ABSTRACT
This article is a transcription of an electronic symposium sponsored by the Brazilian Society of Neuroscience and Behavior (SBNeC). Invited researchers from the European Union, North America and Brazil discussed two issues on anxiety, namely whether panic is a very intense anxiety or something else, and what aspects of clinical anxiety are reproduced by animal models. Concerning the first issue, most participants agreed that generalized anxiety and panic disorder are different on the basis of clinical manifestations, drug response and animal models. Also, underlying brain structures, neurotransmitter modulation and hormonal changes seem to involve important differences. It is also common knowledge that existing animal models generate different types of fear/anxiety. A challenge for future research is to establish a good correlation between animal models and nosological classification
Subject(s)
Humans , Anxiety , Disease Models, Animal , Panic , Anti-Anxiety Agents/pharmacology , Anxiety/drug therapy , Anxiety/physiopathology , Benzodiazepines/pharmacology , Brain/drug effects , Brain/physiopathology , Computer Communication Networks , Fear/drug effects , Panic/drug effects , Periaqueductal Gray/drug effects , Periaqueductal Gray/physiopathology , Serotonin/pharmacologyABSTRACT
The effect of kynurenic acid (20 to 19=60 nmol) microinkected into the dorsal periaqueductal gray matter was measured in rats placed in a elevated plus-maze. Microinjection of 160 nmol of kynurenic acid increased the percentages of open arm entries and of time spent in the open arms. Both of these measures may be considered indexes of anciolysis. Although kynurenic acid also invreased the total number of entries, analysis of covariance shows that the increase in open arm entries is independent of the effect on closed arm entries. Thus, the anxiolytic effect of kynurenic acid detected in the elevated plus-maze strengthens the proposal that glutamatergic neurons of the dorsal periaqueductal gray matter paly an important role in anxiety
Subject(s)
Rats , Animals , Male , Kynurenic Acid/pharmacology , Anxiety/drug therapy , Exploratory Behavior/drug effects , Periaqueductal Gray/physiology , Analysis of Variance , Kynurenic Acid/administration & dosage , Periaqueductal Gray/drug effects , Rats, WistarABSTRACT
The current study assesses the influence of the N-methil-D-aspartate (NMDA) receptor antagonist D-2-amino-7-phosphonohepatanoate (AP7) on the pressor effect of glutamate microinjected into the dorsal periaqueductal gray matter (DPAG) of urethane-anesthetized rats. Glutamate (20, 40 and 80 nmol/site) caused dose-related reproducible increases in systolic and diastolic blood pressure. Microinjection of saline into the DPAG did not alter the pressor effects of glutamate (80 nmol/site). Similar pretreatment with AP7 (2nmol/site) significantly (P < 0.05) attenuated the pressor effects of glutamate from ñ26.5 ñ 7.0 to +3.4 ñ 3.3 mmHg (sistolic blood pressure). We conclude that the pressor efffect of glutamate in the DPAG is mediated largely by activation of NMDA receptors