Although largely overlooked, GH has a number of neurotrophic actions (stimulating neuronal and glial proliferation, increasing myelination, and increasing brain size), whereas GH deficiency is associated with deficits in brain development (see ref. 1 for review). GH deficiency, and more especially GH treatment, are associated with a variety of changes in the major central neurotransmitters, their biosynthetic enzymes, or their receptors (102-106), but a physiological role for endogenous GH, acting directly on these systems, has not yet been established. As mentioned above, the expression of GHRs in the hippocampus is consistent with a role in learning and memory, and some effects of GH have been reported in ameliorating impairments in CNS function in GH-deficient animal models (106,107). The classic hippocampal electrophysiological paradigm for learning and memory is long-term potentiation (LTP), but preliminary results suggest that no obvious defects are seen in the ability to induce LTP in GH-deficient dwarf rats (M. L. Errington and I. C. A. F. Robinson, unpublished). This does not exclude the possibility of local GH effects, or that these animals might show some deficits when tested in behavioral paradigms of learning and memory. Further experiments of this type are clearly warranted in view of the increasing evidence from clinical studies that GH administration to GH-deficient adults may be associated with positive effects on mood and mental performance (56,108). Although it is always difficult to exclude secondary effects of GH treatment (increased muscle strength, loss of fat, increased energy), direct effects of GH on the metabolism or protein synthesis of neural tissue have been demonstrated (109,110). Thus, the presence of central GHRs in human brain tissue certainly encourage the speculation that some of the beneficial effects of GH treatment, assessed by psychological testing, may be direct (111).
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