Neurochemical codes of sympathetic preganglionic neurons activated by glucoprivation.
Glucoprivation or hypoglycemia induces a range of counterregulatory responses, including glucose mobilization, reduced glucose utilization, and de novo glucose synthesis. These responses are mediated in part by the sympathetic nervous system. The aim of this study was to determine the chemical codes of sympathetic preganglionic neurons (SPN) activated by glucoprivation, induced by 2-deoxy-D-glucose (2DG). SPN controlling the adrenal glands and celiac ganglia, which ultimately can innervate the liver and pancreas, were targeted together with the superior cervical ganglia (control). 23.9% ± 1.3% of SPN in the T4-T11 region contained c-Fos immunoreactivity following 2DG; 70.3% ± 1.8% of SPN innervating the adrenal glands and 37.4% ± 3% of SPN innervating celiac ganglia were activated. 14.8% ± 3.5% of SPN (C8-T3) innervating superior cervical ganglia were activated. In the C8-T3 region 55% ± 10% of SPN activated contained PPCART, with only 12% ± 3% expressing PPE mRNA, whereas, in the T4-T11 region, 78% ± 4% contained PPE, with only 6.0% ± 0.6% expressing PPCART mRNA. Thus CART is not involved in glucose mobilization. Two chemically distinct populations of SPN (PPE⁺ 57.4% ± 5%, PPE⁻ ∼40%) were identified to regulate adrenaline release in response to glucoprivation. Multiple chemically distinct SPN populations innervating a specific target could suggest their graded recruitment. The two distinct populations of SPN (PPE⁺ 67.6% ± 9%, PPE⁻ ∼30%) projecting to celiac ganglia activated by glucoprivation could direct pancreatic and hepatic or other counterregulatory responses. Nearly all SPN that expressed PPE mRNA and projected to the adrenal glands or celiac ganglia were activated, suggesting a role for the inhibitory peptide enkephalin in responses evoked by glucoprivation.
The Australian School of Advanced Medicine, Macquarie University, Macquarie Park, 2109 New South Wales, Australia.
Lindsay M
LM
Parker
Natasha N
NN
Kumar
Tina
T
Lonergan
Ann K
AK
Goodchild
D000311:Adrenal Glands / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000187:drug effects; D002772:Cholera Toxin / Q000378:metabolism; D002795:Choline O-Acetyltransferase / Q000235:genetics / Q000378:metabolism; D019439:Chromaffin Cells / Q000378:metabolism; D003847:Deoxyglucose / Q000009:adverse effects / Q000378:metabolism; D004745:Enkephalins / Q000235:genetics / Q000378:metabolism*; D004837:Epinephrine / Q000097:blood; D005456:Fluorescent Dyes / Q000378:metabolism; D005728:Ganglia, Sympathetic / Q000166:cytology* / Q000378:metabolism*; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology*; D007003:Hypoglycemia / Q000097:blood / Q000139:chemically induced / Q000473:pathology*; D008297:Male; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism; D009474:Neurons / Q000378:metabolism*; D010625:Phenylethanolamine N-Methyltransferase / Q000235:genetics / Q000378:metabolism; D011498:Protein Precursors / Q000235:genetics / Q000378:metabolism*; D016760:Proto-Oncogene Proteins c-fos / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013116:Spinal Cord / Q000378:metabolism; D000098882:Cocaine- and Amphetamine-Regulated Transcript Protein
D001786:Blood Glucose; D004745:Enkephalins; D005456:Fluorescent Dyes; D009419:Nerve Tissue Proteins; D011498:Protein Precursors; D016760:Proto-Oncogene Proteins c-fos; D000098882:Cocaine- and Amphetamine-Regulated Transcript Protein; D002772:Cholera Toxin; C033660:preproenkephalin; D003847:Deoxyglucose; D010625:Phenylethanolamine N-Methyltransferase; D002795:Choline O-Acetyltransferase; D004837:Epinephrine