Factors that influence the activity of prefrontal cortex (PFC) pyramidal neurons are likely to play an important role in working memory function. One such factor may be the release of Ca2+ from intracellular stores. Here we investigate the hypothesis that metabotropic glutamate receptors (mGluRs)-mediated waves of internally released Ca2+ can regulate the intrinsic excitability and firing patterns of PFC pyramidal neurons. Synaptic or focal pharmacological activation of mGluRs triggered Ca2+ waves in the dendrites and somata of layer V medial PFC pyramidal neurons. These Ca2+ waves often evoked a transient SK-mediated hyperpolarization followed by a prolonged depolarization that respectively decreased and increased neuronal excitability. Generation of the hyperpolarization depended on whether the Ca2+ wave invaded or came near to the soma. The depolarization also depended on the extent of Ca2+ wave propagation. We tested factors that influence the propagation of Ca2+ waves into the soma. Stimulating more synapses, increasing inositol trisphosphate concentration near the soma, and priming with physiological trains of action potentials all enhanced the amplitude and likelihood of evoking somatic Ca2+ waves. These results suggest that mGluR-mediated Ca2+ waves may regulate firing patterns of PFC pyramidal neurons engaged by working memory, particularly under conditions that favor the propagation of Ca2+ waves into the soma.
We studied inositol-1,4,5-trisphosphate (IP 3 ) receptor-dependent intracellular Ca 2+ waves in CA1 hippocampal and layer V medial prefrontal cortical pyramidal neurons using whole-cell patch-clamp recordings and Ca 2+ fluorescence imaging.
Two forms of short-term plasticity at inhibitory synapses were investigated in adult rat striatal brain slices using intracellular recordings. Intrastriatal stimulation in the presence of the ionotropic glutamate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (20 microM) and D,L-2-amino-5-phosphonovaleric acid (50 microM) produced an inhibitory postsynaptic potential (IPSP) that reversed polarity at -76 +/- 1 (SE) mV and was sensitive to bicuculline (30 microM). The IPSP rectified at hyperpolarized membrane potentials due in part to activation of K(+) channels. The IPSP exhibited two forms of short-term plasticity, paired-pulse depression (PPD) and synaptic augmentation. PPD lasted for several seconds and was greatest at interstimulus intervals (ISIs) of several hundred milliseconds, reducing the IPSP to 80 +/- 2% of its control amplitude at an ISI of 200 ms. Augmentation of the IPSP, elicited by a conditioning train of 15 stimuli applied at 20 Hz, was 119 +/- 1% of control when sampled 2 s after the conditioning train. Augmentation decayed with a time constant of 10 s. We tested if PPD and augmentation modify the ability of the IPSP to prevent the generation of action potentials. A train of action potentials triggered by a depolarizing current injection of constant amplitude could be interrupted by stimulation of an IPSP. If this IPSP was the second in a pair of IPSPs, it was less effective in blocking spikes due to PPD. By contrast, augmented IPSPs were more effective in blocking spikes. The same results were achieved when action potentials were triggered by a depolarizing current injection of varying amplitude, a manipulation that produces nearly identical spike times from trial to trial and approximates the in vivo behavior of these neurons. These results demonstrate that short-term plasticity of inhibition can modify the output of the striatum and thus may be an important component of information processing during behaviors that involve the striatum.
Kainic acid-induced seizure activity in adult rats produces an impairment of long-term potentiation induction in hippocampal slices. As the consequences of seizure activity are different in adult and juvenile rats, we tested the ability of hippocampal slices prepared from kainate-treated juvenile rats to exhibit long-term potentiation. Long-term potentiation was induced by theta-burst stimulation and was not significantly different in slices prepared from control or kainate-injected juvenile rats (16-18 postnatal days). Short-term potentiation, however, was reduced in the kainate-treated juveniles. Calpain inhibitor I has been shown to prevent long-term potentiation formation in adult hippocampal slices, and we evaluated its effect on long-term potentiation in hippocampal slices from juvenile rats. Calpain inhibitor I produced a significant reduction in the degree of long-term potentiation induced by theta-burst stimulation in hippocampal slices prepared from 14-20 postnatal day-old animals. The results are consistent with the notion that, although similar mechanisms participate in the formation of long-term potentiation in juvenile and adult animals, juvenile animals are much more resistant than adult animals to the consequences of seizure activity.
The research was initiated to explore the effects of occupational danger upon an occupation's participants. From work relating to the disaster subculture concept, studies of occupational groups, and research regarding subcultures, it was hypothesized that participants in dangerous occupations adapt to the threats of their work environment by creating and sustaining a protective social mechanism which was named an "occupational subculture of danger." Using a grounded theory approach the article describes how social interaction in a threatening environment leads to the formation of a protective social structure which enables the miners to cope with their hazardous work conditions.
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