Brain-derived neurotrophic factor in arterial baroreceptor pathways: implications for activity-dependent plasticity at baroafferent synapses.
Functional characteristics of the arterial baroreceptor reflex change throughout ontogenesis, including perinatal adjustments of the reflex gain and adult resetting during hypertension. However, the cellular mechanisms that underlie these functional changes are not completely understood. Here, we provide evidence that brain-derived neurotrophic factor (BDNF), a neurotrophin with a well-established role in activity-dependent neuronal plasticity, is abundantly expressed in vivo by a large subset of developing and adult rat baroreceptor afferents. Immunoreactivity to BDNF is present in the cell bodies of baroafferent neurons in the nodose ganglion, their central projections in the solitary tract, and terminal-like structures in the lower brainstem nucleus tractus solitarius. Using ELISA in situ combined with electrical field stimulation, we show that native BDNF is released from cultured newborn nodose ganglion neurons in response to patterns that mimic the in vivo activity of baroreceptor afferents. In particular, high-frequency bursting patterns of baroreceptor firing, which are known to evoke plastic changes at baroreceptor synapses, are significantly more effective at releasing BDNF than tonic patterns of the same average frequency. Together, our study indicates that BDNF expressed by first-order baroreceptor neurons is a likely mediator of both developmental and post-developmental modifications at first-order synapses in arterial baroreceptor pathways.
Martin
Jessica L
JL
Department of Integrative Biosciences, Oregon Health and Science University, Portland, OR 97239, USA.
Jenkins
Victoria K
VK
Hsieh
Hui-ya
HY
Balkowiec
Agnieszka
A
D000367:Age Factors; D000596:Amino Acids; D000818:Animals; D000831:Animals, Newborn; D001158:Arteries / Q000378:metabolism*; D055592:Biophysical Phenomena; D001933:Brain Stem / Q000033:anatomy & histology / Q000378:metabolism; D019208:Brain-Derived Neurotrophic Factor / Q000235:genetics / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002452:Cell Count / Q000379:methods; D002478:Cells, Cultured; D054815:Cyclic Nucleotide-Gated Cation Channels / Q000378:metabolism; D004558:Electric Stimulation / Q000379:methods; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D064428:Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D009475:Neurons, Afferent / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D009620:Nodose Ganglion / Q000166:cytology; D015221:Potassium Channels / Q000378:metabolism; D011311:Pressoreceptors / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013569:Synapses / Q000378:metabolism; D050916:TRPV Cation Channels / Q000378:metabolism
D000596:Amino Acids; D019208:Brain-Derived Neurotrophic Factor; D002121:Calcium Channel Blockers; D054815:Cyclic Nucleotide-Gated Cation Channels; D064428:Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels; D015221:Potassium Channels; D012333:RNA, Messenger; D050916:TRPV Cation Channels; C493921:TRPV1 protein, mouse; C098463:dolaisoleucine