FIG. 1. Nuclei of the rat amygdaloid complex. Coronal sections are drawn from rostral (A) to caudal (D). The different nuclei are divided into three groups as described in text. Areas in blue form part of the basolateral group, areas in yellow are the cortical group, and areas in green form the centromedial group. ABmc, accessory basal magnocellular subdivision; ABpc, accessory basal parvicellular subdivision; Bpc, basal nucleus magnocellular subdivision; e.c., external capsule; Ladl, lateral amygdala medial subdivision; Lam, lateral amygdala medial subdivision; Lavl, lateral amygdala ventrolateral subdivision; Mcd, medial amygdala dorsal subdivision; Mcv, medial amygdala ventral subdivision; Mr, medial amygdala rostral subdivision; Pir, piriform cortex; s.t., stria terminalis. See text for other definitions.
FIG. 2. Summary of the inputs to the amygdaloid nuclei. Neuromodulatory inputs (e.g., acetylcholine, serotonin) have been omitted for clarity. See Fig. 1 and text for definitions.
FIG. 3. Summary of the main outputs from the amygdaloid nuclei.
FIG. 4. Intra-amygdaloid connections as described by anatomical tract tracing studies. Most of the connections between nuclei within the amygdala are glutamatergic. See Fig. 1 and text for definitions.
FIG. 5. An example of the amygdaloid region as it appears in acutely prepared coronal sections. Left: a Nissl-stained hemisection of a rat brain around bregma-3. The areas shown in the outlined region are shown in an acutely prepared coronal brain slice as it appears under brightfield illumination (middle). Shown is the region containing the basolateral complex and central nucleus. Right: approximate regions of the lateral (LA), basal (B), accessory basal (AB) and central nucleus have been outlined. In the central nucleus, the approximate locations of the lateral (CeL) and medial (CeM) subdivisions have also been shown. [Adapted from Paxinos G. and Watson C. The Rat Brain in Stereotaxic Coordinates (2nd ed.). Sydney, Australia: Academic, 1986.]
FIG. 6. Pyramidal-like neurons and interneurons can be distinguished on electrophysiological grounds. Traces show recordings from typical pyramidal-like neuron and interneuron in the basolateral complex. Traces on the left are from a typical pyramidal-like neuron, and those on the right are from an interneuron. A: injection of a 400-ms depolarizing current injection in pyramidal neurons evokes action potentials that show spike frequency adaptation, while similar current injections into interneurons evoke a high-frequency train of action potentials that do not adapt. B: action potentials in interneurons have a shorter duration than in pyramidal cells.
FIG. 7. Electrophysiological and synaptic properties of different types of pyramidal neuron in the basolateral complex. The traces on the left show recordings from neurons which show marked spike frequency adaptation, while the traces on the right are recordings from a repetitively firing neuron. A: response to 600-ms depolarizing current injection (400 pA). The neuron on the left fires a single action potential, whereas the cell on the right fires repetitively throughout the current injection. Spike frequency adaptation is due to activation of a slow afterhyperpolarization. B: the slow afterhyperpolarization (AHP) that follows a train of action potential. The recording on the left shows the AHP that follows two action potentials in a cell which shows complete spike frequency adaptation. Inset: response to a 100-ms, 400-pA current injection which evoked two action potentials. Traces on the right show the AHP evoked in a cell which fires repetitively during a prolonged current injections. Note that the AHP that is evoked is much smaller despite twice the number of action potentials in response to the current injection. C: late firing neuron from the basal nucleus. Traces show the response to a just threshold current injection and one that is suprathreshold. Note the long delay to action potential initiation during a threshold current injection (left). A suprathreshold current injection removes the long delay (right). D: stimulation of the external capsule evokes a depolarizing excitatory postsynaptic potential (inset on left) followed by a hyperpolarizing inhibitory postsynaptic potential (IPSP). The IPSP has two components: a fast component mediated by activation of GABAA receptors and a slow component mediated by activation of GABAB receptors. The amplitudes of the two components are highly variable between cells, and two examples are shown.
FIG. 8. Pyramidal cell and interneurons in the basolateral complex have different types of excitatory inputs. Recordings are shown from a pyramidal-like neuron (left panels) and interneuron (right right) in the lateral amygdala. A: excitatory synaptic currents recorded at the indicated holding potentials following stimulation of the external capsule. In pyramidal cell, a slower current can be seen with membrane depolarization, which is absent in interneurons. Inhibitory synaptic currents have been blocked with picrotoxin (100 µM). B: peak current (I)-voltage (Vm) relationships are shown for the fast inward current in pyramidal neurons and interneurons. Note that the I-V is linear in pyramidal cells but shows marked outward rectification in interneurons, indicating the presence of AMPA receptors which lack GluR2 subunits. C: excitatory synaptic currents in a pyramidal cell recorded at -80 mV and +40 mV (left traces). Application of the NMDA receptor antagonist D-APV (30 µM) blocks the slow component. Records on the right are synaptic currents recorded from an interneuron at -80 mV before and after application of CNQX (10 µM), showing that the current is mediated by AMPA receptors.
FIG. 9. Physiological properties of three types of neuron in the central nucleus. Recordings are from the rat central nucleus showing the three most prominent types of neurons. A: low-threshold spiking neuron. B: regular spiking neuron. C: late firing neuron. In each case, whole cell recordings were made from neurons in the central nucleus and depolarizing and hyperpolarizing currents injected as shown.
FIG. 10. Functional model of the basic pathways and synaptic plasticity proposed to underlie fear conditioning. Sensory stimuli about the conditioned stimulus (CS) and the unconditioned stimulus (US) converge on the lateral nucleus of the amygdala. During fear conditioning, convergence of inputs to single neurons results in enhancement (long-term potentiation) of excitatory postsynaptic potentials (EPSP) evoked by the CS (B). This synaptic plasticity enhances the response of LA projection neurons in response to the CS. CS-evoked information reaches the CeA directly and via the B and AB nucleus. Projections from the central nucleus control the physiological responses, which include behavioral, autonomic nervous system, and hypothalamic-pituitary axis responses. As shown in B, the convergence of the conditioned and unconditioned input to neurons in the LA has been suggested to result in a larger output in response to the CS. All projections, except those from the CeA, are thought to be glutamatergic.