48 Motivation
lesions of the temporal lobe tamed previously fierce monkeys.
Similarly, Kluver and Bucy (1939) described the emotional
disturbances triggered by these large lesions, and Weiskrantz
(1956) reported that many features of the disturbance were
generated by more selective damage to the amygdala. Based
on work done primarily with the Pavlovian fear conditioning
paradigm, three nuclei within the amygdala are known to
make major contributions to fear behavior: the lateral (LA),
basal (BA), and central nuclei (CEA).
The lateral and basal nuclei comprise the frontotemporal
complex(FTC; Swanson & Petrovich, 1998). This complex
communicates most closely with the frontal and temporal
lobes, and it is important in the acquisition of learned fear.
Moreover, the FTC has characteristics that make it a plausi-
ble site of encoding for the learned association that is estab-
lished during fear conditioning (Fanselow & LeDoux, 1999).
First, the FTC receives inputs from all sensory modalities, in-
cluding brain regions that are involved with nociception
(Fendt & Fanselow, 1999). Thus, sensory information of the
CS and pain information of the US converge in the FTC. Sec-
ond, Pavlovian fear conditioning enhances the response of
cells in the FTC that respond to tone CSs (Quirk, Repa, &
LeDoux, 1995). Third, lesions of the FTC produce a pro-
nounced and often total loss of many Pavlovian fear re-
sponses (e.g, Maren, 1998); fourth, chemical inactivation of
this structure is similarly disruptive to fear learning (e.g.,
Gewirtz & Davis, 1997). Thus, the FTC is critical for the ac-
quisition of Pavlovian fear conditioning and is a plausible site
for the encoding and storage of the learned association.
The CEA may be conceived of as the output of the amyg-
dala. It is closely tied with the striatum and is specialized to
modulate motor outflow (Swanson & Petrovich, 1998). The
CEA projects to a variety of structures, including the peri-
aqueductal gray (PAG), the reticular formation, and the lat-
eral hypothalamus. Both the lateral and basal nuclei of the
amygdala project to the CEA. Lesions to the CEA disrupt the
expression of a wide range of defensive behaviors (e.g.,
Kapp, Frysinger, Gallagher, & Haselton, 1979).
The Periaqueductal Gray
The PAG is highly interconnected with the CEA (Rizvi, Ennis,
Behbehani, & Shipley, 1991). This region seems to act as a
coordinator of defensive behaviors, and expression of defen-
sive behaviors can be dissociated within the PAG. For exam-
ple, electrical stimulation of the dorsal-lateral PAG (dlPAG)
triggers robust activity burst–like behavior (Fanselow, 1994),
whereas damage to this structure disrupts the shock-induced
activity burst (Fanselow, 1994). Similarly, chemical stimula-
tion of the caudal third of the dlPAG triggers “bursts of
forward locomotion” that alternate with periods of immobility
(Bandler & Depaulis, 1991, p. 183). Consequently, the dlPAG
seems to coordinate overt defensive reactions, such as flight.
In contrast, similar treatments to the ventral PAG (vPAG)
have very different effects. Chemical or electrical stimulation
of the vPAG triggers freezing behavior, and lesions to this
structure disrupt conditional freezing to aversive CSs
(Fanselow, 1991). Other fear responses can also be dissoci-
ated within the vPAG. For example, the infusion of an opiate
antagonist will disrupt fear-induced analgesia but spare con-
ditioned freezing (Fanselow, 1991). Thus, the vPAG seems to
coordinate conditional freezing and opiate analgesia. Based
on these results, Fanselow (1994) suggested that posten-
counter defenses are related to the vPAG and its inputs from
the amygdala, whereas circa-strike behaviors are related to the
dlPAG and its inputs from the superior colliculus. At this time,
little is known about the neural substrates of preencounter
defenses.Neural Substrates of Unlearned Defensive BehaviorMuch less is known about the neural substrates of innate fear
behavior. Walker and Davis (1997) reported that chemical in-
activation of the bed nucleus of the stria terminalis (BNST)
disrupts light-potentiated startle, but chemical inactivation of
the CEA disrupts only fear-potentiated startle. Inactivation of
the FTC disrupts both behaviors. Thus, available evidence
suggests that learned and unlearned fear responses can be dis-
sociated within a region described as the extended amygdala
(Swanson & Petrovich, 1998). Wallace and Rosen (2001) re-
ported that electrolytic lesions to the LA disrupt freezing to a
predator’s odor, whereas excitotoxic lesions did not. Both
these lesions disrupt freezing to learned fear stimuli. This re-
sult suggests that innate and learned fear can also be dissoci-
ated within the amygdala.SEXUAL MOTIVATIONNothing is more closely tied to evolutionary fitness than
reproductive success. The most direct measure of reproduc-
tive success is the number of offspring that survive, and
therefore the terminal goal of a sexual behavior system is
successful production of offspring. Animal species display a
wide variety of reproductive strategies to produce offspring.
Monogamyinvolves the pairing of a single male and female
for the duration of the reproductive cycle. This strategy oc-
curs mostly in species that split the burden of parental care
across both parents. Polygynyinvolves the association of a
single male with multiple females, and polyandryinvolves