title: Growth hormone treatment affects brain neurotransmitters and thyroxine [see comment].
abstract: OBJECTIVE
  Binding sites specific for growth hormone have been identified in the brain, but the action of GH on the central nervous system is still poorly understood.
  
  
  METHODS
  In a double-blind, placebo-controlled 21-month trial with a cross-over design, with each treatment period lasting for 9 months, we investigated the long-term effect of GH on the cerebrospinal fluid (CSF) concentrations of some brain neurotransmitters and thyroid hormones of importance for mood and cognition.
  
  
  METHODS
  Twenty-four patients with documented GH deficiency acquired in adult life took part.
  
  
  RESULTS
  Analysis of CSF collected at the end of the two treatment periods showed that the GH concentration was related to the administered dose of rhGH (r = 0.56, P = 0.0044). After rhGH treatment the concentration of the dopamine metabolite homovanillic acid (HVA) had decreased from 218 +/- 80 to 193 +/- 82 nmol/l (P = 0.002) and that of the excitatory acid aspartate had increased from 233 +/- 81 to 313 +/- 116 nmol/l (P = 0.032). No effects were observed on the concentrations of 5-hydroxyindoleacetic acid (the serotonin metabolite) and of 3-methoxy-4-hydroxyphenyl glycol (the noradrenaline metabolite), or on those of glutamate, glycine and beta-endorphin. However, both CSF and serum levels of free T4 decreased, from 19.8 +/- 6.1 to 16.6 +/- 5.7 nmol/l (P = 0.0002) and 17.0 +/- 5.0 to 13.7 +/- 4.3 nmol/l (P = 0.0001), respectively. The concentration of total T3 was not measurable in CSF but increased in serum from 1.41 to 1.53 nmol/l (P = 0.01).
  
  
  CONCLUSIONS
  The study demonstrates a passage of GH from the circulation into the CSF. The observed changes in homovanillic acid and free T4 are similar to those reported after successful treatment of depressive disorders with antidepressant drugs, and may reflect a beneficial effect of GH on mood and behaviour.
authors.affiliation: Department of Medicine, University Hospital, Uppsala, Sweden.
authors.forename: P
authors.initials: P
authors.lastname: Burman
authors.forename: J
authors.initials: J
authors.lastname: Hetta
authors.forename: L
authors.initials: L
authors.lastname: Wide
authors.forename: J E
authors.initials: JE
authors.lastname: Månsson
authors.forename: R
authors.initials: R
authors.lastname: Ekman
authors.forename: F A
authors.initials: FA
authors.lastname: Karlsson
mesh_terms: D000328:Adult; D001224:Aspartic Acid / Q000134:cerebrospinal fluid; D018592:Cross-Over Studies; D004311:Double-Blind Method; D005260:Female; D006130:Growth Disorders / Q000097:blood / Q000134:cerebrospinal fluid / Q000188:drug therapy*; D013006:Growth Hormone / Q000134:cerebrospinal fluid / Q000172:deficiency* / Q000627:therapeutic use*; D006719:Homovanillic Acid / Q000134:cerebrospinal fluid; D006801:Humans; D008297:Male; D008875:Middle Aged; D018377:Neurotransmitter Agents / Q000097:blood / Q000134:cerebrospinal fluid*; D011994:Recombinant Proteins / Q000627:therapeutic use; D013963:Thyroid Hormones / Q000097:blood / Q000134:cerebrospinal fluid*; D013974:Thyroxine / Q000097:blood / Q000134:cerebrospinal fluid; D014284:Triiodothyronine / Q000097:blood / Q000134:cerebrospinal fluid
chemical_list: D018377:Neurotransmitter Agents; D011994:Recombinant Proteins; D013963:Thyroid Hormones; D014284:Triiodothyronine; D001224:Aspartic Acid; D013006:Growth Hormone; D013974:Thyroxine; D006719:Homovanillic Acid