Harrell L E, Ayyagari V, Peagler A, Parsons D S
Department of Neurology, Veterans' Administration, Birmingham, Alabama.
Hippocampus. 1994 Apr;4(2):199-203. doi: 10.1002/hipo.450040210.
Cholinergic denervation of the hippocampus by medial septal (MS) lesions results in the ingrowth of peripheral sympathetic fibers, originating from the superior cervical ganglia, into the hippocampus. To determine the effect of hippocampal sympathetic ingrowth (HSI) [3H]-QNB (L-quinuclidinyl [benzilic-4,4(n)] binding was assessed in the dorsal and ventral hippocampus four weeks after MS lesions. In dorsal hippocampus, HSI was found to significantly increase the number (Bmax) of [3H]-QNB binding sites and to normalize the decrease in affinity found in animals with MS lesions plus ganglionectomy (i.e., no ingrowth). In ventral hippocampus, HSI was found to normalize the increased number of binding sites and decreased affinity found in animals with MS lesions without ingrowth. No effect on either Kd or Bmax was found in animals that had undergone ganglionectomy with sham MS lesions. These results suggest that HSI can induce changes in hippocampal muscarinic cholinergic receptors.
内侧隔区（MS）损伤导致海马胆碱能去神经支配，使得源自颈上神经节的外周交感神经纤维长入海马。为了确定海马交感神经长入（HSI）的影响，在MS损伤四周后，评估了[3H]-QNB（L-喹核碱基[苯甲酰-4,4(n)]结合）在背侧和腹侧海马中的情况。在背侧海马中，发现HSI显著增加了[3H]-QNB结合位点的数量（Bmax），并使MS损伤加神经节切除术（即无神经长入）动物中发现的亲和力降低恢复正常。在腹侧海马中，发现HSI使无神经长入的MS损伤动物中增加的结合位点数量和降低的亲和力恢复正常。在接受假MS损伤的神经节切除动物中，未发现对Kd或Bmax有任何影响。这些结果表明，HSI可诱导海马毒蕈碱胆碱能受体发生变化。
