Opioids Inhibit Lateral Amygdala Pyramidal Neurons by Enhancing A Dendritic Potassium Current

Pyramidal neurons in the lateral amygdala discharge trains of action potentials that show marked spike frequency adaptation, which is primarily mediated by activation of a slow calcium-activated potassium current. We show here that these neurons also express an alpha-dendrotoxin- and tityustoxin-Kalpha-sensitive voltage-dependent potassium current that plays a key role in the control of spike discharge frequency. This current is selectively targeted to the primary apical dendrite of these neurons. Activation of mu-opioid receptors by application of morphine or D-Ala(2)-N-Me-Phe(4)-Glycol(5)-enkephalin (DAMGO) potentiates spike frequency adaptation by enhancing the alpha-dendrotoxin-sensitive potassium current. The effects of mu-opioid agonists on spike frequency adaptation were blocked by inhibiting G-proteins with N-ethylmaleimide (NEM) and by blocking phospholipase A(2). Application of arachidonic acid mimicked the actions of DAMGO or morphine. These results show that mu-opioid receptor activation enhances spike frequency adaptation in lateral amygdala neurons by modulating a voltage-dependent potassium channel containing Kv1.2 subunits, through activation of the phospholipase A(2)-arachidonic acid-lipoxygenases cascade.

Quantum-gate characterization in an extended Hilbert space

We describe an approach for characterizing the process performed by a quantum gate using quantum process tomography, by first modeling the gate in an extended Hilbert space, which includes nonqubit degrees of freedom. To prevent unphysical processes from being predicted, present quantum process tomography procedures incorporate mathematical constraints, which make no assumptions as to the actual physical nature of the system being described. By contrast, the procedure presented here assumes a particular class of physical processes, and enforces physicality by fitting the data to this model. This allows quantum process tomography to be performed using a smaller experimental data set, and produces parameters with a direct physical interpretation. The approach is demonstrated by example of mode matching in an all-optical controlled-NOT gate. The techniques described are general and could be applied to other optical circuits or quantum computing architectures.

Independent roles of calcium and voltage-dependent potassium currents in controlling spike frequency adaptation in lateral amygdala pyramidal neurons

The calcium-dependent afterhyperpolarization (AHP) that follows trains of action potentials is responsible for controlling action potential firing patterns in many neuronal cell types. We have previously shown that the slow AHP contributes to spike frequency adaptation in pyramidal neurons in the rat lateral amygdala. In addition, a dendritic voltage-gated potassium current mediated by Kv1.2-containing channels also suppresses action potential firing in these neurons. In this paper we show that this voltage-gated potassium current and the slow AHP act together to control spike frequency adaptation in lateral amygdala pyramidal neurons. The two currents have similar effects on action potential number when firing is evoked either by depolarizing current injections or by synaptic stimulation. However, they differ in their control of firing frequency, with the voltage-gated potassium current but not the slow AHP determining the initial frequency of action potential firing. This dual mechanism of controlling firing patterns is unique to lateral amygdala neurons and is likely to contribute to the very low levels of firing seen in lateral amygdala neurons in vivo.

Batchelor's theory extended to elongated cylindrical or ellipsoidal particles

Extensions to Batchelor's theory have been derived to take into account different shaped particles while relating extensional viscosity enhancement to three parameters - shape, volume fraction and particle aspect ratio. The extended theory now allows calculation of the extensional viscosity enhancement, at a given volume fraction of particles, for either ellipsoidal or cylindrical particles. The formula improves the predictive capability of Batchelor's theory when compared with measurements found in the literature for different rod-like polymer solutions. (c) 2005 Elsevier B.V. All rights reserved.

A new approach to control of MIMO processes with static nonlinearities using an extended IMC framework

In this paper, a new control design method is proposed for stable processes which can be described using Hammerstein-Wiener models. The internal model control (IMC) framework is extended to accommodate multiple IMC controllers, one for each subsystem. The concept of passive systems is used to construct the IMC controllers which approximate the inverses of the subsystems to achieve dynamic control performance. The Passivity Theorem is used to ensure the closed-loop stability. (c) 2005 Elsevier Ltd. All rights reserved.

SK channels regulate excitatory synaptic transmission and plasticity in the lateral amygdala

At glutamatergic synapses, calcium influx through NMDA receptors (NMDARs) is required for long-term potentiation (LTP); this is a proposed cellular mechanism underlying memory and learning. Here we show that in lateral amygdala pyramidal neurons, SK channels are also activated by calcium influx through synaptically activated NMDARs, resulting in depression of the synaptic potential. Thus, blockade of SK channels by apamin potentiates fast glutamatergic synaptic potentials. This potentiation is blocked by the NMDAR antagonist AP5 (D(-)-2-amino-5-phosphono-valeric acid) or by buffering cytosolic calcium with BAPTA. Blockade of SK channels greatly enhances LTP of cortical inputs to lateral amygdala pyramidal neurons. These results show that NMDARs and SK channels are colocalized at glutamatergic synapses in the lateral amygdala. Calcium influx through NMDARs activates SK channels and shunts the resultant excitatory postsynaptic potential. These results demonstrate a new role for SK channels as postsynaptic regulators of synaptic efficacy.

Properties of a unique mutant of Helicoverpa armigera single-nucleocapsid nucleopolyhedrovirus that exhibits a partial many polyhedra and few polyhedra phenotype on extended serial passaging in suspension cell cultures

Serial passaging of wild-type Helicoverpa armigera, single-nucleocapsid (HaSNPV) in H. zea (HzAMI) illsect Cell Cultures results ill rapid selection for the few polyhedra (FP) phenotype. A unique HaSNPV mutant (ppC19) was isolated through plaque purification that exhibited a partial many polyhedra (MP) and FP phenotype. Oil serial passaging in suspension cell cultures, ppC19 produced fivefold more polyhedra than a typical FP mutant (FP8AS) but threefold less polyhedra than the wild-type virus. Most importantly, the polyhedra of ppC19 exhibited MP-like virion occlusion. Furthermore, ppC19 produced the same amount of budded virus (BV) as the FP mutant, which was fivefold higher than that of the wild-type virus. This selective advantage was likely to explain its relative stability in polyhedra production for six passages when compared with the wild-type Virus. However, subsequent passaging of ppC19 resulted in a steel) decline in both BV and polyhedra yields, which was also experienced by FP8AS and the wild-type virus Lit high passage numbers. Genomic deoxyribonueleic Licid profiling of the latter suggested that defective interfering particles (DIPS) were implicated in this phenomenon and represented another Undesirable mutation during serial passaging of HaSNPV Hence, a strategy to isolate HaSNPV Clones that exhibited MP-like polyhedra production but FP-like BV production, coupled with low multiplicities of infection during scale-up to avoid accumulation of DIPS, could prove commerically invaluable.

Synaptic activation of transient receptor potential channels by metabotropic glutamate receptors in the lateral amygdala

Classical mammalian transient receptor potential channels form non-selective cation channels that open in response to activation of phospholipase C-coupled metabotropic receptors, and are thought to play a key role in calcium homeostasis in non-excitable cells. Within the nervous system transient receptor potential channels are widely distributed but their physiological roles are not well understood. Here we show that in the rat lateral amygdala transient receptor potential channels mediate an excitatory synaptic response to glutamate. Activation of group l etabotropic glutamate receptors on pyramidal neurons in the lateral amygdala with either exogenous or synaptically released glutamate evokes an inward current at negative potentials with a current voltage relationship showing a region of negative slope and steep outward rectification. This current is blocked by inhibiting G protein function with GTP-beta-S, by inhibiting phospholipase C or by infusing transient receptor potential antibodies into lateral amygdala pyramidal neurons. Using RT-PCR and Western blotting we show that transient receptor potential 1, transient receptor potential 4 and transient receptor potential 5 are present in the lateral amygdala. Single cell PCR confirms the presence of transient receptor potential 1 and transient receptor potential 5 in pyramidal neurons and we show by co-immunoprecipitation that transient receptor potential 1 and transient receptor potential 5 co-assemble as a heteromultimers in the amygdala. These results show that in lateral amygdala pyramidal neurons synaptically released glutamate activates transient receptor potential channels, which we propose are likely to be heteromultimeric channels containing transient receptor potential 1 and transient receptor potential 5/transient receptor potential 4. (c) 2005 Published by Elsevier Ltd on behalf of IBRO.

GABAergic excitation in the basolateral amygdala

GABA-containing interneurons are a diverse population of cells whose primary mode of action in the mature nervous system is inhibition of postsynaptic target neurons. Using paired recordings from parvalbumin-positive interneurons in the basolateral amygdala, we show that, in a subpopulation of interneurons, single action potentials in one interneuron evoke in the postsynaptic interneuron a monosynaptic inhibitory synaptic current, followed by a disynaptic excitatory glutamatergic synaptic current. Interneuron-evoked glutamatergic events were blocked by antagonists of either AMPA/kainate or GABA(A) receptors, and could be seen concurrently in both presynaptic and postsynaptic interneurons. These results show that single action potentials in a GABAergic interneuron can drive glutamatergic principal neurons to threshold, resulting in both feedforward and feedback excitation. In interneuron pairs that both receive glutamatergic inputs after an interneuron spike, electrical coupling and bidirectional GABAergic connections occur with a higher probability relative to other interneuron pairs. We propose that this form of GABAergic excitation provides a means for the reliable and specific recruitment of homogeneous interneuron networks in the basal amygdala.

Genetic and Cultural Transmission of Smoking Initiation: An Extended Twin Kinship Model

Background Considerable evidence from twin and adoption studies indicates that genetic and shared environmental factors play a significant role in the initiation of smoking behavior. Although twin and adoption designs are powerful to detect genetic and environmental influences, they do not provide information on the processes of assortative mating and parent–offspring transmission and their contribution to the variability explained by genetic and/or environmental factors. Methods We examined the role of genetic and environmental factors for smoking initiation using an extended kinship design. This design allows the simultaneous testing of additive and non-additive genetic, shared and individual-specific environmental factors, as well as sex differences in the expression of genes and environment in the presence of assortative mating and combined genetic and cultural transmission. A dichotomous lifetime smoking measure was obtained from twins and relatives in the Virginia 30,000 sample. Results Results demonstrate that both genetic and environmental factors play a significant role in the liability to smoking initiation. Major influences on individual differences appeared to be additive genetic and unique environmental effects, with smaller contributions from assortative mating, shared sibling environment, twin environment, cultural transmission and resulting genotype–environment covariance. The finding of negative cultural transmission without dominance led us to investigate more closely two possible mechanisms for the lower parent–offspring correlations compared to the sibling and DZ twin correlations in subsets of the data: (i) age × gene interaction, and (ii) social homogamy. Neither mechanism provided a significantly better explanation of the data, although age regression was significant. Conclusions This study showed significant heritability, partly due to assortment, and significant effects of primarily non-parental shared environment on smoking initiation.