PubMed · 15485447
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Michael R Franz. 2004. "Reconstituting" restitution?. https://doi.org/10.1046/j.1540-8167.2004.04458.x
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The central nucleus of the amygdala (CeA) orchestrates autonomic and other behavioral and physiological responses to conditioned stimuli that are aversive or elicit fear. As a related CeA function is the expression of hypoalgesia induced by conditioned stimuli or systemic morphine administration, we examined postsynaptic opioid modulation of neurons in each major CeA subdivision. Following electrophysiological recording, biocytin-filled neurons were precisely located in CeA regions identified by chemoarchitecture (enkephalin-immunoreactivity) and cytoarchitecture (DAPI nuclear staining) in fixed adult rat brain slices. This revealed a striking distribution of physiological types, as 92% of neurons in capsular CeA were classified as late-firing, whereas no neurons in the medial CeA were of this class. In contrast, 60% or more of neurons in the lateral and medial CeA were low-threshold bursting neurons. Mu-opioid receptor (MOPR) agonists induced postsynaptic inhibitory potassium currents in 61% of CeA cells, and this ratio was maintained in each subdivision and for each physiological class of neuron. However, MOPR agonists more frequently inhibited bipolar/fusiform cells than triangular or multipolar neurons. A subpopulation of MOPR-expressing neurons were also inhibited by delta opioid receptor agonists, whereas a separate population were inhibited kappa opioid receptors (KOPR). The MOPR agonist DAMGO inhibited 9/9 CeM neurons with projections to the parabrachial nucleus identified by retrograde tracer injection. These data support models of striatopallidal organization that have identified striatal-like and pallidal-like CeA regions. Opioids can directly inhibit output from each subdivision by activating postsynaptic MOPRs or KOPRs on distinct subpopulations of opioid-sensitive neurons.
We report a study on the characterization of voltage-activated calcium currents (I(Ca)) in retinal ganglion cells (RGCs) and the topographic distribution of RGCs that express different types of I(Ca) in zebrafish retinas. In acutely isolated zebrafish RGCs, both high-voltage-activated (HVA; peak activation potential +7.4 +/- 1.1 mV) and low-voltage-activated (LVA; peak activation potential -33.0 +/- 1.2 mV) I(Ca) were recorded. HVA I(Ca) were recorded in all of the tested RGCs, whereas LVA I(Ca) were recorded in approximately one-third of the tested cells. In RGCs that expressed both HVA and LVA I(Ca), the two currents were readily separated by depolarizing the cell membrane to different voltages from different holding potentials. Among RGCs that expressed LVA I(Ca), some cells expressed large LVA I(Ca) (up to 130 pA), whereas others expressed small LVA I(Ca) (approximately 20 pA). RGCs that expressed large and small LVA I(Ca) were designated as class I and class II cells, respectively, and RGCs that expressed only HVA I(Ca) were designated as class III cells. The topographic distribution of cell classes was similar in various areas of the retina. In the nasal-ventral retina, for example, class III cells outnumbered class I and class II cells by 10.8- and 2.6-fold, respectively. In the temporal and dorsal retinas, the density of class III cells slightly decreased, whereas the density of class I and class II cells increased. The differential expression of I(Ca) in RGCs may correlate with the development and function of the retina.
The steroid hormone 17beta-estradiol and its respective receptors have been found in several cardiovascular nuclei in the central nervous system including the parabrachial nucleus. In a previous study, we provided evidence that 17beta-estradiol attenuated an outward potassium conductance in parabrachial neurons of male rats, using an in vitro slice preparation. In this study we sought to enhance the comprehensive information provided previously on estradiol's postsynaptic effects in the parabrachial nucleus by directly examining whether 17beta-estradiol application will modulate excitatory synaptic neurotransmission. Using a pontine slice preparation and whole-cell patch-clamp recording, bath application of either 17beta-estradiol (20-100 muM) or BSA-17beta-estradiol (50 muM) decreased the amplitude of evoked excitatory postsynaptic currents (from 30-60% of control) recorded from neurons in the parabrachial nucleus. The paired pulse ratio was not significantly affected and suggests a post-synaptic site of action. The inhibitory effect on the synaptic current was relatively long-lasting (non-reversible) and was blocked by the selective estrogen receptor antagonist, ICI 182,780. Furthermore, 17beta-estradiol reduced the maximum current elicited by a ramp protocol, increased the input resistance measured between resting membrane potential and action potential threshold and caused an increase in the firing frequency of the cells under current-clamp. In summary, 17beta-estradiol caused 3 effects: first, a depolarization; second, a reduction in evoked excitatory postsynaptic potentials; and third, an enhancement of action potential firing frequency in neurons of the parabrachial nucleus. These observations are consistent with our previous findings and support a role for estrogen in modulating neurotransmission in this nucleus.