Sah, P., E. S. L. Faber, M. Lopez de Armentia, and J. Power. The Amygdaloid Complex: Anatomy and Physiology. Physiol Rev 83: 803–834, 2003; 10.1152/physrev.00002.2003.—A converging body of literature over the last 50 years has implicated the amygdala in assigning emotional significance or value to sensory information. In particular, the amygdala has been shown to be an essential component of the circuitry underlying fear-related responses. Disorders in the processing of fear-related information are likely to be the underlying cause of some anxiety disorders in humans such as posttraumatic stress. The amygdaloid complex is a group of more than 10 nuclei that are located in the midtemporal lobe. These nuclei can be distinguished both on cytoarchitectonic and connectional grounds. Anatomical tract tracing studies have shown that these nuclei have extensive intranuclear and internuclear connections. The afferent and efferent connections of the amygdala have also been mapped in detail, showing that the amygdaloid complex has extensive connections with cortical and subcortical regions. Analysis of fear conditioning in rats has suggested that long-term synaptic plasticity of inputs to the amygdala underlies the acquisition and perhaps storage of the fear memory. In agreement with this proposal, synaptic plasticity has been demonstrated at synapses in the amygdala in both in vitro and in vivo studies. In this review, we examine the anatomical and physiological substrates proposed to underlie amygdala function.

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Small-conductance Ca(2+)-activated K(+) channels (SK channels) are widely expressed throughout the central nervous system. These channels are activated solely by increases in intracellular Ca(2+). SK channels are stable macromolecular complexes of the ion pore-forming subunits with calmodulin, which serves as the intrinsic Ca(2+) gating subunit, as well as with protein kinase CK2 and protein phosphatase 2A, which modulate Ca(2+) sensitivity. Well-known for their roles in regulating somatic excitability in central neurons, SK channels are also expressed in the postsynaptic membrane of glutamatergic synapses, where their activation and regulated trafficking modulate synaptic transmission and the induction and expression of synaptic plasticity, thereby affecting learning and memory. In this review we discuss the molecular and functional properties of SK channels and their physiological roles in central neurons.

SUMMARY1. The pharmacological and biophysical properties of excitatory synapses in the CAI region of the hippocampus were studied using patch electrodes and whole-cell recording from thin slices.2. Excitatory postsynaptic currents (EPSCs) had a fast component whose amplitude was voltage insensitive and a slow component whose amplitude was voltage dependent with a region of negative slope resistance in the range of -70 to -30 mV.3. The voltage-dependent component was abolished by the N-methyl-D-aspartate (NMDA) receptor antagonist DL-2-amino-5-phosphonovalerate (APV; 50 /uM), which had no effect on the fast component. Conversely, the fast voltage-insensitive component was abolished by the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 (1M) which had no effect on the slow component.4. In Ringer solution with no added Mg2+ the current-voltage relation of the NMDA component was linear over a much larger voltage range than in the presence of 1-3 mM-Mg2+.5. The NMDA component of the EPSC could be switched off with a hyperpolarizing voltage step at the soma. The kinetics of this switch-off was used to estimate the speed of clamp control of the subsynaptic membrane as well as the electrotonic distance from the soma. The kinetic analysis of the EPSC was restricted to synapses which were judged to be under adequate voltage control.6. For those synapses that were close to the soma the time constant for decay for the non-NMDA component, which was voltage insensitive, ranged from 4-8 ms.7. The rise time for the NMDA component was 8-20 ms and the time constant for decay ranged from 60-150 ms.8. During increased transmitter release with post-tetanic potentiation or application of phorbol esters, both components of the EPSC increased to a similar extent.9. These experiments provide a detailed description of the dual receptor mechanism operating at hippocampal excitatory synapses. In addition, the MS 7663 S. HESTRIN AND OTHERS experiments provide an electrophysiological method for estimating the electrotonic distance of synaptic inputs.