Key result
Chemical lesioning of the ipsilateral dorsal medulla abolished the pressor response to glutamate in the PFTG, while lesioning the RVLM changed the PFTL depressor effect to a pressor one.
This preclinical study maps central cardiovascular regulatory pathways, demonstrating that PFTG pressor actions are mediated unilaterally via the ipsilateral DM, while PFTL depressor effects depend on the integrity of both the DM and RVLM.
The present project studies the effects of chemical lesioning in the dorsal medulla (DM) or rostral ventrolateral medulla (RVLM) on glutamate-induced cardiovascular action of the pontine gigantocellular tegmental field (PFTG) and lateral tegmental field (PFTL) in cats. Experiments were performed on 39 adult cats anesthetized with intraperitoneal injection of a mixture of alpha-chloralose and urethane. Systemic arterial blood pressure (SAP), heart rate (HR) and vertebral nerve sympathetic activity (VNA) were continuously monitored. Microinjections of the glutamate solution (Glu, 0.25 M of sodium glutamate dissolved in artificial cerebrospinal fluid with 0.5% pontamine sky blue) in 50- to 70- nl aliquots were made in the PFTG and PFTL. SAP, HR, and VNA were measured before and after chemical lesioning of the DM and/or RVLM and compared. The DM or the RVLM was lesioned by injection of 150-200 nl of kainic acid (24 mM) acutely. We found that when the ipsilateral DM was lesioned, microinjection of Glu into PFTG no longer elicited a pressor response. In contrast, when the contralateral DM was lesioned, the Glu-induced PFTG pressor response was little affected. Lesioning of either the ipsi- or contralateral RVLM affected the PFTG response very little. This suggests that the connection between PFTG in producing the pressor action is principally unilateral through the ipsilateral DM. When the ipsi- or contralateral DM was lesioned, injection of Glu into the PFTL no longer could elicit a depressor response. Interestingly, when either the ipsi- or contralateral RVLM was lesioned, the PFTL-induced depressor effect changed to a pressor one. These results suggest that the PFTL depressor effect is dependent on the integrity of both the DM and RVLM. Furthermore, there may be a mixture of sympathoexcitatory and parasympathoexcitatory neurons in the PFTL.
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Hsieh et al. (2000) studied this question. Chemical lesioning of the dorsal medulla (DM) or rostral ventrolateral medulla (RVLM) vs. Before chemical lesioning was evaluated on Systemic arterial blood pressure (SAP), heart rate (HR) and vertebral nerve sympathetic activity (VNA) responses to glutamate microinjection. Chemical lesioning of the ipsilateral dorsal medulla abolished the pressor response to glutamate in the PFTG, while lesioning the RVLM changed the PFTL depressor effect to a pressor one.
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