MK-212 increases anxiety and decreases locomotor activity. The anxiogenic-like profile of 5-HT2 receptor activation is prevented by the blockade of 5-HT2 receptors within the BLA, which does not have an effect by itself upon basal anxiety levels triggered by the EPM.
Transcranial magnetic stimulation (TMS) has recently been investigated as a possible adjuvant treatment for many neuropsychiatric disorders, and has already been approved for the treatment of drug-resistant depression in the United States and in Brazil, among other countries. Although its use in other neuropsychiatric disorders is still largely experimental, many physicians have been using it as an off-label add-on therapy for various disorders. More recently, another technique, transcranial direct current stimulation (tDCS), has also become available as a much cheaper and portable alternative to TMS, although its mechanisms of action are different from those of TMS. The use of off-label therapeutic TMS or tDCS tends to occur in the setting of diseases that are notoriously resistant to other treatment modalities. Here we discuss the case of anxiety disorders, namely panic and post-traumatic stress disorders, highlighting the uncertainties and potential problems and benefits of the clinical use of these neuromodulatory techniques at the current stage of knowledge.
The present study investigated the effects of midazolam and pentylenetetrazole upon repeating and varying sequences of responses. Rats were exposed to a multiple schedule with two components. Under the VARY component, water was provided if the current sequence of four responses differed from each of the five previous ones; under the REPEAT component, water delivery was contingent upon a particular four-response sequence. Each component was signaled by specific exteroceptive stimuli. Overall, sequence variability was affected by midazolam, and to a lesser degree, by pentylenetetrazole. With the REPEAT contingency, drug administration increased behavior variation, thus reducing accuracy; with the VARY contingency, behavior variation and accuracy were not altered. These results were explained on the basis of the disruptive effects of both drugs upon the discriminative control exerted by previous responses within a sequence and by exteroceptive stimuli.
Electrical or chemical stimulation of the dorsal periaqueductal gray (DPAG) has been accepted as an animal model of panic attacks. This study investigates the influence of anticipatory anxiety in the occurrence of panic-like behavior induced by N-methyl-Daspartate (NMDA) microinjection into the DPAG of rats. Behavioral (i.e., contextual fear conditioning) and pharmacological (i.e., pentylenetetrazol) manipulations were employed as animal models of anticipatory anxiety. In the first experiment, animals exposed to contextual cues that had been previously associated with electric footshocks through contextual fear conditioning were less likely than non-conditioned control animals to display defensive reactions such as running and jumping in response to microinjection of NMDA (0.3 µl of 15.0 µg/µl) into the DPAG. In the second experiment, rats were injected intraperitoneally with the anxiogenic drug pentylenetetrazol (PTZ, 15 mg/kg) 5 minutes before receiving intra-DPAG microinfusion with the same dose of NMDA as in Experiment 1. Panic-related behaviors were registered in an experimental arena immediately after NMDA microinfusion. As compared with saline pre-treated animals, PTZ significantly attenuated NMDA-induced panic-like reactions. These results further demonstrate the usefulness of DPAG chemical stimulation as an animal model of panic attacks and suggest that behavioral and pharmacological activation of the brain mechanisms underlying anticipatory anxiety might exert an antipanic-like effect.
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