Slow and Fast (Gamma) Neuronal Oscillations in the Perirhinal Cortex and Lateral Amygdala

Abstract

Most lesion studies emphasize the distinct contributions of the amygdala and perirhinal cortex to memory. Yet, the presence of strong reciprocal excitatory projections between these two structures suggests that they are functionally coupled. To gain some insight into this issue, the present study examined whether the close anatomical ties existing between perirhinal and lateral amygdala (LA) neurons are expressed in their spontaneous activity. To this end, multiple simultaneous recordings of single unit discharges and local field potentials were performed in the LA and perirhinal cortex in ketamine-xylazine anesthetized cats. The perirhinal cortex and LA exhibited a similar pattern of spontaneous activity. Recordings at both sites were dominated by a slow focal oscillation at 1 Hz onto which was superimposed a faster rhythm (approximately 30 Hz) whose amplitude fluctuated cyclically. Computing crosscorrelograms between focal waves recorded simultaneously in the perirhinal cortex and LA revealed a close relationship between their spontaneous activity. Even when recording sites were separated by as much as 8 mm, the slow focal oscillation remained highly correlated (r > or = 0.7). In contrast, the correlation between fast oscillations was usually lower (r approximately 0.3). Perievent histograms of neuronal discharges revealed that the firing probability of most LA and perirhinal neurons increased during the depth-negative component of the slow oscillation. In addition, respectively, 47 and 64% of LA and perirhinal neurons exhibited a significant modulation of firing probability in relation to the fast oscillations. Finally, crosscorrelating unit discharges simultaneously recorded in the LA and perirhinal cortex confirmed the presence of phase-related oscillatory events in both structures. In summary, our results suggest that the interconnections existing between the perirhinal cortex and LA can support the genesis of coherent neuronal activities at various frequencies. These results imply that cooperative interactions must be taking place between these structures.

Systemic administration of the benzodiazepine receptor partial inverse agonist FG‐7142 disrupts corticolimbic network interactions

“…The LFP activity pattern mirrored that of neuronal firing in each region such that the initial negative deflection in potential coincided with neuronal bursting in mPFC and BLA. This temporal association between unit and LFP activity has been reported previously in both cortical and amygdaloid regions (Collins et al, 2001;Steriade, 1997). It should be noted that the low frequency LFP activity seen under basal conditions and in response to vehicle is not due to true slow wave oscillations but rather to the \average" of high frequency activity of short duration and the very low activity periods of longer duration observed during the 150 s epoch.…”

Hippocampal Slow Oscillation: A Novel EEG State and Its Coordination with Ongoing Neocortical Activity

“…Our hippocampal CSD, EC field and EC multiunit recordings implicate the temporo-ammonic pathway (EC layer III to the apical dendritic zone of CA1, i.e., SLM) as providing robust, rhythmic, excitatory input at slow frequencies during the SO. In support of this, the SO has been noted previously in the EC of both the ketamine-xylazine anesthetized and naturally sleeping cat (Collins et al, 1999(Collins et al, , 2001 as well as the urethane-anesthetized rat (Isomura et al, 2005). Furthermore, preliminary evidence from our laboratory (Dickson et al, 2005) suggests that lesions of the perforant pathway also affect the hippocampal SO.…”

GABAergic Excitation in the Basolateral Amygdala

“…Given that these strong connections are clustered, and the highly nonrandom nature of synaptic connectivity, it is conceivable that pyramidal neurons with strong connections may be the recipient of suprathreshold AAC excitation. This provides an ideal mechanism for the rapid activation of large numbers of pyramidal neurons, as occurs in the transition from a hyperpolarized network Down state to the depolarized Up state (Steriade et al, 1993;Cossart et al, 2003;Haider et al, 2006), a phenomenon that has been observed not only in the cortex but also in the amygdala (Collins et al, 2001).…”