Increased sympathetic nerve activity induced by excitation/lesions of the gigantocellular depressor area (GiDA) is not affected by rostral medullary transection

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GiDA stimulation produced sympathoinhibition and hypotension, while microinjections of kainic acid (KA) in this region produced increased levels of sympathetic nerve activity (SNA) and hypertension. The present study sought to determine whether the effects of KA in GiDA are dependent on either RVLM activity or forebrain projections. Recordings of arterial pressure (AP) and heart rate (HR) and postganglionic splanchnic SNA were made from male Sprague-Dawley rats (300–500 g) anesthetized with urethane/chloralose, paralyzed, and artificially ventilated. Bilateral microinjections of KA (20mM) into GiDA produced hypertension (154±11mmHg) and increased SNA to 175% of control. SNA remained elevated (201±51% of control) following a transection of the neuraxis between GiDA and RVLM (2.3 mm rostral to calamus scriptorius), although AP was reduced to 88±13 mmHg. In a separate group of animals, bilateral muscimol microinjections into the RVLM decreased SNA (−55±4% of control) and AP (54±6 mmHg). Under these conditions, KA into the GiDA increased SNA to 260±16% of control and AP to a peak of 167±8 mmHg. SNA was unchanged (257±16% of control) following a transection rostral to RVLM (3.5 mm rostral to calamus scriptorius), although AP was reduced to 80±12 mmHg. These results suggest that an increase in SNA and a hypertension can be induced by KA into the GiDA during muscimol inhibition of the RVLM and in the absence of connections between GiDA and forebrain structures. Financial support: CAPES.