gramicidin-a and biocytin

The striatum, the input stage of the basal ganglia, is a critical brain structure for the learning of stimulus-response habits as well as motor, perceptual, and cognitive skills. Roles of dopamine (DA) and acetylcholine (ACh) in this form of implicit memory have long been considered essential, but the underlying cellular mechanism is still unclear. By means of patch-clamp recordings from corticostriatal slices of the mouse, we studied whether the identified striatal cholinergic interneurons undergo long-term synaptic changes after tetanic stimulation of cortico- and thalamostriatal fibers. Electrical stimulation of the fibers revealed a depolarizing and hyperpolarizing postsynaptic potential in the striatal cholinergic interneurons. The early depolarizing phase was considered to be a cortico/thalamostriatal glutamatergic EPSP, and the hyperpolarizing component was considered to be an intrastriatally evoked GABAergic IPSP. Tetanic stimulation of cortico/thalamostriatal fibers was found to induce simultaneously occurring long-term potentiation (LTP) of the EPSPs as well as the disynaptically mediated IPSPs. The induction of LTP of EPSP required a rise in intracellular Ca(2+) concentration and dopamine D(5), but not D(2) receptor activation. Ca(2+)-permeable AMPA receptors might also play a part in the LTP induction. Blockade of NMDA receptors, metabotropic glutamate receptors, or serotonin receptors had no significant effects. The long-term enhancement of the disynaptic IPSPs was caused by a long-term increase in the occurrence rate but not the amplitude of disynaptically mediated IPSP in the striatal cholinergic interneurons. This dual mechanism of synaptic plasticity may be responsible for the long-term modulation of the cortico/thalamostriatal synaptic transmission.

Topics: Acetylcholine; Animals; Calcium; Chelating Agents; Corpus Striatum; Dopamine; Egtazic Acid; Electric Stimulation; Excitatory Amino Acid Antagonists; Excitatory Postsynaptic Potentials; Gramicidin; In Vitro Techniques; Interneurons; Long-Term Potentiation; Lysine; Male; Memory; Mice; Mice, Inbred C57BL; Neuronal Plasticity; Patch-Clamp Techniques; Receptors, Dopamine; Receptors, N-Methyl-D-Aspartate; Synapses

This study assessed the mechanism of uptake of biotin by the fetal-facing (basolateral) membrane of the term human placenta. Using membrane vesicles, we showed that most of the uptake was attributable to transfer of the vitamin into the vesicle and that the uptake was saturable, Na-dependent, carrier-mediated, and electroneutral. The rate of uptake was less than for biotin uptake by the maternal-facing (apical) membrane of the human placenta. Because ethanol inhibits biotin uptake by the apical membrane, the effect of ethanol on uptake by basolateral vesicles was investigated. With 10-hr exposure at a concentration of 2 and 3 mg/ml, but not 1 mg/ml, ethanol modestly inhibited biotin uptake. The mechanism of inhibition by alcohol is not known.

Topics: Biotin; Cell Membrane; Ethanol; Female; Gramicidin; Humans; In Vitro Techniques; Kinetics; Lysine; Mannitol; Membrane Potentials; Osmolar Concentration; Placenta; Valinomycin