Abstract– In a previous publication (Wheeler & Hollingsworth, 1978), a model was presented which accounted for the role of sodium in the high affinity transport of glutamic acid in rat brain synaptosomes. Subsequent studies confirmed a lack of fit of the model to the data at the higher sodium and glutamate concentrations. The model has therefore been reexamined and refined. By removing some of the restrictions placed on the original model, a model emerges which fits the data at all sodium and glutamate concentrations with an average per cent error of only 2.14% per experimental data point. The kinetic constants describing uptake have been redefined and recalculated in accordance with this revised model.

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Pituitary hormones were measured in plasma in unanesthetized male and female rats prepared with venous and ventricular cannulae following ventricular infusions of adenosine and two adenosine receptor agonists. Adenosine (10, 100, and 200 nmol) injected intraventricularly caused dose-related rises in plasma prolactin (PRL) in males; in females, only the 100- and 200-nmol doses increased PRL. Similar doses of adenosine had little effect on plasma levels of luteinizing hormone (LH) and thyrotropin (TSH) in the same animals. The adenosine receptor agonists L-N⁶-phenylisopropyladenosine (L-PIA) and 5’-N-ethyl-carboxamideadenosine (NECA) potently stimulated prolactin secretion at doses of 10 and 50 nmol when administered into the lateral ventricle, and at a dose of 2.5 nmol when administered into the third ventricle. The secretion of PRL was antagonized by the adenosine receptor antagonist theophylline (25 nmol), when theophylline was coadministered with NECA and L-PIA. TSH levels were reduced slightly but significantly following the 10- and 50-nmol infusions of L-PIA into the lateral ventricle. The less potent D-isomer of PIA (D-PIA) did not significantly stimulate PRL release. Coupled with studies indicating the presence of adenosine in the basal hypothalamus, our observations indicate a potential neuroendocrine role for this purine in prolactin secretion.

—The kinetics of sodium dependent glutamic acid transport have been studied in desheathed frog sciatic nerve. Initial velocities have been measured as a function of both glulamic acid and sodium concentration. Lineweaver–Burk plots are constructed from these data, and the kinetic constants describing uptake are estimated. Vmax is unaffected by sodium concentration, which implies that translocation is not directly affected by sodium. K1 is sodium dependent, which implies that sodium affects the affinity of the carrier for glutamic acid. Reciprocal plots of velocity vs [Na] or K1 vs 1/[Na] are linear, suggesting that glutamic acid and sodium are co‐transported on a one‐to‐one basis. t, the sodium concentration giving half maximal velocity of uptake, was found to vary from about 57 mm to 48 mm at glutamic acid concentrations of 1.0–10.0 ± 10−6m. A model of a mechanism by which sodium and glutamate could be co‐transported is presented; the model is in very good agreement with the experimental data.