because neurotransmitter release is dependent on the influx of Ca2+ into presynaptic terminals and varicosities, an underlying disturbance in calcium metabolism could cause compensatory alterations in the regulation of neurotransmitter release.
The hyperactivity observed in ADHD children has been suggested to be because of increased cAMP levels in the prefrontal cortex and striatum (60). Increased expression of Gia genes has been demonstrated in very young SHRs at 2 wk of age (8). Inactivation of Gia proteins by intraperitoneal injection of pertussis toxin into 2-wk-old SHRs delayed the development of hypertension (61). These results suggest that the increased expression of genes for Gi proteins, with a consequent decrease in cAMP levels and impaired regulation of cellular function, precedes the elevation of blood pressure and may contribute to the development of hypertension and ADHD symptoms in SHRs. If striatal Gia proteins are also increased, then activation of D2 receptors may give rise to enhanced D2 receptor-mediated inhibition of dopamine release from SHR nucleus accumbens and caudate-putamen slices (20-22).
Downregulation of a2-adrenoceptors observed in the SHR central nervous system may have been a compensatory response to increased Gia-mediated inhibition of adenylyl cyclase in an attempt to increase stimulus-evoked release of norepinephrine (37).
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Attention Deficit Disorder or ADD is a very complicated, and time and again misinterpreted, disorder. Its beginning is physiological, but it can have a multitude of consequences that come alongside with it. That apart, what is the differentiation between ADHD and ADD ADHD is the abbreviated form of Attention Deficit Hyperactive Disorder, its major indications being noticeable hyperactivity and impulsivity.