Exposure of rats to an odor of a predator can elicit an innate fear response. In addition, such exposure has been shown to activate limbic brain regions such as the amygdala. However, there is a paucity of data on the phenotypic characteristics of the activated amygdalar neurons following predator odor exposure. In the current experiments, rats were exposed to cloth which contained either ferret odor, butyric acid, or no odor for 30 minutes. Ferret odor-exposed rats displayed an increase in defensive burying versus control rats. Sections of the brains were prepared for dual-labeled immunohistochemistry and counts of c-Fos co-localized with Ca2+/calmodulin-dependent protein kinase II (CAMKII), parvalbumin, or calbindin were made in the basolateral (BLA), central (CEA), and medial (MEA) nucleus of the amygdala. Dual-labeled immunohistochemistry showed a significant increase in the percentage of CAMKII–positive neurons also immunoreactive for c-Fos in the BLA, CEA and MEA of ferret odor-exposed rats compared to control and butyric acid-exposed groups. Further results showed a significant decrease in calbindin-immunoreactive neurons that were also c-Fos-positive in the anterior portion of the BLA of ferret odor-exposed rats compared to control and butyric acid-exposed rats, whereas the MEA expressed a significant decrease in calbindin/c-Fos dual-labeled neurons in butyric acid-exposed rats compared to controls and ferret odor-exposed groups. These results enhance our understanding of the functioning of the amygdala following exposure to predator threats by showing phenotypic characteristics of activated amygdalar neurons. With this knowledge, specific neuronal populations could be targeted to further elucidate the fundamental underpinnings of anxiety and could possibly indicate new targets for the therapeutic treatment of anxiety.

SUMMARY The inhibitory effect of IB interneurons on motoneurons was tested in both legs of six hemiplegic adults. On the normal side, an inhibition of 10 ms, (14-6%) was observed in all cases and was similar to that described previously. On the spastic side, the same technique results in a facilitation of same duration reaching a maximum of 15%. Hence the IB inhibitory effect is, at least functionally, absent in spasticity. Disappearance of IB inhibition is an additional mechanism to be considered in interpreting spasticity.In cat, Golgi tendon organs, sensitive to muscle tension, project via large diameter fibres (IB fibres) on to the motoneurons of the muscle from which they originate, to inhibit them. Their activation results in a postsynaptic short lasting inhibition (IB inhibition). This latter appears after a short latency indicating that the interneuronal IB pathway is di-(eventually tri) synaptic. The IB inhibition, also named autogenic, is mediated through a special interneuron' which is thought to be glycinergic. The IB interneuron receives many segmentary afferents both cutaneous and proprioceptive. It is also influenced by supraspinal excitatory (from the cortico-and rubrospinal tracts) as well as inhibitory (from the dorsal reticulospinal tract) projections. A tonic inhibition of the IB interneuron has been described in the cat decerebrate rigidity preparation.2For a long time, the IB inhibition has been considered as a protective mechanism against muscle extreme tension. However, the demonstration that active contraction of only few motor units is able to activate Golgi tendon organs suggests rather that-IB inhibition plays a role in the ongoing control of the motor output.34In the intact man, it is generally believed that the IB pathway is similar to that described in the cat.7 It has been suggested that it could play a role in the claspknife phenomenon described in spastic patients. In fact, it is not known whether IB interneuron excitability is modified in human spasticity and, if so, Address for reprint requests: Dr P J Delwaide, University Dept of Neurology, H6pital de la Citadelle, Liege, Belgium.

Rats exposed to the odor of a predator or to the elevated plus maze (EPM) express unique unconditioned fear behaviors. The extended amygdala has previously been demonstrated to mediate the response to both predator odor and the EPM. We seek to determine if divergent amygdalar microcircuits are associated with the different behavioral responses. The current experiments compared activation of corticotropin-releasing factor (CRF)-containing neuronal populations in the central amygdala and bed nucleus of the stria terminalis (BNST) of rats exposed to either the EPM (5 minutes) versus home cage controls, or predator ferret odor versus butyric acid, or no odor (30 minutes). Sections of the brains were prepared for dual-labeled immunohistochemistry and counts of c-Fos co-localized with CRF were made in the centrolateral and centromedial amygdala (CLA and CMA) as well as the dorsolateral (dl), dorsomedial (dm), and ventral (v) BNST. Ferret odor-exposed rats displayed an increase in duration and a decrease in latency of defensive burying versus control rats. Exposure to both predator stress and EPM induced neuronal activation in the BNST, but not the central amygdala, and similar levels of neuronal activation were seen in both the high and low anxiety groups in the BNST after EPM exposure. Dual-labeled immunohistochemistry showed a significant increase in the percentage of CRF/c-Fos co-localization in the vBNST of ferret odor-exposed rats compared to control and butyric acid-exposed groups as well as EPM-exposed rats compared to home cage controls. In addition, an increase in the percentage of CRF-containing neurons co-localized with c-Fos was observed in the dmBNST after EPM exposure. No changes in co-localization of CRF with c-Fos was observed with these treatments in either the CLA or CMA. These results suggest that predator odor and EPM exposure activates CRF neurons in the BNST to a much greater extent than CRF neurons of the central amygdala, and indicates unconditioned anxiogenic stimuli may activate unique anatomical circuits in the extended amygdala.

The amygdala is a bilateral temporal lobe brain region which plays an important role in emotional processing. Past studies on the amygdala have shown hemispheric differences in amygdalar processes and responses associated with specific pain and fear behaviors. Despite the functional differences in the amygdala, few studies have been performed to characterize whether anatomical differences exist between the left and right amygdala. Parvalbumin (PV) is a phenotypic marker for an inhibitory interneuronal population in cortical brain structures such as the basolateral amygdala complex (BLC). This study examined the number of PV-positive neurons in the left and right BLC of adult, male Long-Evans rats using unbiased stereology. Coronal sections through the rostral-caudal extent of the BLC were immunohistochemically-stained for PV and the optical fractionator method was used to obtain an unbiased estimate of the number of PV-positive neurons in subdivisions through the BLC. The lateral and basolateral amygdala divisions of the BLC were analyzed, were subdivided into the dorsolateral, ventrolateral and ventromedial and the posterior, anterior and ventral subdivisions, respectively. The results indicate that there are significantly more PV-positive neurons in the left basolateral amygdala compared to the right, with a significant difference specifically in the posterior subdivision. This difference in PV neuronal number could help explain the distinct hemispheric roles of the BLC in the behavioral processing following exposure to painful and fearful stimuli.