Introduction
The relations between anxiety and nociception can be an-
alysed from two perspectives: the influence of anxiety on
nociception or the impact of nociception on anxiety. Re-
garding the former, there are clinical reports establishing
that under stressful conditions pain perception is increased
whereas in relaxed situations pain is less intense (Cornwall
and Donderi 1988; Jones and Zachariae 2002). Addition-
ally, studies in animals indicate that exposure to cues that
produce anxiety-like responses result in antinociceptive
actions. Thus, Lee and Rodgers (1990) were the first to
demonstrate that exposure to the elevated plus maze (an
anxiety test) results in a long-lasting elevation in tail-flick
latency (an antinociceptive response). This kind of anti-
nociception seems to be non-opioid mediated, since it is not
blocked by naltrexone nor does it show cross-tolerance with
morphine (Lee and Rodgers 1990). This response, however,
is sensitive to a variety of benzodiazepines and 5-HT1A
agonists including diazepam (Rodgers and Randall 1987),
buspirone, gepirone, ipsapirone (Rodgers and Shepherd
1989), midazolam and 8-OH-DPAT (Nunes-de-Souza et al.
2000). The finding that various anxiolytic drugs block the
antinociception induced by exposure to the elevated plus
maze is most likely a direct result of the anxiolytic-like
effect of these compounds, indicating the close relations
between experimental anxiety and nociception.