Effects of GABA on acutely isolated neurons from the gustatory zone of the rat nucleus of the solitary tract

Responses of acutely isolated neurons from the rostral nucleus of the solitary tract (rNST) to GABA receptor agonists and antagonists were investigated using whole-cell recording in current clamp mode. The isolated neurons retain their morphology and can be divided into multipolar, elongate and ovoid cell types. Most rNST neurons (97%), including all three cell types, respond to GABA with membrane hyperpolarization and a reduction in input resistance. The GABA(A) receptor agonist muscimol reduces neuronal input resistance in a concentration-dependent manner, whereas the GABA(B) receptor agonist baclofen had no effect on any of the neurons tested. The GABA and muscimol reversal potentials were both found to be -75 mV Both the GABA competitive antagonist picrotoxin and the GABA(A) receptor antagonist bicuculline block the effect of GABA in a concentration-dependent manner. These results suggest that GABA activates all neurons in the rNST and that inhibitory synaptic activity is important in brainstem processing of gustatory and somatosensory information.      

The metabolism of L-glutamate and L-5-carboxy-pyrrolidone by mouse cells (NCTC clone 929) under conditions of defined nutrition

The utilization of L-glutamate by clone 929 mouse cells growing in a synthetic medium, MAL 294/2, was studied with the aid of carbon-14 labeled L-glutamate. The rate of consumption of extracellular glutamate was rapid even though the extracellular concentration of this substance has been found to remain constant or to increase. The rate of uptake during an interval of otpimal growth was calculated to be approximately 42 mμmoles/mg of cell protein per hour. Among the metabolic products that are derived from the carbon of glutamate and secreted from the cells are carbon dioxide, lactic acid, proline, alanine, alpha-ketoglutaric acid and 5-carboxypyrrolidone. Aspartic acid, although produced by the cells in amounts sufficient to meet the needs for growth, does not appear as an extracellular product of glutamate metabolism. Extracts of L cells were found to exhibit four times as much glutamic-oxaloacetic as glutamic-pyruvic transaminase activities. Failure to secrete aspartic acid must not be due to a deficiency in the transaminase. The transaminase concentrations are apparently not affected by variations in the concentrations of aspartic acid and alanine in the medium, both of which are absent from MAL 294/2. 5-Carboxypyrrolidone, although produced from L-glutamate by L cells, is metabolically inert in this system. Likewise, mouse fetal lung cells, cultured in a similar way, use glutamic acid as extensively as L cells and fail to metabolize exogenous 5-carboxypyrrolidone.     

Replacement of receptor cells in the hamster vomeronasal epithelium after nerve transection

Chemoreceptor cells in the vomeronasal and olfactory epithelium are replaced following experimentally induced degeneration. This study analyzes quantitatively the time course and degree of vomeronasal receptor cell replacement. Unilateral transection of the vomeronasal nerves in adult hamster was used to induce a retrograde degeneration of receptor cells in the vomeronasal organ. Histological measurement of both number of receptor cells and epithelial thickness were made for recovery times from 0 to 60 days. After nerve transection, there was a gradual degeneration of receptor cells, the number decreasing to 50% of control by day 2 and 16% by day 6. During days 7-15 maximum receptor cell replacement was observed. Cell number increased rapidly and reached a peak on day 15. At recovery times of 40-60 days, cell number returned to the control level. Epithelial thickness, however, decreased to 60-70% during the degeneration period (days 4-6) and did not return to control levels. After 40-60 days epithelial thickness remained at 70% of control. These results demonstrate that vomeronasal receptor cells are replaced following degeneration, but epithelial thickness does not return to control levels. These findings suggest that the number of replacement cells is not limited by the reduced thickness of the epithelium, and that recovery mechanisms may function to restore an optimum number of receptor cells.