Changes in extracellular glutamate and pressor response during muscle contraction following AMPA-receptor blockade in the RVLM and CVLM.

We examined whether modulation of cardiovascular responses by administering 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, an AMPA-receptor antagonist) into the rostral (RVLM) or caudal (CVLM) ventrolateral medulla are mediated via changes in extracellular levels of glutamate. Microdialysis probes were inserted bilaterally into the RVLM or the CVLM. For the RVLM experiments (n=8), muscle contraction for 2 min increased mean arterial pressure (MAP) and heart rate (HR) by 18+/-3 mmHg and 24+/-5 bpm, respectively. Extracellular glutamate concentrations increased from 1.5+/-0.3 to 4.3+/-0.9 ng/5 microl during the contraction. Microdialysis of CNQX (1.0 microM) for 30 min into the RVLM attenuated the increases in MAP, HR, and glutamate concentration in response to a muscle contraction (8+/-2 mmHg, 11+/-3 bpm, and 2.2+/-0.7 ng/5 microl, respectively). Developed tensions did not change during contractions before and after CNQX. Microdialysis of CNQX into the CVLM (n=8) potentiated the contraction-evoked responses in MAP (19+/-3 vs. 34+/-3 mmHg) and HR (25+/-4 vs. 49+/-5 bpm) without a change in developed tension. Following CNQX perfusion into the CVLM, the levels of extracellular glutamate in the CVLM were also augmented during the contraction. Results suggests that AMPA-receptors within the RVLM and CVLM differentially modulate cardiovascular responses during static muscle contraction via increasing and decreasing, respectively, extracellular glutamate concentrations.

Lateralized effects of ethanol on aggression and serotonergic systems in Anolis carolinensis.

The lateralized effects of ethanol (ETOH) upon behavior and monoamine biochemistry in the lizard, Anolis carolinensis, were examined. Eight adult male anoles consumed solutions of 19% ethanol (ETOH) twice daily over the course of 18 days, while controls consumed water. ETOH decreased the use of the left eye/right hemisphere, but not the right eye/left hemisphere, during territorial aggression (p<0.05). During crossover (i.e., ETOH to water and vice versa) this effect was reversible and replicable. Biochemically, an asymmetry was observed in 5-HT levels in the raphe both in ETOH and controls. ETOH increased levels of serotonin (5-HT; p<0.05), and 5-HIAA/5-HT ratios (p<0.05) in the raphe; serotonin levels in several brain regions correlated with aggressive responses. These results suggest that ETOH boosts 5-HT levels in animals subchronically exposed to ETOH. They further suggest that asymmetry in endogenous 5-HT systems may account for the asymmetrical regulation of aggression generally, and may explain the behavioral effects of ETOH upon lateralized aggression.

Cardiovascular responses to muscle contraction following microdialysis of nitric oxide precursor into ventrolateral medulla.

We determined the effects of administering L-arginine, a precursor for the synthesis of nitric oxide, and L-NMMA (NG-monomethyl-L-arginine), a nitric oxide synthase blocker, into the rostral (RVLM) and caudal (CVLM) ventrolateral medulla on cardiovascular responses elicited during static contraction of the triceps surae muscle. Two microdialysis probes were inserted bilaterally into the RVLM or CVLM of anesthetized Sprague-Dawley rats using stereotaxic guides. For RVLM experiments, static muscle contraction evoked by stimulation of the tibial nerve increased mean arterial pressure (MAP) and heart rate (HR) by 29+/-3 mmHg and 44+/-7 bpm, respectively (n=8). Microdialysis of L-arginine (1.0 microM) for 30 min attenuated the contraction-evoked increases in MAP and HR. After discontinuing L-arginine, L-NMMA (1.0 microM) was microdialyzed into the RVLM for an additional 30 min followed by a muscle contraction. This contraction augmented the pressor response (37+/-4 mmHg) and HR (61+/-11 bpm) with respect to control values. For CVLM experiments, muscle contraction increased MAP and HR by 23+/-3 mmHg and 25+/-5 bpm, respectively (n=9). Microdialysis of L-arginine (1.0 microM) for 30 min potentiated the contraction-evoked increases in MAP and HR. Subsequent administration of L-NMMA (1.0 microM) into the CVLM for an additional 30 min blocked the augmented MAP and HR responses. Developed tensions did not alter during contractions throughout both RVLM and CVLM protocols. These results suggest that nitric oxide, within the RVLM and CVLM, plays an opposing role in modulating cardiovascular responses during static muscle contraction.