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Department of Ophthalmology and Visual Science, Yale University School of Medicine, New Haven, Connecticut 06520
Submitted 24 March 2004; accepted in final form 17 June 2004
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
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-S) in patch pipette, suggesting an involvement of postsynaptic group I metabotropic glutamate receptors (mGluRs). These results indicate that LTD in developing rat visual cortex varies with layer: LTD was absent in layer IV, suggesting a unique plasticity mechanism at geniculocortical synapses; LTD in layers II/III and V depends on NMDA receptors but not mGluRs, and LTD in layer VI requires mGluRs but not NMDA receptors. |
INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
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; Wiesel and Hubel 1963). It has been known that the critical period for this sensory-dependent plasticity in the visual cortex varies with layer, ending first in layer IV. Extragranular layers (layers II, III, V, and VI) remain plastic for longer than layer IV (Daw et al. 1992; Mower et al. 1985; Shatz and Stryker 1978). More recently, initial changes from monocular deprivation have been demonstrated to occur in layers II and III, earlier than in layer IV (Trachtenberg et al. 2000).
Although the mechanism underlying ocular dominance plasticity is not yet fully understood, the involvement of both ionic and metabotropic glutamate receptors in the visual cortex have been implicated. Blockade of N-methyl-D-aspartate receptors (NMDARs) in vivo prevents the ocular dominance shift (Bear et al. 1990; Daw et al. 1999a). The laminar expression, subunit variants, and function of NMDARs are correlated with the critical period, and all are modified by visual experience (Carmignoto and Vicini 1992; Chen et al. 2000; Fox et al. 1989; Hestrin 1992; Monyer et al. 1994; Quinlan et al. 1999; Sheng et al. 1994). In addition to ionotropic receptors, G-protein-coupled metabotropic glutamate receptors (mGluRs) are also pointed to be crucial in modulating ocular dominance plasticity. The developmental changes of mGluR-linked phosphoinositide (PI) turnover are parallel with the changes of visual cortical plasticity (Bear and Dudek 1991; Dudek and Bear 1989). Moreover, the laminar distribution of mGluRs changes with critical period and is sensitive to dark rearing (Beaver et al. 1999; Daw et al. 1999b; Reid and Romano 2001; Reid et al. 1997).
The mechanisms of LTD and long-term potentiation (LTP) of excitatory synaptic transmission from in vitro brain slice preparations have been correlated with the development of normal ocular dominance and the ocular dominance shift due to MD in vivo. Of particular interest is the observation that developmental declines in LTP and LTD in visual cortex correlate well with the age-dependent loss of experience-dependent plasticity (Dudek and Friedlander 1996; Kirkwood et al. 1995). Inhibitors for NMDARs (Bear et al. 1990; Daw et al. 1999a; Kirkwood and Bear 1994a, b) or protein kinase A (Beaver et al. 2001; Liu et al. 2003) can block LTD and LTP in vitro and ocular dominance plasticity in vivo. However, experiments with genetic and pharmacological manipulations, on the other hand, revealed a dissociation between either LTD or LTP and ocular dominance plasticity. Knockout of the RII subunit of PKA (Fischer et al. 2002; Rao et al. 2002) or GABA synthesizing enzyme GAD65 (Choi et al. 2002; Hensch et al. 1998a) impairs LTD and ocular dominance plasticity but not LTP. RI mutant mice showed absence of LTD and some forms of LTP and presence of ocular dominance plasticity (Hensch et al. 1998b). LTD is absent and ocular dominance plasticity is present in kitten after infusion of the mGluRs antagonist 
-methyl-4-carboxyphenlglycine (MCPG) as well as in mice mutant for the mGluR2 (Hensch and Stryker 1996; Renger et al. 2002).
Because most of the studies on LTP/LTD in visual cortex have been done by recording of field potentials in layer II/III with stimulation of layer IV and ocular dominance plasticity is monitored by recording cells in all layers, it is reasonable to hypothesize that the dissociation of LTP/LTD from ocular dominance plasticity found in these experiments may be due to different mechanisms for plasticity in different layers. Indeed, our previous work has shown that LTP in various layers has different mechanisms, depending on NMDARs or group I mGluRs distinctly (Wang and Daw 2003). However, there are no systematic studies of LTD in various layers of visual cortex so far. Therefore in the present experiments, by using whole cell recording, the laminar variations in the mechanisms of LTD were compared by applying antagonist against either NMDARs or mGluRs.
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METHODS |
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Sprague-Dawley rats (18–25 days old) were decapitated under halothane anesthesia. The brain was rapidly removed and placed in ice-cold cutting solution consisting of (in mM) 215 sucrose, 2.5 KCl, 2.8 MgCl2, 1.0 NaH2PO4, 10.0 glucose, 26.2 NaHCO3, and 1.0 CaCl2 at pH 7.3 when equilibrated with 95% O2-5% CO2. Coronal slices (400 µm) were cut using a vibroslicer and incubated at room temperature for 2 h in an interface chamber containing (in mM) 124 NaCl, 5 KCl, 1.3 MgCl2, 1 NaH2PO4, 10 Glucose, 26 NaHCO3, and 2.5 CaCl2, pH 7.3 when equilibrated with 95% O2-5% CO2. Osmolarity was adjusted to 310 mosM with H2O.
Electrophysiology
For whole cell voltage-clamp recording, slices were submerged in a chamber perfused with artificial cerebrospinal fluid (ACSF; 32°C). Patch pipettes were filled with internal solution containing (in mM) 130 K-gluconate, 5 MgCl2, 10 HEPES, 0.5 EGTA, 5 Tris salt-ATP, 1 Tris salt-GTP, 10 KCl, 10 Di-tris salt phosphocreatine, and 4 Di-sodium phosphocreatine, pH was adjusted to 7.3 with KOH and osmolarity was adjusted to 290 mosM with H2O. Whole cell recordings were obtained from neurons in layers II/III, IV, V, or VI of visual cortex with a patch-clamp amplifier (Dagan 3900A, Dagan, Minneapolis, MN). The neurons were visualized using an Olympus BX51WI upright microscope with DIC optics. A bipolar matrix stimulating electrode (No. MX21XEP, Frederick Haer) was located within the border between layer VI and white matter for recording in layer IV, in layer II/III for recording in layer V or VI, and in layer IV for recording in layer II/III. The boundaries between layers occur at 5–10% of the distance between pia and white matter for the layer I to layer II boundary, 32–36% for the layer III to layer IV boundary, 47–52% for the layer IV to layer V boundary, and 72–75% for the layer V to layer VI boundary (Reid and Juraska 1991). After a whole cell recording was obtained, with resting potential less or equal to –55 mV, neurons were voltage-clamped at –70 mV. Throughout the recording, series resistance was monitored continuously by applying a –10-mV voltage step, and the recording was terminated if it varied by >10%. A bipolar test stimulus (0.1-ms duration) was used to elicit an excitatory postsynaptic current (EPSC) every 15 s. EPSCs were included in the analysis if the rise time and decay time constants were monotonic and possessed no obvious multiple EPSCs or polysynaptic waveforms. After a stable control level of EPSC was recorded for 10 min, LTD was induced using 1-Hz stimulation for 10 min paired with postsynaptic depolarization to –40 mV. Data were collected at 20.0 kHz (HEKA Lambrecht) and stored for off-line analysis. For data analysis, a custom-written IGOR Pro program was used for calculating the amplitude of EPSCs, and every four samples were averaged and EPSCs amplitudes were normalized to baseline and expressed as the means ± SE The magnitude of LTD was calculated by comparing the EPSC amplitude for the period of 30–40 min after induction, with that for the period of 10 min prior to induction. Slices were interleaved for control and drug-treated groups. Student's t-test determined significant difference at P values <0.05.
D-aminophosphonovaleric acid (D-AP5, Tocris), (2S)-amino-2-[(1S,2S)-2-carboxycycloprop-1-yl]-3-(xanth-9-yl) propanoic acid (LY341495, Tocris), and (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA, Tocris) were diluted from stock solution (H2O, DMSO, or NaOH, respectively). The slices were preincubated with D-AP5 or LY341495 or AIDA for 
30 min prior to experiment to eliminate any effects of the drugs on baseline. Guanosine 5'-O-(2-thiodiphosphate) thilothium salt (GDP--S, Sigma) was added directly into the recording pipette.
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RESULTS |
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). LY341495 is a nanomolar potent and selective antagonist at group II mGluRs but can be used in higher concentrations to block all mGluRs (Fitzjohn et al. 1998; Kingston et al. 1998). So in the present study, LY341495 was used to block all mGluRs at 100 µM and to inhibit group II mGluRs at 1 µM, and AIDA (500 µM) was used to block group I mGluRs. LTD in layer II/III depends on NMDARs but not mGluRs
In layer II/III of control slices, after 10-min baseline period of stable EPSCs were collected, LTD was induced by 10-min 1-Hz afferent stimulation paired with postsynaptic depolarization to –40 mV (pairing protocol). The peak amplitude of EPSCs showed obvious depression lasting for 40 min after induction (Fig. 1). Administration of 50 µM D-AP5, a specific NMDAR antagonist, could totally block the LTD induced by the pairing protocol (94.5 ± 5.8%, n = 6; P < 0.01, compared with control, 64.4 ± 6.6%, n = 6; Fig. 1A), while significant LTD was induced in the presence of 100 µM LY341495 (70.4 ± 3.1%, n = 5; P > 0.4, compared with control, 74.7 ± 3.1%, n = 7; Fig. 1B). These results indicated that the LTD in layer II/III is NMDAR dependent and mGluR independent.
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In layer IV, the pairing protocol did not induce significant depression of EPSCs in layer IV (91.7 ± 5.2%, n = 5; P > 0.1, compared with baseline; data not shown), demonstrating that LTD is significantly suppressed under these conditions.
LTD in layer V is also NMDARs but not mGluRs dependent
As was the case in layer II/III, 10-min 1-Hz afferent stimulation paired with postsynaptic depolarization to –40 mV elicited a significant LTD in layer V neurons. Application of 50 µM D-AP5 prevented the induction of LTD (103.2 ± 8.6%, n = 5; P < 0.005, compared with control, 58.2 ± 7.3%, n = 5; Fig. 2A), indicating a dependence of LTD on NMDARs in layer V. However, in the presence of 100 µM LY 341495 in the bath solution, LTD could still be induced in layer V (70.8 ± 7.0%, n = 6), which was not significantly different from the control (66.8 ± 7.1%, n = 6, P > 0.7; Fig. 2B), suggesting that mGluRs are not involved in the induction of LTD in layer V of visual cortex.
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Pairing protocol is also effective to induce LTD in layer VI. However, in contrast to the LTD in layers II/III and V, LTD induced in layer VI was not abolished by 50 µM D-AP5. The peak amplitudes of EPSCs in D-AP5-treated slices (76.8 ± 5.3%, n = 4) were not significantly different from that in control slices (71.4 ± 5.7%, n = 4; P > 0.3; Fig. 3A). As shown in Fig. 3B, 100 µM LY341495 treatment blocked induction of LTD in layer VI totally (n = 9; P < 0.02, compared with control, n = 7; Fig. 3B). These data suggested the dependence of LTD in layer VI on mGluRs but not NMDARs.
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-S inside the patch pipette, which prevents GTP binding to the G protein thereby halting the functions of postsynaptic mGluRs, was used to identify the involvement of postsynaptic mGluRs in LTD in layer VI. When GDP--S was included in recording pipette, the amplitude of LTD (80.1 ± 5.4%, n = 6; P < 0.05, compared with baseline, paired t-test) in layer VI was significantly smaller than control level (56.3 ± 7.3%, n = 6; P < 0.03; Fig. 3C), demonstrating the involvement of postsynaptic mGluRs in LTD in layer VI. Meanwhile, because GDP--S in recording pipette only partially inhibited the amplitude of LTD, it suggests that presynaptic mGluRs might also participate in LTD induction in layer VI.
The possible contribution of group II or/and group I mGluRs to the mGluR-dependent LTD in layer VI were also examined in the present study. Our previous work of mGluRs on the synaptic effects have shown that group II mGluRs are depressive in visual cortex (Beaver et al. 1999; Daw et al. 1999b). We first examined the effects of group II mGluRs on LTD in layer VI. As shown in Fig. 3D, 1 µM LY341495, which is believed to block just group II mGluRs at this low concentration, had no effect on LTD induced by pairing protocol. The peak amplitude of EPSCs in drug treated slices at 30–40 min after induction (60.5 ± 10.9%, n = 4) had no significant difference from that in control slices (54.6 ± 8.4%, n = 4; P > 0.4), demonstrating that group II receptors are not involved in the mGluR-dependent LTD in layer VI. On the other hand, the group I mGluR-specific antagonist AIDA (500 µM) blocked the LTD in layer VI totally (93.1 ± 5.0%, n = 8; P < 0.005, compared with control, 66.1 ± 5.1%, n = 6; Fig. 3E), indicating a dependence of LTD on group I mGluRs in layer VI.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
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), this may very well occur because there are different mechanisms of plasticity in different layers (present results; Wang and Daw 2003).
Consistent with previous data, we found that LTD in layer II/III induced by a pairing protocol is NMDAR-dependent (Kirkwood and Bear 1994b; Sawtell et al. 1999). In addition, this LTD does not need the participation of mGluRs because 100 µM LY341495, which is the most potent mGluRs antagonist at all known mGluR subtypes (Kingston et al. 1998) and can competitively antagonize glutamate-stimulated PI hydrolysis in visual cortical synaptoneurosomes (Sawtell et al. 1999), has no effect on induction of LTD in layer II/III, indicating that mGluRs are not involved in NMDAR-dependent LTD in layer II/III under our experimental conditions. In agreement with our results, previous studies showed that NMDAR-dependent LTD induced by low-frequency stimulation (LFS) in either layer II/III of visual cortex (Sawtell et al. 1999) or CA1 region of hippocampus (Fitzjohn et al. 1998) cannot be blocked by LY341495. However, our findings are at odds with other reports that (S)-MCPG blocks LFS-induced LTD in layer II/III (Haruta et al. 1994; Hensch and Stryker 1996). It should be noted that (S)-MCPG, which once was believed to act as a competitive antagonist of cell-surface mGluRs, fails to block PI turnover and changes in spike adaptation stimulated by glutamate, the endogenous ligand (Huber et al. 1998), thus it is likely that (S)-MCPG works on an unknown, (S)-MCPG-sensitive and LY341495-insensitive mGluR. Moreover, our result in layer II/III is also consistent with the finding that mGluR5 mutant mice have normal LTD in layer II/III of visual cortex (Sawtell et al. 1999). We cannot rule out the possibility that an alternative, mGluRs-dependent LTD also exists in layer II/III of visual cortex because of the fact that multiple forms of LTD can coexist at the same neurons (Oliet et al. 1997). It is possible that such a type of LTD, distinct from the LTD in the present study, might be revealed under some conditions. Recently Renger et al. (2002) reported that both NMDAR- and group II mGluR-dependent LTD were induced by LFS in layer II/III of visual cortex, and mGluR2 mutant mice showed deficits in this LTD.
LTD was not induced with a pairing protocol in layer IV in the present study; this confirms prior report showing the induction of LTD in layer IV was not reliable (Dudek and Friedlander 1996). Because the absence of LTP was also found in layer IV (Wang and Daw 2003), these data suggest that the mechanisms of plasticity at the geniculocortical synapses are different from those at intracortical synapses.
Of particular interest, LTD of excitatory synaptic transmission was also induced in layers V and VI by 10-min 1-Hz presynaptic stimulation paired with postsynaptic depolarization to –40 mV with stimulating electrode placed at layer II/III. We found LTD in layer V was abolished in the presence of 50 µM D-AP5 in the bath solution, which implies that the LTD in layer V is similar to the LTD in layer II/III, also depending on NMDARs but not mGluRs. However, the mechanism of LTD in layer VI depends on mGluRs but not NMDARs. Similar results are seen with mossy fiber LTD (Kobayashi et al. 1996).
We were also able to examine the possible involvement of group II and group I mGluRs in LTD in layer VI. At first, for several reasons, we focused on group II mGluRs: group II mGluRs are well-known presynaptic autoreceptors, and activation of these receptors by accumulating glutamate may inhibit transmitter release through G-protein-coupled Ca2+ channel (Scanziani et al. 1997; Sladeczek et al. 1993); group II mGluRs depress the visual response in all layers at an early age; and its laminar expression and sensitivity to agonists is correlated with the critical period in kittens, and all are delayed by dark-rearing (Beaver et al. 1999; Reid and Romano 2001). However, it is unexpected that group II mGluRs are not involved in the mGluRs-dependent LTD in layer VI: our results showed that 1 µM LY341495 had no effect on the induction of LTD.
Group I mGluRs are mGluR1 and mGluR5, which couple to phospholipase C to increase levels of diacylglycerol and inositol trisphosphate, and these messengers activate PKC and release of Ca2+ from internal stores, respectively. Recently, it has been reported that mGluR-dependent and NMDAR-independent LTD can be induced by activation of group I mGluRs (Fitzjohn et al. 1999; Huber et al. 2000; Oliet et al. 1997; Palmer et al. 1997; Snyder et al. 2001). Both pre- and postsynaptic mechanisms underlying this LTD have been suggested; this is consistent with the fact that group I mGluRs exist at both sites. Group I mGluRs might reduce transmitter release by modulating presynaptic calcium influx (Faas et al. 2002; Fitzjohn et al. 2001; Stefani et al. 1996; Swartz and Bean 1992; Yoshino and Kamiya 1995), or postsynaptically modulate dendritic protein synthesis or internalization of glutamate receptors (Huber et al. 2000; Snyder et al. 2001). Jin et al. (2001) have revealed that prolonged application of dihydroxyphenylglycine (DHPG), a group I mGluRs agonist, in the cat visual cortex, after the initial excitatory effect, produces depression. By using group I mGluRs inhibitor, the present study demonstrates that the mGluR-dependent LTD in layer VI is mediated by group I mGluRs, which probably involves both pre- and postsynaptic mechanisms as indicated by the results showing that GDP--S in recording pipette can only partially block LTD.
Finally, the present results showed that LTD in developing rat visual cortex varies with layer: LTD was absent in layer IV, suggesting a unique plasticity mechanism at geniculocortical synapses; LTD in layers II/III and V depends on NMDARs but not mGluRs; and LTD in layer VI depends on mGluRs but not NMDARs. Combined with our previous results showing that mechanisms of LTP also vary with layer in developing visual cortex (Wang and Daw 2003), it is suggested that attention should be taken to layer variations when trying to interpret the dissociation between ocular dominance plasticity in vivo and LTP/LTD in visual cortex in vitro.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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Address for reprint requests and other correspondence: Y. Rao, Dept. of Ophthalmology and Visual Science, Yale University Medical School, 330 Cedar St., New Haven, CT 06520-8061 (E-mail: yan.rao{at}yale.edu).
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