Figure 1.
IPSC regulation by mGluR on second-order medial NTS neurons in brainstem slices. After identifying second-order NTS neurons by their minimal (<150 μsec) synaptic jitter to ST activation (data not shown; see Materials and Methods), ST-evoked postsynaptic responses were blocked by addition of ionotropic Glu antagonists NBQX (20 μm) and AP-5 (100 μm). Typically, second-order medial NTS neurons appeared spindle shaped, with two major processes exiting the poles of the long axis of the cell (top right micrograph). After ionotropic GluR blockade, large-amplitude, long-duration spontaneous GABAergic IPSCs were prominent (Control traces, left and right). ST activation consisted of trains of five shocks (T2) or 10 shocks (T3) with intershock intervals of 20 msec (i.e., 50 Hz), delivered as short bursts that were repeated every 0.5 sec as depicted at the top left; horizontal bars mark periods of ST stimulation. Note that IPSCs were inward because of the high Cl- (50 mm) internal solution and holding potentials of -60 mV. Left, In decrease-type neurons, ST stimulation decreased the sIPSC rate in a frequency-dependent manner; bottom, 20 consecutive original traces superimposed for each condition. The lowest trace shows that T3 stimulation nearly eliminated IPSCs. Bin plots indicate that sIPSC rates rapidly rebound to near control levels within 10-20 sec after the halt of stimulation. Right, In increase-type neurons, ST stimulation strongly increased the sIPSC rates in a frequency-dependent manner; bottom, 10 consecutive original traces superimposed for each condition. Bin plots indicate that sIPSC rates increase more rapidly for T3 than T2. For clarity, stimulus artifacts have been truncated in some of the original traces.