The Nervous Heart video lecture notes


  Dr. Crystal Ripplinger

5:40 nerve:myocyte ratio similar to capillary myocyte ratio; all myocytes in ventricular myocardium are in contact with at least one neuronal process   

6:27 more nerves at base of heart than apex, more sympathetic in epicardium, more parasympathetic in endocardium  

11:15 how sympathetic nerve loss contributes to arrhythmia post-myocardial infarction (heart attack) 12:52 heterogeneity in innervation can be arrhythmogenic  

13:02 nerve loss, lack of norepinephrine can lead to beta adrenergic receptor hypersenstitivity & supersensitive response to neurotransmitters 

 14:03 Chondroitin sulfate proteoglycans (CSPGs) inhibit sympathetic regeneration after infarction, also prevent spinal cord regeneration  

20:22 localized lesioning with anti-DBH-saporin; anti-dopamine beta hydroxylase antibody conjugated to toxin that gets into cell via synaptic vesicle  

28:30 differences between larger animals (rabbits) and mice in how sympathetic stimulation affects action potential duration, differences in fight or flight responses  

32:30 model mouse for studying cAMP second messenger activity  

40:00 mapping spatial kinetics of cAMP activity  

41:29 regional differences in phosphodiesterase activity (nice movie)  

43:26 electrophysiological responses relative to cAMP activity 

 47:30 Q&A  

48:00 too much sympathetic activity in heart failure leads to decreased beta adrenergic receptor sensitivity  

52:15 depth of tissue affected by painting with anti-DBH-saporin 

 52:45 reperfusion injury; in absence of reperfusion nerve re-growth is possible and may even result in hyperinnervation since no CSPGs  

54:45 what is source of CSPGs? 

 56:10 technical issues - FRET signal drift, NADH autoflourescence, change in NADH metabolism with sympathetic activity

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