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1 Neuroscience, Pennington Biomedical Research Center- LSU System, Baton Rouge, LA, USA
* To whom correspondence should be addressed. E-mail: travagra{at}pbrc.edu.
Cholecystokinin (CCK) is released from enteroendocrine cells following ingestion of nutrients and induces multiple effects along the gastrointestinal tract, including gastric relaxation and short-term satiety. We used whole cell patch clamp and immunohistochemical techniques in rat brainstem slices to characterize the effects of CCK. In 45% of the neurons of nucleus tractus solitarius subnucleus centralis (cNTS), perfusion with the sulfated form of CCK (CCK8s) increased the frequency of spontaneous excitatory currents (sEPSCs) in a concentration-dependent manner (1-300nM). The threshold for the CCK-8s excitatory effect was 1nM, the EC50 was 20nM and Emax was 100nM. The excitatory effects of CCK-8s were still present when the slices were preincubated with tetrodotoxin or bicuculline and when the recordings were conducted with Cs+ electrodes. Pretreatment with the CCK-A receptor antagonist, lorglumide (1µM), antagonized the effects of CCK-8s, while perfusion with the CCK-B preferring agonist CCK-8 non sulfated (CCKns, 1µM) did not affect the frequency of sEPSCs. Similarly, pretreatment with the CCK-B receptor antagonist, triglumide (1µM), did not prevent the actions of CCK8s. While the majority (i.e. 76%) of CCK8s unresponsive cNTS neurons had a bipolar somata shape and were TH-IR negative, no differences were found in either the morphological or the neurochemical phenotype of cNTS neurons responsive to CCK8s. Our results suggest that the excitatory effects of CCK8s on terminals impinging on a subpopulation of cNTS neurons are mediated by CCK-A receptors; these responsive neurons, however, do not have morphological or neurochemical characteristics that automatically distinguish them from non responsive neurons.
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