TY - JOUR
T1 - Developmental expression of tyrosine hydroxylase, D2-dopamine receptor and substance P genes in the carotid body of the rat
AU - Gauda, E. B.
AU - Bamford, O.
AU - Gerfen, C. R.
PY - 1996/12
Y1 - 1996/12
N2 - Alterations in the level of putative neurotransmitters/neuromodulators and corresponding receptors may be a possible mechanism involved in changes in chemosensitivity of peripheral chemoreceptors in the carotid body during development. Using quantitative in situ hybridization histochemistry, levels of messenger RNAs encoding tyrosine hydroxylase, the rate-limiting enzyme for dopamine synthesis, the D2-dopamine receptor and substance P of newborn rats at postnatal days 0, 2, 14 and 21 were determined. For comparison, during the same time points during development, we also determined the level of expression of these messenger RNAs in the cells of the superior cervical ganglion which are not chemosensitive. Tyrosine hydroxylase and D2-dopamine receptor messenger RNAs were co-localized in many of the cells in both the carotid body and the superior cervical ganglion. In the carotid body, the level of tyrosine hydroxylase messenger RNA expression was greatest at birth, significantly decreased by 48 h postnatal age and remained decreased at 14 and 21 postnatal days. In contrast, D2-dopamine receptor messenger RNA levels significantly increased with postnatal age in the carotid body. This profile of an inverse relationship between the level of expression of the messenger RNAs for tyrosine hydroxylase and D2-dopamine receptor was not observed in the superior cervical ganglion where tyrosine hydroxylase and D2-dopamine receptor messenger RNAs levels did not significantly change from postnatal days 0 to 21. Lastly, in the rat carotid body, substance P messenger RNA was not detected. However, substance P messenger RNA was abundant in the nodose and petrosal ganglion. The increasing contribution of carotid body on ventilation with increasing postnatal age is associated with changes in levels of gene expression for tryosine hydroxylase and D2-dopamine receptor in the carotid body.
AB - Alterations in the level of putative neurotransmitters/neuromodulators and corresponding receptors may be a possible mechanism involved in changes in chemosensitivity of peripheral chemoreceptors in the carotid body during development. Using quantitative in situ hybridization histochemistry, levels of messenger RNAs encoding tyrosine hydroxylase, the rate-limiting enzyme for dopamine synthesis, the D2-dopamine receptor and substance P of newborn rats at postnatal days 0, 2, 14 and 21 were determined. For comparison, during the same time points during development, we also determined the level of expression of these messenger RNAs in the cells of the superior cervical ganglion which are not chemosensitive. Tyrosine hydroxylase and D2-dopamine receptor messenger RNAs were co-localized in many of the cells in both the carotid body and the superior cervical ganglion. In the carotid body, the level of tyrosine hydroxylase messenger RNA expression was greatest at birth, significantly decreased by 48 h postnatal age and remained decreased at 14 and 21 postnatal days. In contrast, D2-dopamine receptor messenger RNA levels significantly increased with postnatal age in the carotid body. This profile of an inverse relationship between the level of expression of the messenger RNAs for tyrosine hydroxylase and D2-dopamine receptor was not observed in the superior cervical ganglion where tyrosine hydroxylase and D2-dopamine receptor messenger RNAs levels did not significantly change from postnatal days 0 to 21. Lastly, in the rat carotid body, substance P messenger RNA was not detected. However, substance P messenger RNA was abundant in the nodose and petrosal ganglion. The increasing contribution of carotid body on ventilation with increasing postnatal age is associated with changes in levels of gene expression for tryosine hydroxylase and D2-dopamine receptor in the carotid body.
KW - arterial chemoreceptors
KW - glomus cells
UR - http://www.scopus.com/inward/record.url?scp=0030561606&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030561606&partnerID=8YFLogxK
U2 - 10.1016/0306-4522(96)00312-0
DO - 10.1016/0306-4522(96)00312-0
M3 - Article
C2 - 8951888
AN - SCOPUS:0030561606
SN - 0306-4522
VL - 75
SP - 969
EP - 977
JO - Neuroscience
JF - Neuroscience
IS - 3
ER -