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Ventral hippocampus modulates bradycardic response to peripheral chemoreflex activation in awake rats
Author(s) -
Kuntze Luciana Bärg,
FerreiraJunior Nilson Carlos,
Lagatta Davi Campos,
Resstel Leonardo Barbosa Moraes
Publication year - 2016
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/ep085393
Subject(s) - neuroscience , hippocampus , peripheral , medicine , biology , psychology
New FindingsWhat is the central question of this study? Does reversible synaptic inactivation by CoCl 2 in the dorsal (DH) or ventral (VH) portions of the hippocampus have a modulatory effect on cardiovascular and respiratory responses evoked by chemoreflex activation in awake rats?What is the main finding and its importance? Using i.v . infusion of KCN to activate the peripheral chemoreflex before and after microinjection of CoCl 2 into VH, we showed that the bradycardic response was increased, but not the pressor and tachypnoeic responses even if the tidal volume had been increased. Thus, VH but not DH may be involved in the modulation of the parasympathoexcitatory component of the peripheral chemoreflex.In rats, peripheral chemoreflex activation evokes pressor and bradycardic responses as well as a tachypnoeic response. Studies have shown that limbic structures, such as the hippocampus, can modulate autonomic reflexes. Evidence suggests that the dorsal (DH) and the ventral (VH) portions of the hippocampus are structurally and functionally distinct; therefore, in the present study we tested the hypothesis that local neurotransmission of the DH and VH are involved in the neural pathways of the cardiovascular and ventilatory responses to chemoreflex activation. Thus, the goal of the present study was to compare the chemoreflex responses elicited by i.v . injection of KCN (40 μg per rat) in awake rats before and after DH and VH synaptic transmission was temporarily inhibited by bilateral microinjections of 500 nl of the unspecific synapse blocker, CoCl 2 (1 m m ). Bilateral inhibition of VH, but not DH, 10 min before KCN infusion was able to enhance the bradycardic response ( P < 0.05), with no changes in the typical pressor and tachypnoeic responses evoked by chemoreflex activation ( P > 0.05). Furthermore, the tidal volume was significantly increased ( P < 0.05) even though no other respiratory parameter had been significantly changed ( P > 0.05), suggesting that VH can exert a tonic modulatory action on tidal volume. Therefore, the present study reports, for the first time, that DH neurotransmission did not exert an influence on chemoreflex responses, whereas VH mediates, at least in part, the parasympathoexcitatory component of the peripheral chemoreflex.