Ithaca College

Shannon Ryan (Biology '12).  Poster presentation, "Changes in synaptic efficiency in the guinea pig intrinsic cardiac plexus: Effects of acute myocardial infarction and neuromodulators."  Society for Neuroscience. Washington, DC. November 2011

Research was conducted under the supervision of Jean Hardwick.  The Society for Neuroscience meetings are attended annually by over 30,000 scientists from around the world.

Abstract:

Chronic heart disease has been shown to induce both phenotypic and functional remodeling of neurons within the intrinsic cardiac plexus of the guinea pig. The current study examined the time scale of this remodeling process, looking specifically at changes in synaptic efficiency at different time points following surgically-induced heart disease. Heart disease can be surgically-induced in the guinea pig to model myocardial infarction (MI) by ligature of the coronary artery and dorsal vein on the heart leaving an ischemic area on the surface of the ventricle. Fifteen male Hartley guinea pigs (Charles River) weighing between 300 and 500 grams were given myocardial infarctions and allowed to recover for either 4, 7, or 14 days. Nine animals, with no surgery, were used as controls. Animals were euthanized via CO2 inhalation and exsanguination. The heart and lungs were removed and the heart was dissected to expose the intrinsic cardiac plexus as a whole mount preparation for intracellular voltage recordings. An extracellular focal electrode was placed on nerve bundles connecting to the individual neuron used for recording. Fibers were stimulated with suprathreshold stimuli for 2seconds at a frequency of 10, 20, or 30Hz and the number of action potentials produced by the postsynaptic cells was determined. Previous studies found that animals with chronic MI (6 week recovery) show no difference in frequency output compared to control animals.  Conversely, in the acute MI studies, the 7 day recovery animals showed a significant increase in frequency output (p<0.002 at 30Hz) that was not seen at either 4 or 14 days post MI. Previous studies also demonstrated that several neuromodulators, such as norepinephrine (NE), PACAP27 (P27), and substance P (SP), increase neuronal excitability in these cells. Therefore the ability of these substances to increase frequency output with fiber tract stimulation (FTS) was tested. NE (Sigma, 10-3M), P27 (American Peptide, 10-5M), and SP (American Peptide, 10-4M) were applied by local pressure ejection to individual neurons. FTS (20Hz) was tested in with and without the application of either NE, P27, or SP. In both control and all three acute recovery time points, there was no significant differences in output frequency with neuromodulator application. This suggests that the increased excitability seen with disease at 7 days post MI is not due to enhanced adrenergic or neuropeptide release, but rather to an as yet, undetermined mechanism. Supported by NIH HL098589 to JCH.