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Department of Pharmacology and Toxicology, Ponce School of Medicine, Ponce, Puerto Rico, 00732
Submitted 3 January 2004; accepted in final form 8 July 2004
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
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), plays a critical role in this processing by determining receptive field sizes and temporal interactions between adjoining receptive fields (Alloway et al. 1989; Dykes et al. 1984; Kyriazi et al. 1996b). In addition, cortical inhibition plays a role in activity-induced plasticity (Hensch et al. 1998; Knott et al. 2002; Micheva and Beaulieu 1995; Welker et al. 1989). For example in the rodent somatosensory system, repeated whisker stimulation induces a long-lasting increase in the number of inhibitory synapses in the corresponding cortical barrel (Knott et al. 2002) and in the enzyme glutamic acid decarboxylase, which synthesizes GABA (Welker et al. 1989).
Cortical inhibition is mediated by the stimulation of GABAA receptors, which are ligand-gated chloride channels, and G-protein-coupled GABAB receptors. Although many studies have focused on inhibition through GABAA receptors, several in vivo studies in the barrel cortex and other areas of the primary somatosensory cortex indicate that GABAB receptors also modulate the processing of thalamocortical inputs by regulating receptive field sizes and allowing for the temporal encoding of sensory inputs (Ajima et al. 1999; Chowdhury and Rasmusson 2002a, b, 2003; Kaneko and Hicks 1988, 1990). Mechanistically, this modulation could occur through the stimulation of presynaptic GABAB receptors on the thalamocortical axon terminals or postsynaptic GABAB receptors on the dendrites and cell bodies of the cortical neurons. GABAB receptors exist on many glutamatergic terminals where they decrease the release of glutamate by inhibiting voltage-dependent Ca2+ channels (VDCCs) and thus presynaptic calcium influx (Wu and Saggau 1995, 1997) and on dendrites and cell bodies where they activate inwardly rectifying K+ channels to cause inhibition (Luscher et al. 1997; Sodickson and Bean 1996). A previous study showed that GABAB receptor activation does not inhibit thalamocortical synapses onto layer II/III pyramidal neurons (Gil et al. 1997), suggesting that thalamocortical synapses are not presynaptically regulated by GABAB receptors. However, in the present study, we demonstrate that presynaptic GABAB receptors exist at thalamocortical synapses onto inhibitory neurons in layer IV and excitatory neurons in layers II–III and IV of the mouse "barrel" cortex where they reduce the thalamic activation of cortical inhibition and excitation.
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METHODS |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
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The Institutional Animal Care and Use Committee of the Ponce School of Medicine in compliance with National Institutes of Health guidelines for the care and use of laboratory animals (Publication DHHS 86-23) approved all procedures involving animals. Mice (10–23 days postnatal) were anesthetized with halothane and decapitated under deep anesthesia. The brain was dissected out and put in ice-cold artificial cerebral spinal fluid (ACSF) containing (in mM) 126 NaCl, 3 KCl, 1.25 NaH2PO4, 1 MgSO4, 26 NaHCO3, 20 glucose, and 2 CaCl2 and bubbled with 95% O2-5% CO2. Thalamocortical slices (300 µm thick) were obtained as previously described (Agmon and Connors 1991) with modifications (Porter et al. 2001) using a Vibratome 1000 Plus (Vibratome, St. Louis, MO). Slices were incubated at room temperature in ACSF for an hour prior to experiments. Most of the slices from animals >18 days old were incubated with ACSF containing 10 µM MK-801 to block NMDA receptors.
Electrophysiology
Slices were transferred to a submersion recording chamber mounted on an upright E600FN microscope (Nikon Instruments, Melville, NY) and perfused at 2–3 ml/min with room-temperature ACSF. Neurons were visualized with infrared video microscopy using a x40 water-immersion objective. Neurons were tentatively identified as inhibitory or excitatory based on differences in somatic sizes. In layer IV, excitatory neurons generally had smaller, rounder somas than inhibitory neurons. Whole cell recordings were done with glass pipettes of 3–5 M
filled with an internal solution consisting of (in mM) 12 KCl, 140 KGluconate, 0.2 EGTA, 10 HEPES, 0.3 GTP, and 0.4 ATP (pH 7.3, 285 mosM) or 12 TEA-Cl, 140 CsGluconate, 0.2 Cs-EGTA, 10 HEPES, 0.1 spermine, 0.3 GTP, and 0.4 mM ATP (pH 7.3, 285 mosM). QX-314 (1 mM) was included in the Cs+-based internal solution for experiments done on layer II–III pyramidal neurons and experiments examining the effect of baclofen on NMDA receptor-mediated EPSCs. Using a patch-clamp amplifier (MultiClamp 700A, Axon Instruments, Union City, CA) in current-clamp mode, action potential discharges were elicited with the injection of current pulses to distinguish between inhibitory and excitatory cells as previously described (Porter et al. 2001). To record EPSCs, cells were held in voltage-clamp mode at –60 mV, and the ventrobasal nucleus of the thalamus was stimulated (25–130 µA of current; A-M Systems, Carlsborg, WA) with pairs of stimuli separated by a 50-ms interval with a unipolar tungsten electrode (WPI, Sarasota, FL) every 10–15 s to evoke EPSCs. Recordings were filtered at 4 kHz, digitized at 10 kHz, and saved to computer using pCLAMP8 (Axon Instruments). Membrane potentials were not corrected for the junction potential. Recordings were not compensated for series resistance, but changes in series resistance were monitored throughout the recordings with a 500-ms prepulse in every sweep. Experiments in which the series resistance changed by >15% were eliminated from analysis. All experiments, except those in which NMDA receptor-mediated EPSCs were recorded, were done with 10 µM bicuculline and 100 µM DL-2-amino-5-phosphonopentanoic acid (AP5) in the bath to block GABAA and NMDA receptors, respectively. The remaining current was blocked by 6-cyano-7- nitroquinoxaline-2,3-dione (CNQX; n = 3), confirming that the recorded EPSCs are AMPA receptor-mediated. It is unlikely that the EPSCs were mediated by kainate receptors because thalamocortical stimulation of kainite receptors generates EPSCs with much slower kinetics (Kidd and Isaac 1999).
Baclofen, bicuculline, AP5, CNQX, and MK-801 were purchased from Sigma (St. Louis, MO). CGP 35348 was purchased from Tocris (Ellisville, MO).
Data analysis and statistics
Experiments were accepted for analysis if the effect of baclofen on the EPSCs reversed on removal of the drug, and there was no confounding di- or polysynaptic activity in the EPSCs. Data were analyzed using Clampfit (Axon Instruments). To calculate the paired-pulse ratio (PPR) for a given cell, the thalamus was stimulated with pairs of stimuli 50 ms apart, and the mean amplitude of the EPSC generated by the second stimulus (EPSC2) was divided by the mean amplitude of the EPSC generated by the first stimulus (EPSC1). The average EPSCs were taken from 10 consecutive traces including failures before, during, and after baclofen perfusion. The coefficient of variation (CV) was calculated from 10 consecutive traces including failures before, during, and after baclofen application as the SD of the EPSC amplitude divided by the mean EPSC amplitude. The CV was corrected for changes in baseline noise by subtracting the variance of the baseline noise from the variance of the EPSC. Concentration response curves were generated with SigmaPlot (Aspire Software International, Leesburg, VA) and fitted with the equation, y = min + (max – min)/[1 + (x/EC50)Hillslope]. The results presented were analyzed using the Student's t-test or ANOVA with Tukey's post hoc analysis where appropriate. Statistical significance was set at P < 0.05. Values are reported as the means ± SE.
Morphology
For post hoc morphological identification of inhibitory and excitatory cells, 5 mM biocytin was included in the recording solution to label the neurons. After the electrophysiological recordings, the slices were fixed and refrigerated overnight in 4% paraformaldehyde, and the labeled neurons were subsequently revealed with a standard advidin-biotin peroxidase procedure (Vectastain ABC kit, Vector Laboratories, Burlingame, CA) as previously described (Porter et al. 2001). Images of the labeled neurons were taken with a cooled CCD camera (CoolSNAPcf, Roper Scientific, Trenton, NJ) using a x40 objective on an upright microscope (Olympus America, Melville, NY).
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RESULTS |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
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Using the thalamocortical slice preparation (Agmon and Connors 1991), we examined the modulation of thalamic input onto inhibitory and excitatory cells in layer IV of the mouse barrel cortex by GABAB receptors in mice 10–23 days old. Inhibitory interneurons were distinguished from excitatory neurons by their action potential discharge patterns in response to injected depolarizing current pulses or post hoc morphology as previously described (Connors and Gutnick 1990; Porter et al. 2001). Twenty-seven neurons were identified by both discharge pattern and morphology. In each case, the morphology confirmed the classification based on the discharge pattern. Seventeen neurons were identified by action potential discharge pattern alone, and 32 neurons were identified by morphology alone. To confirm that the studied EPSCs were of thalamocortical origin, several different parameters were measured. The latency of the EPSCs was measured and the range, and the coefficient of variation of the latencies were calculated. Previous studies have demonstrated that monosynaptic thalamocortical EPSCs exhibit latencies which vary by <1 ms (Agmon et al. 1996; Beierlein and Connors 2002) and coefficients of variation of <0.06 ms (Laurent et al. 2002). Consistent with this, the EPSCs in our study had latencies that varied by <1 ms and a coefficient of variation of 0.046 ± 0.002 (n = 97), identifying them as monosynaptic events. The latencies of the evoked EPSCs showed an age-dependent decline with an average latency from the beginning of the stimulation artifact of 6.09 ± 0.18 ms in slices from mice 10–13 postnatal days old (n = 47) and 3.37 ± 0.09 ms in slices from mice 16–23 postnatal days old (n = 50). These latencies are consistent with the latencies of thalamocortical EPSCs measured in slices from similarly aged animals (Agmon and O'Dowd 1992; Agmon et al. 1996; Crair and Malenka 1995; Laurent et al. 2002; Lu et al. 2001). It is unlikely that corticothalamic fibers activated antidromically from the thalamus contributed to the responses because corticothalamic EPSCs exhibit paired-pulse facilitation (Beierlein and Connors 2002) and the EPSCs that we studied exhibited paired-pulse depression (Fig. 5) like thalamocortical EPSCs examined in previous studies (Gibson et al. 1999; Gil et al. 1997; Porter et al. 2001).
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; Kawaguchi and Kubota 1997; Porter et al. 1999). Post hoc morphological analysis demonstrates that this cell exhibits a nonpyramidal morphology with aspiny dendrites (Fig. 1B), confirming its electrophysiological classification as an inhibitory cortical neuron (Meinecke and Peters 1987; Ribak 1978). Furthermore, in this example the neuron forms putative synaptic contacts with an unlabeled cell body. Such perisomatic synapses are typical of inhibitory cortical basket cells (Kawaguchi and Kubota 1997; Somogyi et al. 1983). In the presence of bicuculline and AP5 to block GABAA and NMDA receptors, respectively, stimulation of the ventrobasal nucleus of the thalamus induced thalamocortical EPSCs in this neuron. Bath application of 10 µM baclofen, a selective GABAB receptor agonist, reversibly reduced the amplitude of the thalamocortical EPSCs by 40% (Fig. 1, C and D), indicating that thalamic activation of cortical inhibitory circuits is modulated by GABAB receptors.
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; Porter et al. 2001; Simons and Woolsey 1984). Bath application of 10 µM baclofen reduced the thalamocortical EPSCs recorded in this neuron by 68% (Fig. 2, C and D), demonstrating that baclofen also modulates thalamic stimulation of cortical excitatory circuits. Within the population of neurons examined, the percent inhibition of thalamocortical EPSCs produced by baclofen in inhibitory interneurons (45 ± 8%; n = 12) did not statistically differ from that of excitatory spiny stellate cells (49 ± 6%; n = 13; t-test, P > 0.1; Fig. 2E).
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) was used. As shown in Fig. 3, bath application of 5 µM baclofen reduced the thalamocortical EPSC recorded in the layer IV interneuron by 47%. In the continued presence of baclofen, the subsequent application of 100 µM CGP 35348 reversed the EPSC reduction to 90% of control values. In the four neurons tested, CGP 35348 reversed the baclofen-mediated reduction to 83 ± 3% of control values (Fig. 3C), indicating that the inhibition required the stimulation of GABAB receptors.
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The effect of baclofen could be due to stimulation of either pre- or postsynaptic GABAB receptors. Presynaptic GABAB receptors inhibit VDCCs to decrease the release of neurotransmitter (Wu and Saggau 1995, 1997), while postsynaptic GABAB receptors generally activate inwardly rectifying K+ channels causing hyperpolarization (Luscher et al. 1997; Sodickson and Bean 1996). Within the population of neurons examined, baclofen did not significantly affect the holding current or the membrane resistance (n = 24; ANOVA, P > 0.05); however, in a few neurons, there was a decrease in the holding current, and the input resistance consistent with the postsynaptic activation of GABAB receptors (Fig. 4A). These results suggest that baclofen's effect was not mediated postsynaptically. To further determine whether a postsynaptic effect of baclofen produced the reduction in EPSC amplitude, we used a Cs+-based recording solution to inhibit the K+ currents activated by GABAB receptors (Jarolimek et al. 1994; Morishita and Sastry 1995). As shown in the example in Fig. 4B, with Cs+ in the patch pipette baclofen reduced thalamocortical EPSCs without changing the holding current or the input resistance. Baclofen did not affect the holding current or membrane resistance of the cells recorded with intracellular Cs+ (n = 32; ANOVA; P > 0.05). In the population studied, 10 µM baclofen reduced thalamocortical EPSCs in inhibitory interneurons recorded in the presence of intracellular Cs+ by 54 ± 3% (n = 20) and in excitatory neurons by 49 ± 5% (n = 17). As in experiments without Cs+ in the internal solution, the inhibition observed in both cell types was not statistically different (P > 0.1, t-test), so the data from both cell types were grouped for the remaining analyses. As shown in Fig. 4C, there was no difference between the percent inhibition produced by baclofen with Cs+ in the internal solution (52 ± 3%; n = 37) and without Cs+ (47 ± 5%; n = 25; P > 0.1, t-test), suggesting that presynaptic GABAB receptors mediate the reduction in thalamocortical EPSC amplitudes.
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; Zucker 1989). Typical of thalamocortical synapses (Amitai 2001; Gil and Amitai 1996), paired stimuli evoked strongly depressing EPSCs (Fig. 5A). Scaling the average traces taken before and during the perfusion of baclofen, so that the first EPSC is the same amplitude in both traces, indicates that baclofen increased the PPR from 0.08 to 0.59. An overlay of the 10 consecutive traces used to generate the average traces demonstrates that baclofen also increased the CV from 0.07 to 0.14 (Fig. 5B). The combined data from the experiments done with and without Cs+ in the internal solution indicate that baclofen reversibly increased the PPR from 0.59 ± 0.03 to 1.49 ± 0.42 (n = 67; ANOVA, P < 0.05) and the CV from 0.15 ± 0.02 to 0.53 ± 0.10 (n = 30; ANOVA, P < 0.05; Fig. 5, C and D). A monoexponential function fit to the decay of EPSC1 gave time constants of 6.36 ± 0.48 ms in control conditions and 6.10 ± 0.52 ms in the presence of baclofen for the excitatory neurons (n = 14). For the inhibitory neurons (n = 15), the decay time constants were 3.28 ± 0.35 and 2.98 ± 0.39 ms in the absence and presence of baclofen, respectively. Therefore baclofen did not affect the kinetics of the EPSCs, suggesting that the postsynaptic AMPA receptors were not modified by the application of baclofen (P > 0.05 for both excitatory and inhibitory neurons). Together these results are most consistent with the presynaptic inhibition of glutamate release by baclofen. Although the hyperpolarization of thalamocortical projecting neurons by baclofen could reduce the number of thalamocortical neurons that discharge in response to the stimulation and thus reduce the resultant EPSCs recorded in the cortical neurons, our results are unlikely to be caused by this mechanism because a general inhibition of the thalamocortical neurons should equally affect both the first EPSC and the second EPSC and should; therefore not affect the PPR of the EPSCs. Furthermore, baclofen reduced thalamocortical EPSCs evoked by stimulating the internal capsule (66 ± 10%, n = 3) which contains only axons (data not shown).
GABAB receptors modulate thalamocortical inputs onto layer II–III pyramidal cells
Because previous results indicated that thalamocortical EPSCs onto layer II–III pyramidal neurons were not modulated by baclofen, our results raised the possibility that thalamocortical synapses in layer IV could be selectively modulated by baclofen. To directly test this possibility, we examined the effects of baclofen on thalamocortical EPSCs onto layer II–III pyramidal neurons from mice 14 to 20 days postnatal. In response to injected current pulses, layer II–III pyramidal neurons exhibited strongly adapting spikes and small and slowly repolarizing AHPs (Fig. 6A) similar to the excitatory spiny stellate neurons. Post hoc morphological analysis confirmed that the six recorded neurons were layer II–III pyramidal neurons with prominent apical dendrites and dendrites (Fig. 6B). After recording the response to injected current, the neuron in Fig. 6 was repatched with an internal solution containing both Cs+ and 1 mM QX-314 to block postsynaptic GABAB receptor-mediated effects. Stimulation of the thalamus evoked EPSCs in the presence of bicuculline and AP5. Consistent with thalamocortical EPSCs, the evoked currents exhibited paired-pulse depression with a paired pulse ratio of 0.49 ± 0.15 (Fig. 6E; n = 6) and latencies that varied by <1 ms. The application of 10 µM baclofen reversibly reduced the thalamocortical EPSCs recorded in the layer II–III pyramidal neurons (n = 6) by an average of 74 ± 9% (Fig. 6, C–F). Given that corticothalamic EPSCs exhibit paired-pulse facilitation (Beierlein and Connors 2002), our results are most consistent with GABAB receptor-mediated inhibition of thalamocortical synaptic transmission.
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). Because the previous study had shown that intracortical inputs were modulated by baclofen, we needed to confirm that we were recording monosynaptic thalamocortical synaptic currents. Based on the fact that the latency of the evoked EPSCs varied by <1 ms suggests that they are indeed monosynaptic (Agmon et al. 1996; Beierlein and Connors 2002). To further confirm that monosynaptic EPSCs evoked by stimulating the thalamus are modulated by baclofen, we examined the effect of baclofen on NMDA receptor-mediated synaptic currents. Slices were perfused with 10 µM bicuculline and 10 µM CNQX to essentially block synaptic transmission by blocking GABAA and AMPA/kainate receptors, respectively. The thalamus was stimulated and NMDA receptor-mediated synaptic currents were recorded in cortical neurons voltage-clamped at +60 mV to remove the Mg2+ block of the NMDA receptors. Under these conditions, all synaptic transmission except for the monosynaptic input to the recorded neuron should be blocked. Application of 10 µM baclofen reversibly reduced the NMDA receptor-mediated synaptic currents recorded under these conditions by 73 ± 10% (n = 4; 2 layer IV inhibitory neurons and 2 layer II–III pyramidal neurons; Fig. 7A–C). These experiments further confirm that monosynaptic inputs coming from the thalamus are modulated by GABAB receptors.
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) used 1 µM baclofen and we were using 10 µM baclofen, we decided to test the concentration dependency of the baclofen-mediated inhibition of thalamocortical EPSCs. A concentration-response curve generated by applying different concentrations of baclofen gave an EC50 of 4.4 µM with an average inhibition of only 8 ± 5% produced by 1 µM baclofen (Fig. 7D). These results are consistent with the EC50 of baclofen-mediated inhibition of hippocampal EPSCs (Lei and McBain 2003; Wu and Saggau 1995). Therefore the apparent discrepancy between our results and the previous study can be accounted for by the difference in the concentrations of baclofen. |
DISCUSSION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
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Our experiments demonstrate the existence of GABAB receptors presynaptically on the thalamocortical terminals. Stimulation of postsynaptic GABAB receptors does not mediate the inhibition of thalamocortical EPSCs produced by baclofen because blocking the postsynaptic effects of baclofen with intracellular Cs+ did not decrease the baclofen-mediated inhibition of evoked EPSCs in either the excitatory or the inhibitory neurons. Furthermore, with and without Cs+ in the pipette, baclofen induced an increase in both the PPR and the CV of the EPSCs; this is indicative of a reduction in neurotransmitter release (Ohana and Sakmann 1998; Zucker 1989). The lack of effect of intracellular Cs+ together with the increase in PPR and CV suggest that the stimulation of GABAB receptors on presynaptic thalamocortical terminals produces the reduction of EPSCs. Presynaptic GABAB receptors have been shown to reduce the release of glutamate from a variety of different synapses (Batchelor and Garthwaite 1992; Chen and Regehr 2003; Gaiarsa et al. 1995; Isaacson 1998; Kombian et al. 1996; Lei and McBain 2003; Morishita and Sastry 1995; Nisenbaum et al. 1992; Wu and Saggau 1995; Yamada et al. 1999), including intracortical glutamatergic synapses in the cerebral cortex (Chu and Hablitz 2003; Fukuda et al. 1993; Gil et al. 1997; Zilberter et al. 1999).
The results of present study represent the first demonstration that afferents within the cortex can be modulated by presynaptic GABAB receptors. Previous studies have demonstrated that perforant path synapses in the hippocampus (Colbert and Levy 1992) and afferent fibers in the olfactory cortex (Tang and Hasselmo 1994) are not modulated by GABAB receptors. Because baclofen does modulate the intrinsic fibers of both of these brain regions, it has been proposed that GABAB receptors are selectively targeted to the intracortical synaptic terminals (Hasselmo 1995). Based on our results, the models of how GABAB receptors regulate the processing of incoming afferent signals should be modified to include the inhibition of sensory afferents in the primary somatosensory cortex. The structural similarities between the olfactory cortex and the hippocampus (Tang and Hasselmo 1994) suggest the possibility that GABAB receptors may be selectively targeted to intrinsic fibers only in cortical areas that lack the six-layer structure of the primary somatosensory cortex. However, the selective modulation of intrinsic fibers in the primary somatosensory cortex may still occur since the intracortical fibers (Gil et al. 1997) were inhibited by lower concentrations of baclofen than the thalamocortical fibers.
In conclusion, our results demonstrate that glutamate release from thalamocortical synapses onto both inhibitory layer IV neurons and excitatory neurons in layers II–III and IV is regulated by the activity of presynaptic GABAB receptors. This mechanism could account for the in vivo observations that indicate that GABAB receptors are involved in the processing of sensory information in the primary somatosensory cortex (Kaneko and Hicks 1988, 1990). A reduction in glutamate release from thalamocortical terminals would preferentially suppress weak and longer latency inputs leading to a reduction in receptive field sizes (Chowdhury and Rasmusson 2002a, b; Kyriazi et al. 1996a). For example, the prior stimulation of an adjacent whisker inhibits the cortical response to the principle whisker (Simons 1985; Simons and Carvell 1989). A recent study indicates that the stimulation of adjacent whiskers reduces the thalamocortical EPSP by a mechanism other than hyperpolarization or shunting inhibition (Higley and Contreras 2003). The activation of presynaptic GABAB receptors by the stimulation of the adjacent whisker could explain these findings because the presynaptic inhibition of glutamate release would cause a reduction in the EPSP without changing the membrane potential or input resistance of the cortical neuron. Consistent with this hypothesis, blocking GABAB receptors reduces adjacent whisker-mediated inhibition (Ajima et al. 1999; Chowdhury and Rasmusson 2003).
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
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ACKNOWLEDGMENTS |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
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FOOTNOTES |
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Address for reprint requests and other correspondence: J. T. Porter, PO Box 7004, Dept. of Pharmacology and Toxicology, Ponce School of Medicine, Ponce, PR 00732 (E-mail: jporter{at}psm.edu).
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REFERENCES |
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) and lack of adaptation of the action potentials. B: image of the biocytin-labeled inhibitory interneuron that exhibited the pattern of action potential discharge in A. Scale bar, 30 µm. Inset: putative synaptic contacts made by this interneuron with the soma of an unlabeled neuron. Scale bar, 10 µm. C: time course showing the effect of 10 µM baclofen on the evoked thalamocortical EPSCs in this interneuron. D: averages of 10 consecutive EPSCs taken at the times indicated in C.
