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Activation of NMDA receptors in the medial prefrontal cortex attenuates the cardiovascular response to acute stress
Author(s) -
MüllerRibeiro Flávia Camargos,
Zaretsky Dmitry V,
Zaretskaia Maria V,
DiMicco Joseph A,
Fontes Marco Peliky
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.645.8
The infralimbic region (IL) of the medial prefrontal cortex modulates autonomic and neuroendocrine functions via projections to subcortical structures involved in the response to stress. We evaluated the contribution of IL to the cardiovascular response evoked by acute stress. Under anesthesia (80 mg/kg ketamine and 11.5 mg/kg xylazine), rats were implanted with telemetry probes or arterial lines for recording heart rate and blood pressure. Guide cannulas were implanted in the IL for microinjection of muscimol (100 pmol/100 nl), NMDA (6 pmol/100 nl) or vehicle (100 nl). Microinjection of muscimol into the IL had no effect on stress‐evoked cardiovascular, thermogenic or behavioral changes in any of the paradigms evaluated (cage switch, restraint plus air jet noise, or air jet stress). However, microinjection of the excitatory amino acid NMDA attenuated the pressor (Δ MAP: 19 ± 2 mmHg vs. 12 ± 1 mmHg; P<0.05) and tachycardic (Δ HR: 124 ± 10 bpm vs. 82 ± 13 bpm; P<0.05) response to air jet stress. Pretreatment with the NMDA antagonist (AP‐5, 100 pmol/100 nl) blocked the effect of NMDA on the response to air jet stress. We conclude that 1) IL region is not tonically involved in the cardiovascular, thermogenic and behavioral control during stress or baseline conditions, 2) activation of NMDA receptors in the IL can suppress the cardiovascular response to acute stress exposure. Support: FAPEMIG, CAPES, CNPq, USPHS Grant NS 19883