ABSTRACT
The escape response to electrical or chemical stimulation of the dorsal periaqueductal gray matter (DPAG) has been associated with panic attacks. In order to explore the validity of the DPAG stimulation model for the study of panic disorder, we determined if the aversive consequences of the electrical or chemical stimulation of this midbrain area can be detected subsequently in the elevated T-maze. This animal model, derived from the elevated plus-maze, permits the measurement in the same rat of a generalized anxiety- and a panic-related defensive response, i.e., inhibitory avoidance and escape, respectively. Facilitation of inhibitory avoidance, suggesting an anxiogenic effect, was detected in male Wistar rats (200-220 g) tested in the elevated T-maze 30 min after DPAG electrical stimulation (current generated by a sine-wave stimulator, frequency at 60 Hz) or after local microinjection of the GABA A receptor antagonist bicuculline (5 pmol). Previous electrical (5, 15, 30 min, or 24 h before testing) or chemical stimulation of this midbrain area did not affect escape performance in the elevated T-maze or locomotion in an open-field. No change in the two behavioral tasks measured by the elevated T-maze was observed after repetitive (3 trials) electrical stimulation of the DPAG. The results indicate that activation of the DPAG caused a short-lived, but selective, increase in defensive behaviors associated with generalized anxiety.
Subject(s)
Animals , Male , Rats , Anxiety/physiopathology , Behavior, Animal/drug effects , Escape Reaction/drug effects , Panic Disorder/physiopathology , Periaqueductal Gray/drug effects , Behavior, Animal/physiology , Bicuculline/pharmacology , Electrodes, Implanted , Escape Reaction/physiology , Maze Learning/drug effects , Maze Learning/physiology , Periaqueductal Gray/physiology , Rats, WistarABSTRACT
We investigated the effect of acute oral treatment with a water-alcohol extract of the inflorescence of Erythrina mulungu (EM, Leguminosae-Papilionaceae) (100, 200 and 400 mg/kg) on rats submitted to different anxiety models: the elevated T-maze (for inhibitory avoidance and escape measurements), the light/dark transition, and the cat odor test. These models were selected for their presumed capacity to demonstrate specific subtypes of anxiety disorders as recognized in clinical practice. Treatment with 200 mg/kg EM impaired avoidance latencies (avoidance 1 - 200 mg/kg EM: 18 + or - 0 7 s, control group: 40 or - 9 s; avoidance 2 - 200 mg/kg EM: 15 + or - 4 s, control group: 110.33 + or - 38 s) in a way similar to the reference drug diazepam (avoidance 1: 3 + or - 0.79 s; avoidance 2: 3 + or - 0.76 s), without altering escape. Additionally, the same treatments increased the number of transitions (200 mg/kg EM: 6.33 + or - 0.90, diazepam: 10 + or - 1.54, control group: 2.78 + or - 0.60) between the two compartments and the time spent in the lighted compartment in the light/dark transition model (200 mg/kg EM: 39 + or - 7 s; diazepam: 61 + or - 9 s; control group: 14 + or - 4 s). The dose of 400 mg/kg EM also increased this last measurement (38 + or - 8 s). These results were not due to motor alterations since no significant effects were detected in the number of crossings or rearings in the arena. Furthermore, neither EM nor diazepam altered the behavioral responses of rats to a cloth impregnated with cat odor. These observations suggest that EM exerts anxiolytic-like effects on a specific subset of defensive behaviors, particularly those that have been shown to be sensitive to low doses of benzodiazepines