Article Figures & Data
Figures
- Fig. 1.
Histological localization and antidromic identification of neurons in the BL amygdaloid complex. A, Microelectrode track through the lateral nucleus on three consecutive frontal sections displayed from caudal (1) to rostral (3). B, Histological control of two microelectrode tracks (1–2) through the BL nucleus. InA and B, curved arrows point to electrolytic lesions performed to facilitate histological reconstruction of electrode tracks. C, ENT stimulation (arrowheads) elicits antidromic spikes in a neuron located in the caudal part of the BM nucleus. Note constant latency of antidromic responses, ability to follow high-frequency stimulation (C1), and collision with a spontaneous action potential (arrows in C2). AHA, Amygdalohippocampal area; HF, hippocampal formation;ME, medial amygdaloid nucleus; OT, optic tract;PAC, periamygdaloid cortex; PU, putamen;V, ventricle.
- Fig. 2.
Bursting neuron of the BL nucleus. A, ISIHs of a BL neuron in S and PS. Bins of 1 msec (left) and 10 msec (right). X, Mean interval; s, standard deviation; F, firing rate in Hz; EI%, percentage of intervals outside the depicted range; N, number of intervals. The inset (upper left) shows superimposed spike doublets in S using the first spike as a temporal reference. Curved arrow in A points to late mode in ISIH of PS. Examples of isolated doublets (*) and bursts (**) in PS are displayed below the histograms. B, Silencing of BL bursting cell during a transient period of W and bursting discharge pattern in S. Curved arrows point to eye movements generated in the W. Inset shows superimposed spike bursts.
- Fig. 11.
Bursting neurons of the BL nucleus fire during the depth-negative phase of ENT theta during PS. A, Samples of theta-related activity in a BL bursting cell. B, Superimposed STA and PEH using the negative peak of depth ENT EEG as zero-time. Same cell as in A. Bins of 10 msec. PEH was smoothed with a moving average of three bins.
- Fig. 3.
Tonically active neuron of the BL nucleus during the sleep–waking cycle. A, ISIHs of neuronal discharges inW, S, and PS with bins of 1 msec (left) and 5 msec (right). Abbreviations as in Figure 2. B, Sample of the activity generated by a tonic neuron in S. Same neuron as in A. The spike train marked by the number 2 in B1 is expanded inB2.
- Fig. 4.
Fast-firing neuron of the BL nucleus generating high-frequency spike trains on a silent background. A, ISIHs of neuronal discharges in W, S, and PSwith bins of 1 msec (left) and 5 msec (right). Note presence of intervals longer than 400 msec (EI%) in all states (5.5% of intervals in PS compared with 0.9 and 1.4% in W and S, respectively). Abbreviations as in Figure 2. B, High-frequency spike trains occurring on a silent background in S. Same neuron as in A. The spike train marked by the number2 in B1 is expanded in B2.
- Fig. 5.
Orthodromic response of a phasic neuron of the BL nucleus to ENT stimuli. Orthodromic responses are shown with slow (A1) and fast (B1) time bases. Corresponding poststimulus histograms with bins of 10 msec (A2) and 2 msec (B2). C, Counts (number of shocks); N, number of spikes.
- Fig. 6.
State-dependent fluctuations in antidromic responsiveness of a silent neuron of the lateral nucleus to PRH stimuli. Double-shock paradigm (interstimulus interval, 90 msec). InA, 20 pairs of PRH stimuli were applied in each state, but only 10 of the 20 shocks are displayed. Numbers at thetop of the figure indicate the proportion of shocks eliciting antidromic spikes for the first (S1) and second (S2) stimuli. In response to the first shock (left response), this silent projection cell generated 3, 10, and 9 antidromic responses in W, S, and PScompared with 18, 20, and 20 responses to the second shock (right response). B is a superimposition of antidromic responses in S with a faster time base, demonstrating the constant latency of antidromic spikes.
- Fig. 7.
Rhythmic modulation of neuronal discharge in the delta frequency range during S. Lateral amygdaloid projection neuron that was backfired from the PRH cortex and had an average firing rate of 2.2 Hz in S. A, Left, Superimposed STA and PEH of neuronal discharges using the negative peak of digitally filtered (0.1–4 Hz) focal waves (top), ENT EEG (middle), or PRH EEG (bottom) as the zero-time. Bins of 30 msec. PEHs were smoothed with a moving average of three bins. See Paré et al. (1995) for methodological details. Ns, Number of spikes;Nr, number of references. Right, Cross-correlograms (CROSS) between focal waves and ENT EEG (top), between focal waves and PRH EEG (middle), and between ENT and PRH EEG (bottom). B, Epoch of spontaneous activity during S. Same cells as in A.
- Fig. 9.
Activation of a phasic neuron of the BL nucleus in relation to ENT SPs. A, Simultaneously recorded phasic BL neuron and bipolar ENT EEG. The neuronal events marked by 1 and 2 in A are shown with a faster time base inC1 and C2, respectively. B, Peri-SP histogram of neuronal discharges for the same cell using the negative peaks of ENT SPs as zero-time. Bins of 10 msec.
- Fig. 8.
Delta (A) and SP-related (B) modulation of neuronal activity in the BL nucleus. Grouped PEHs of fast-firing cells (1) and bursting neurons (2) using the depth-negative peak of digitally filtered ENT delta waves (A) and ENT SPs (B) as zero-time. Bins of 20 msec in A and 5 msec in B. Ordinate in 1 and 2 indicates percentage of spikes per bin. Average of ENT delta (A3) and ENT SPs (B3) obtained by computing an average of all delta waves and ENT SPs, giving an equal weight to all cells. Selection criteria for cells included in grouped PEHs: for delta, we considered only cells that were recorded for long (>90 sec) epochs of slow-wave sleep devoid of SPs for the grouped PEHs, whereas for SPs, only cells with a significant number of SPs (>20) were considered. In the grouped PEH displayed in A1, the flanking troughs that could be seen in individual PEHs were erased by variations in the delta frequency.
- Fig. 10.
Theta-related modulation of unit activity in the BL nucleus during PS. A1, Superimposed STA and PEH of neuronal discharge using the negative peaks of ENT theta as zero-time. Bins of 10 msec. PEH was smoothed with a moving average of three bins.Ns, Number of spikes; Nr, number of references.A2, Envelope of PEH after shuffling the interspike intervals. B, Autocorrelogram (Auto) of Focal (1) and ENT (2) waves. B3, Cross-correlogram between focal and ENT waves. All waves digitally filtered between 4 and 8 Hz. C, Epoch of spontaneous activity during PS. The period marked by the number 1 inC2 is expanded in C1. Same cells as inA.
Tables
- Table 1.
Distribution of recorded cells in the basolateral complex and central nuclei and their response to stimulation of the parahippocampal cortices
Recording site Basolateral complex Central nucleus Lateral BL BM Total CEM CEL Total No. recorded cells 124 212 80 416 46 70 116 Antidromically invaded (%) 42 15 13 30 0 0 0 Latency (msec) 12.3 ± 0.6 12.1 ± 1.6 2.3 12.6 ± 0.7 – – – Orthodromic spiking (%) 32 43 38 36 64 40 45 Latency (msec) 15.1 ± 1.3 14.3 ± 1.0 11.2 ± 1.1 14.4 ± 0.7 12.3 ± 2.4 13.3 ± 1.3 12.9 ± 1.1 Unresponsive units (%) 26 43 50 34 36 60 55 No. tested cells 66 47 8 121 11 40 51 - Table 2.
Discharge rates (spikes/sec) of BL and lateral amygdaloid neurons during the sleep–waking cycle
BL nucleus Lateral nucleus Bursting Fast-firing Silent Tonic Tonic Phasic W 0.5 ± 0.47 13.3 ± 6.1 15.1 ± 6.2 <0.02 10.1 ± 4.1 S 0.92 ± 0.34 15 ± 6.4 18 ± 6.6 <0.02 10.4 ± 4.3 PS 0.96 ± 0.86 13.7 ± 6.7 15.8 ± 6.9 <0.02 12.2 ± 4.5
