Differential ontogenetic appearance and regulation of stimulatory G protein isoforms in rat cerebral cortex by thyroid hormone deficiency

Thyroid hormone regulates Gαi1 gene expression in the rat cerebellar cortex during post‐natal development

“…In this regard, it is interesting that other authors have suggested that changes in the half life and distribution of G proteins underlie the action of T 3 , which seems to be the case of thyroid hormone induction of Gαs protein in ventricular myocytes in culture (Bahouth 1995). Concurrent with our results, other authors did not observed changes in the content of Gαi1, Gαi2 and Gα0 proteins in the cerebral cortex of hypothyroid neonates (Wong et al . 1994; Li et al .…”

Developmentally-induced hypothyroidism alters the expression of Egr-1 and Arc genes and the sensitivity to cannabinoid agonists in the hippocampus. Possible implications for memory and learning

“…In addition to the lack of changes in the amount of CB1R, it is unlikely that these differences are due to differences in the hippocampal content of G proteins. Previous work from our group has shown that there are no changes in the hippocampal amount of Gi and Go transcripts between control and hypothyroid rats (Alvarez et al, 2005) and to our knowledge, no differences in the brain levels of G proteins have been described by others (Li et al, 1995;Wong et al, 1994). Finally, the possibility that an alternative cannabinoid receptor could be responsible for the increased cannabinoid response in the hippocampus of hypothyroid animals it is very unlikely.…”

Signal Transduction Processes in the Developing Brain: Perturbations of G Protein Alpha-Subunit Abundances by Perinatal Hypothyroidism

“…We are unaware of any published studies of the effect of perinatal hypothy roidism on CNS adenylyl cyclase activities or their regu lation. However, one can advance some tentative quali tative predictions based on our present findings and those of Wong et al [10]. From approximately day 10 to day 22 post-partum, hypothyroidism significantly decreases the abundance of Gsa in rat cortical mem branes [10] which might be expected to blunt stimulation of all forms of cyclase, although possibly less so in the case of cyclases I and VIII where stimulation by G^a (rather than by CaJ7calmodulin) is relatively mild [44].…”

“…However, one can advance some tentative quali tative predictions based on our present findings and those of Wong et al [10]. From approximately day 10 to day 22 post-partum, hypothyroidism significantly decreases the abundance of Gsa in rat cortical mem branes [10] which might be expected to blunt stimulation of all forms of cyclase, although possibly less so in the case of cyclases I and VIII where stimulation by G^a (rather than by CaJ7calmodulin) is relatively mild [44]. Cyclases I, V and VI can be inhibited by G^a, and G,2a [48] and cyclase type I can also be inhibited via G"a [48] (types II, II and IV are unaffected by G, or G" a-subunits [48]).…”

“…Recently Wong et al [10], using a methimazole-induced model of hypothyroidism, showed that hypothyroidism substantially reduced the expression of the 45-kD splice variant Gvsa in a cerebral cortex crude membrane prepa ration from rats aged 10-22 days. By contrast, no sig nificant differences were observed for G ,la, G,2a, Goa, Gt| /1,oc or Gsla in the same crude membrane preparation.…”