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RAPID REPORTS |
1 Experimental Neurology Laboratory, I.R.C.C.S. Fondazione Santa Lucia, Rome, Italy2 Clinica Neurologica, University of Rome Tor Vergata, Rome, Italy3 Interdisciplinary Centre for Neurosciences (IZN), University of Heidelberg, Heidelberg, Germany
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Abstract |
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(Received 10 December 2003;
accepted after revision 14 January 2004;
first published online 14 January 2004)
Corresponding author N. B. Mercuri: Experimental Neurology Laboratory, IRCCS Fondazione Santa Lucia, Via Ardeatina 306, 00179 Roma, Italy. Email: Mercurin{at}med.uniroma2.it
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Introduction |
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In dopamine neurones, mGluR-I activates either an inhibitory or an excitatory response depending on the recording conditions and the stimulus strength. Brief afferent stimulation (5 pulses) produces an IPSC mediated by mGluR-I and small conductance Ca2+-activated K+ channels (sK) while longer stimulation (10 pulses) evokes a complex response due to the summation of inhibitory and excitatory components (Shen & Johnson, 1997; Fiorillo & Williams, 1998; Iribe et al. 1999). Using a gluconate-based intracellular solution with moderate Ca2+ buffering which inhibits sK (Velumian et al. 1997), our group has studied isolated excitatory currents evoked by the agonist (S)-3,5-dihydroxyphenylglycine (DHPG, local application by pressure ejection through micropipettes) mediated selectively by mGluR1 in dopamine neurones of the SNc (Guatteo et al. 1999). DHPG activates a TRP-like cationic conductance with a reversal potential near 0 mV and sensitivity to several TRP channel blockers (Tozzi et al. 2003).
We wished to assess the involvement of TRP channels in mGluR1-mediated EPSCs in acute slice preparations of dopamine neurones. Thus we pharmacologically isolated a mGluR1-mediated synaptic current evoked by electrical stimulation and characterized its reversal potential and sensitivity to TRP channel blockers. This study demonstrates that TRP-like channels also mediate mGluR1-activated EPSCs in the SNc.
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Methods |
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All experiments were carried out according to guidelines of the Ethics Committee of the Tor Vergata University for the use of animals in research. Albino Wistar rats of either sex (P22-28) were anaesthetized with 2-bromo-2-chloro-1,1,1-trifluoroethane (Sigma) inhalation and killed by decapitation. The brain was rapidly removed and horizontal slices (thickness 240 µm) were cut in 8–12°C artificial cerebrospinal fluid (ACSF) using a vibratome. ACSF contained (mM): NaCl, 126; KCl, 2.5; MgCl2, 1.2; NaH2PO4, 1.2; CaCl2, 2.4; glucose, 10; NaHCO3, 24; equilibrated with 95% O2 and 5% CO2. After incubation in a reservoir (1–4 h, 34°C), single slices were transferred into a recording chamber and completely submerged in continuously flowing ACSF (2.5 ml min-1, 33–34°C, pH 7.4). The chamber was mounted on the stage of an upright Axioskop microscope (Carl Zeiss, Oberkochen, Germany) equipped for infrared video microscopy (Hamamatsu, Hamamatsu City, Japan).
Electrophysiology
Whole cell patch-clamp recordings were obtained with an amplifier (Axopatch 1D, Axon Instruments) from visually and electrophysiologically identified dopamine neurones (Guatteo et al. 1999) of the SNc using patch pipettes (3–4 M
) made from borosilicate glass 1.5 mm (WPI, Sarasota, FL, USA) using a PP 83 Narishige puller (Tokyo, Japan). Membrane currents were digitized at 5 kHz through a Digidata 1322A A/D converter, acquired and analysed using pCLAMP software (Axon Instruments).
EPSCs were evoked using a pair of tungsten electrodes positioned on either side and within 2 mm of the patched cell. All EPSCs were recorded in the presence of CNQX (10 µM), AP5 (50 µM), picrotoxin (100 µM), CGP 55845 (0.5 µM), atropine (3 µM) and strychnine (1 µM) to block AMPA, NMDA, GABAA, GABAB, muscarinic and glycinergic receptors, respectively. In all cells, the identification of the residual EPSC was confirmed by blockade with the mGluR1 selective antagonist CPCCOEt (100 µM).
Recording pipettes were filled with a standard internal solution containing (mM): potassium gluconate 145; CaCl2, 0.1; MgCl2, 2; Hepes, 10; EGTA, 0.75; Mg2-ATP, 2; Na3GTP, 0.3; (pH 7.35 with KOH). For measurement of current–voltage relationships (I–Vs), potassium gluconate was replaced with caesium gluconate (pH 7.35 with CsOH). For EPSC I–V measurement, QX-314 (2 mM) was added to the internal solution to block Na+ currents and the h current (Ih) and ketamine 100 µM was added to the extracellular solution to ensure the blockade of NMDA receptor-mediated currents at depolarized potentials. For the measurement of DHPG I–Vs, the extracellular solution contained Na+, K+, Ih and GABAA channel blockers (containing in mM: NaCl, 106; TEA-Cl, 30; 4-aminopyridine (4AP), 5; KCl, 2.5; MgCl2, 1.2; CsCl, 2; CaCl2, 2.4; NaH2PO4, 1.2; NaHCO3, 24; glucose, 10; tetrodotoxin (TTX), 0.001; picrotoxin, 0.1). Extracellular channel blockers were applied for at least 10 min before measuring I–Vs and did not affect DHPG response amplitudes which measured 90 ± 8% of control responses measured in the same cell in standard ACSF (n= 6,Vh: -75 mV).
All results and figures have been corrected for calculated junction potential of 13–15 mV and should be noted when comparing these results with uncorrected data reported elsewhere.
Drugs
(S)-3,5-dihydroxyphenylglycine (DHPG), 1-[2-(4-Methoxyphenyl)-2-[3-(4-methoxyphenyl)propoxy]ethyl-1H-imidazole hydrochloride (SKF 96365), 7(hydroxyimino)cyclopropa[b]chromen-1a-carboxylate (CPCCOEt), picrotoxin, CGP 55845 and amino-5-phosphonoeptanoic acid (AP5) were obtained from Tocris Cookson (Bristol, UK); ruthenium red was from Fluka Chemie (Buchs, Switzerland); tetrodotoxin and N-(2,6-dimethylphenylcarbamoylmethyl) triethylammonium chloride (QX-314) were from Alomone Laboratories (Jerusalem, Israel); strychnine hydrochloride was from Roth (Karlsruhe, Germany); N-[3(trifluoromethyl)phenyl]anthranylic acid (flufenamic acid), atropine, ketamine, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and all other products were obtained from Sigma (Milan, Italy).
Picrotoxin, ruthenium red, flufenamic acid and strychnine were dissolved on the day of use. CPCCOEt and CGP 55845 were dissolved in DMSO, picrotoxin was dissolved in extracellular solution, QX-314 was dissolved in the intracellular solution and all other substances were dissolved in water. The final concentration of DMSO did not exceed 0.1% extracellularly which produced no independent effects on the neurones.
DHPG (100 µM) in extracellular solution was applied through a glass pipette whose open end (approx. 2 µM diameter) was positioned 30–50 µM from the cell body of the patched neurone. The DHPG pipette was connected to a pneumatic pico-pump (Picospritzer, WPI) set at 20 p.s.i., delivering a pressure-ejection pulse (1 s). Other drugs were bath-applied by switching the solution of the perfusion system using three-way taps with complete exchange of the solution in the recording chamber occurring in about 1 min.
All values in the text are expressed as mean ± standard error of the mean.
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Results |
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mGluR1 receptor-mediated EPSCs with a peak amplitude of 273 ± 35 pA (Vh=-73 mV, n= 15) were pharmacologically isolated (see Methods) from postsynaptic current responses to a 300 Hz stimulus train lasting 50 ms (i.e. 15 stimulations). This response peak occurred 381 ± 25 ms after the end of the stimulus train. Single exponential fits of mGluR1 EPSCs gave time constants of 0.199 ± 0.025 s for the increase in current amplitude and 0.809 ± 0.092 s for the decay.
Evoked EPSCs mediated by mGluR-I reverse near -10 mV
To investigate their I–V, mGluR1 EPSCs were recorded at holding potentials between -73 and +47 mV in seven cells. EPSCs were then re-recorded in the presence of the selective mGluR1 antagonist CPCCOEt (100 µM), which confirmed the absence of non-mGluR1-mediated components of the EPSC at all potentials in all cells (Fig. 1A). The EPSCs of three cells, including the example in Fig. 1A, were larger at -53 mV than at -73 mV, indicating a region of negative slope conductance in the I–V at hyperpolarized potentials. Another four cells, however, did not display this phenomenon with a positive slope conductance at all potentials. The EPSCs of all seven cells were inward at -33 mV and outward at +7 mV although EPSCs recorded at -13 mV showed both inward and outward components in some cells (not shown). An I–V of the mGluR1 EPSC was formed from the average EPSC amplitude of all cells and showed a reversal potential estimated to be -10 mV by extrapolation (Fig. 1B).
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) values measured at -75 mV. Responses to pressure ejection of an mGluR1 agonist reverse near -17 mV
Local pressure-ejection application of DHPG selectively activates mGluR1 receptors in midbrain dopamine neurones (Guatteo et al. 1999). Responses to DHPG (100 µM, 1 s) showed an amplitude of 340 ± 61 pA with time constants of 0.96 ± 0.09 s for the increase in current amplitude and 3.10 ± 0.34 s for the decay (Vh=-75 mV, n= 9). In comparison to synaptically mediated mGluR1 currents, DHPG-activated currents showed similar amplitudes (125% of mean EPSC amplitude, P= 0.42) but much slower kinetics (482 and 383% of mean EPSC on and off, respectively, P < 0.0001 between-groups t tests).
We have recently demonstrated the involvement of Na+- and K+-permeable TRP-like channels in the DHPG response of dopamine neurones, where a reversal potential of 0 mV was determined using ramp I–V protocols. To more directly compare mGluR1 EPSCs to agonist-evoked currents across a range of holding potentials, we measured responses to pressure ejection of DHPG at holding potentials between -75 and +45 mV in 20 mV intervals (Fig. 2A). In all nine cells, the DHPG current reversed polarity between -35 and +5 mV with a reversal potential of -17 mV estimated by extrapolation (Fig. 2B). As for mGluR1-mediated EPSCs measured near the reversal potential, the DHPG response at -15 mV showed inward followed by outward components in several cells (see example Fig. 2A).
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mGluR1 EPSCs are blocked by TRP channel blockers
mGluR1 receptor-mediated EPSCs were diminished by extracellular application of non-selective compounds known to block TRP channels and store-operated channels (SOCs). The imidazole SKF 96365 blocks SOCs and TRPC3, TRPC5, TRPC6 and TRPC7 channels at concentrations of 25–100 µM (Zhu et al. 1998; Halaszovich et al. 2000; Inoue et al. 2001; Clapham et al. 2002). SKF 96365 (100 µM) reversibly inhibited mGluR-mediated EPSCs to 3.9 ± 3.9% of control (n= 4; P < 0.05; Fig. 3A).
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Ruthenium red is a non-selective ryanodine receptor antagonist, which blocks TRPV-mediated responses (Zucchi & Ronca-Testoni, 1997), mitochondrial Ca2+ uptake (Rigoni & Deana, 1986) and voltage-operated Ca2+ channels (Cibulsky & Sather, 1999). Ruthenium red (20 µM) applied extracellularly rapidly and reversibly inhibited mGluR1-mediated EPSCs to 20 ± 7% of control (n= 4; P < 0.05; Fig. 3C).
After washout of the effects of SKF 96365, flufenamic acid or ruthenium red in all cells, CPCCOEt 100 µM was applied and shown to block the evoked EPSCs (5 ± 2% of control; n= 12; see Fig. 3). Thus the evoked EPSCs blocked by these TRP channel blockers were mediated by mGluR1.
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Discussion |
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mGluR1 EPSC I–V is consistent with a cationic TRP channel
mGluR1 EPSCs reversed at a membrane potential of -10 mV, consistent with the involvement of a cationic channel and similar to the reversal potential of channels activated by DHPG, which we have previously shown to be permeable to K+ and Na+ (Guatteo et al. 1999; Tozzi et al. 2003). The reversal potential of the DHPG current measured at various holding potentials (-17 mV, current results) was more negative than estimates generated from ramp protocols (+1 mV, Tozzi et al. 2003). This may be due to a diminished contribution of the slow activating outward current components in rapid voltage ramp measurements, or the contribution of voltage-activated conductances in distal dendritic compartments where the voltage clamp may have been compromised.
The form of the mGluR1 EPSC I–V displayed double rectification with minimal outward current between -10 and +27 mV. Negative slope conductance at hyperpolarized potentials (< -53 mV) was also present in some cells. These properties also characterize TRPC channels in the TRPC1/4/5 subfamily studied in expression systems (Strubing et al. 2001; Plant & Schaefer, 2003). We have recently reported the presence of mRNA for individual or multiple combinations of these isoforms in dopamine cells. (Tozzi et al. 2003) Negative slope conductance at potentials more negative than -60 mV is revealed when multiple isoforms of this subfamily are coexpressed, but is lost during strong channel activation. The presence of negative slope conductance of the mGluR1 EPSC in some dopamine neurones may reflect the presence of multiple TRPC isoforms in these cells or differences in the degree of channel activation.
Voltage-dependent kinetics of mGluR1 responses
The kinetics of mGluR1-mediated EPSCs in dopamine neurones at hyperpolarized potentials was typical of the relatively slow synaptic currents mediated by metabotropic receptors including mGluR-I-mediated EPSCs in cerebellar Purkinje neurones (Reichelt & Knopfel, 2002; Kim et al. 2003) and dopamine neurones (Shen & Johnson, 1997). EPSC response latencies may also reflect diffusion delays introduced by the extra-synaptic location of mGluR1 receptors and/or the effector channels. Since time constants for EPSCs were roughly 4 times faster than those of currents evoked by localized pressure ejection of DHPG, mGluR1 receptors are probably located close to terminals (i.e. synaptic or perisynaptic).
The time course of both mGluR1-activated EPSCs and responses to brief activation of mGluR1 with an exogenous agonist were greatly retarded at depolarized potentials. The voltage dependence of mGluR1 response kinetics is unlikely to relate to the spatial relationship of receptors and effectors or second messengers but may reflect gating properties of the TRP-like channel involved. NMDA-mediated EPSCs (for example Anchisi et al. 2001) show a similar I–V shape and exhibit qualitatively similar voltage dependence in their kinetics.
Although mGluR1 EPSCs were much smaller at positive membrane potentials, they activated and deactivated/inactivated much more slowly. This may act to sustain mGluR1-activated excitatory currents following burst initiation when the membrane potential spends significant amounts of time at positive potentials.
Pharmacological identification of TRP channels mediating mGluR1 EPSCs
The sensitivity of mGluR1 EPSCs to TRP channel antagonists parallels that of current responses to DHPG pressure ejection. Although SKF 96365, flufenamic acid and ruthenium red have non-selective actions (see Results), we previously demonstrated the insensitivity of DHPG responses to blockers of voltage-activated Ca2+, Na+, K+ and h-current channels and that the inhibition of mGluR1 responses by ruthenium red was not mediated by its intracellular actions (Tozzi et al. 2003). Thus, we propose that mGluR1 EPSCs, like agonist-activated currents, are mediated by a TRP-like channel.
mGluR1-mediated EPSCs in cerebellar Purkinje neurones were also inhibited by SKF 96365 (Kim et al. 2003), despite previous evidence to the contrary (Tempia et al. 2001). TRPC1 channels, which mediate EPSCs in Purkinje neurones may also be involved in the mGluR1 EPSCs of dopamine neurones, most of which contain TRPC1 mRNA (Tozzi et al. 2003).
Physiological implications
Burst firing of afferent glutamatergic neurones is likely to activate mGluR1-mediated EPSCs in dopamine neurones. Glutamatergic neurones in the subthalamic nucleus project directly on to dopamine neurones in the substantia nigra. (Iribe et al. 1999). Subthalamic nucleus neurones display burst activity with 10–15 spikes per burst at frequencies of 100–400 Hz in vivo (Hollerman & Grace, 1992; Urbain et al. 2002). Such bursting activity in vivo is expected to cause mGluR1 EPSCs such as those recorded here using 15 stimuli at 300 Hz. Complex interactions between concurrent metabotropic and ionotropic glutamate receptor-mediated EPSCs and metabotropic IPSCs are likely, however.
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