6 research outputs found
Locus of the effect of DA on EPSCs.
<p><b>A</b>: Current traces of the responses evoked by a pair of single local electrical stimuli 50 ms apart at holding membrane potentials of −100 mV to record the AMPA response before (1) and during (2) superfusion with DA (50 µM). 3: overlay of the responses before and during DA superfusion; the amplitude of the 2nd response in the presence of DA was scaled to match the amplitude of the 2nd response during control. Note that the 1st response proportionally decreased more than the 2nd response in the presence of DA and that there is no substantial changes in the time course of the EPSCs. Current traces represent the average of 6 sweeps and BMI (10 µM) was present in the superfusing medium throughout recording. Panel 4 (4. PPR) shows the average amplitude of the PPR from 12 neurons before and during superfusion with DA. * Statistically different from control, Student’s paired t-test, <i>P</i><0.05. <b>B</b>: Average holding membrane current before and during superfusion with DA (50 µM). No statistically significant differences were found at any holding membrane potential. <b>C</b>: current traces of the response evoked by local pressure ejection of glutamate (10 mM; vertical arrow) from a patch pipette before (1) and during (2) superfusion with DA (50 µM) at a holding membrane potential of –100 mV in the presence of tetrodotoxin (1 µM) and BMI (10 µM). 3: the overlay of the responses recorded in panels 1 and 2. 4: amplitude of the peak response recorded at a holding membrane potential of −100 mV for 5 neurons before and during superfusion with DA. No statistically significant difference in the amplitude of the glutamate response during control and during DA superfusion (Student’s paired <i>t</i>-test, <i>P</i>>0.75, n = 5).</p
Nature of the EPSC evoked by local electrical stimulus in the presence of BMI (10 µM).
<p><b>A</b>: current traces of the response evoked by single local electrical stimulus and recorded at holding membrane potentials of −40 and −100 mV before glutamatergic antagonists application (1.Control) and during superfusion with CNQX (20 µM; 2.CNQX), APV (50 µM) following CNQX wash out (3. APV) and CNQX and APV (4. CNQX+APV). Recordings were obtained in a MS neuron from a P20 animal. Current traces represent the average of 6 sweeps. <b>B</b>: Current-voltage relationship of the response recorded between −120 mV and 20 mV. The early component of the EPSC was measured 9 ms after the stimulus as indicated by the left vertical arrow in A. The late component was measured 53 ms after the stimulus as indicated by the right vertical arrow in A.</p
Effect of DA (50 µM) on pharmacologically isolated NMDA and AMPA/KA receptor-mediated EPSCs.
<p><b>A</b>: Current traces of pharmacologically isolated AMPA/KA EPSC recorded with APV (50 µM) present in the superfusing medium before (1), during (2) and after (3) superfusion with dopamine at a holding membrane potential of −100 mV. 4: the overlay of the responses before and during DA superfusion. <b>B</b>: Current traces of pharmacologically isolated NMDA receptor-mediated EPSC recorded with CNQX (20 µM) present in the superfusing medium before (1), during (2) and after (3) superfusion with dopamine at a holding membrane potential of −20 mV. 4: the overlay of the responses before and during DA superfusion. Traces in A and B represent the average of 6 sweeps. <b>C</b>: average effect of dopamine on isolated NMDA and AMPA/KA receptor-mediated EPSCs. NMDA receptor-mediated EPSC was measured at the membrane potential the response was largest, −40 mV or −20 mV and AMPA/KA receptor-mediated EPSC was measured at a holding membrane potential of −100 mV. The left and right vertical axis are for the NMDA and AMPA/KA receptor-mediated EPSCs respectively. * Statistically different from control, Student’s paired t-test, <i>P</i><0.001. <b>D</b>: Time course of the inhibitory effect (in percentage) of dopamine on AMPA/KA and on NMDA receptor-mediated EPSC shown in A and B respectively. Response was recorded every 15 s and each filled circle represent the average of 4 sweeps recorded over one minute period. The dashed rectangle represent the period during which DA (50 µM) was added to the superfusing medium, from 4 to 14 min.</p
Effect D<sub>1</sub>-like receptor agonist and antagonist on dopaminergic inhibition of EPSC.
<p><b>A</b>: Current traces of glutamatergic EPSC recorded before (1), during (2) and after (3) superfusion with SKF 38393 (10 µM) at a holding membrane potential of −100 mV. 4: the overlay of the responses before and during SKF 38393 superfusion. <b>B</b>: Current traces of glutamatergic EPSC recorded during superfusion with SCH23390 (1), with SCH23390 and DA (2) and with DA following the washout of SCH23390 (3) at a holding membrane potential of −100 mV. 4: the overlay of the responses during SCH23390 and DA and during DA. <b>C</b>: summary of the effect of DA in the presence or absence of SCH23390 at holding membrane potential −100 mV and −40 mV (n = 9). * Statistically different from SCH23390 and DA, Student’s paired t-test, <i>P</i><0.01.</p
Effect of dopamine on the EPSC.
<p><b>A</b>: Current traces of the response evoked by single electrical stimulus recorded at holding potentials of −20 mV (upper row) and −100 mV (lower row) before (1), during (2), and after (3) superfusion with dopamine (DA 50 µM). 4: the overlay of the responses before and during DA superfusion. Current traces represent the average of 6 sweeps. Recordings were obtained in a slice from a P7 animal. Left and right vertical arrows in 1 indicate where the AMPA/KA and NMDA responses were measured. <b>B</b>: Average current-voltage relationship of the AMPA/KA (n = 51; 1) and NMDA (n = 51; 2) responses recorded before and during superfusion with DA. The I<sub>R</sub>-V<sub>m</sub> of the late response were aligned on the holding membrane potential at which the response was maximum before averaging (usually at −20 mV or −40 mV). Asterisks indicate a statistically significant difference between control and DA treatment at this holding membrane potential (Student’s <i>t</i>-test, <i>P</i><0.05).</p
Effects of QX314 on Dopamine modulation of Glutamatergic EPSCs.
<p><b>A</b>: Comparison of the average change in amplitude of the early component of the glutamatergic EPSCs (in pA) measured at −60 mV, on superfusion of DA in the presence and absence of QX314. The solid bar represents the average response in 80 neurons (n = 80), in the presence of QX314 and the dashed bar represents the average of 8 neurons (n = 8) in the absence of QX314. No statistically significant difference was found between the two groups (Paired Student’s t test p<0.050, p = 0.471). <b>B</b>: Comparison of the average change in amplitude of the late component of the glutamatergic EPSCs (in pA) measured at −20 mV, on superfusion of DA in the presence and absence of QX314. The solid bar represents the average of 70 neurons (n = 70), in the presence of QX314 and the dashed bar represents the average of 7 neurons (n = 7) in the absence of QX314. No statistically significant difference was found between the two groups (Paired Student’s t test p<0.048, p = 0.500).</p