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F Stratta

Publications and source records attributed to F Stratta.

At least 19 recordsLinked to original sources

Cognitive allocentric representations of visual space shape pointing errors.

Subjects reached in three-dimensional space to a set of remembered targets whose position was varied randomly from trial to trial, but always fell along a "virtual" line (line condition). Targets were presented briefly, one-by-one and in an empty visual field. After a short delay, subjects were required to point to the remembered target location. Under these conditions, the target was presented in the complete absence of allocentric visual cues as to its position in space. However, because the subjects were informed prior to the experiment that all targets would fall on a straight line, they could conceivably imagine each point target as belonging to a single rigid object with a particular geometry and orientation in space, although this virtual object was never explicitly shown to the subjects. We compared the responses to repeated measurements of each target with those measured for targets presented in a directionally neutral configuration (sphere condition), and used the variable errors to infer the putative reference frames underlying the corresponding sensorimotor transformation. Performance in the different tasks was compared under two different lighting conditions (dim light or total darkness) and two memory delays (0.5 or 5 s). The pattern of variable errors differed significantly between the sphere condition and the line condition. In the former case, the errors were always accounted for by egocentric reference frames. By contrast the errors in the line condition revealed both egocentric and allocentric components, consistent with the hypothesis that target information can be defined concurrently in both egocentric and allocentric frames of reference, resulting in two independent coexisting representations.

Adult↗

Analysis of pointing errors reveals properties of data representations and coordinate transformations within the central nervous system.

The execution of a simple pointing task invokes a chain of processing that includes visual acquisition of the target, coordination of multimodal proprioceptive signals, and ultimately the generation of a motor command that will drive the finger to the desired target location. These processes in the sensorimotor chain can be described in terms of internal representations of the target or limb positions and coordinate transformations between different internal reference frames. In this article we first describe how different types of error analysis can be used to identify properties of the internal representations and coordinate transformations within the central nervous system. We then describe a series of experiments in which subjects pointed to remembered 3D visual targets under two lighting conditions (dim light and total darkness) and after two different memory delays (0.5 and 5.0 s) and report results in terms of variable error, constant error, and local distortion. Finally, we present a set of simulations to help explain the patterns of errors produced in this pointing task. These analyses and experiments provide insight into the structure of the underlying sensorimotor processes employed by the central nervous system.

Central Nervous System↗

Basal ganglia and gait control: apomorphine administration and internal pallidum stimulation in Parkinson's disease.

Gait coordination was analyzed (four-camera 100 Hz ELITE system) in two groups of idiopathic Parkinson disease (PD) patients. Five patients underwent continuous infusion of apomorphine and were recorded in two different sessions (APO OFF and APO ON) in the same day. Three patients with a previous chronic electrode implantation in both internal globi pallidi (GPi) were recorded in the same experimental session with the electrodes on and off (STIM ON and STIM OFF). The orientation of both the trunk and the lower-limb segments was described with respect to the vertical in the sagittal plane. Lower-limb inter-segmental coordination was evaluated by analyzing the co-variation between thigh, shank, and foot elevation angles by means of orthogonal planar regression. At least 30 gait cycles per experimental condition were processed. We found that the trunk was bent forward in STIM OFF, whereas it was better aligned with the vertical in STIM ON in both PD groups. The legs never fully extended during the gait cycle in STIM OFF, whereas they extended before heel strike in STIM ON. The multisegmental coordination of the lower limb changed almost in parallel with the changes in trunk orientation. In STIM OFF, both the shape and the spatial orientation of the planar gait loops (thigh angle vs. shank angle vs. foot angle) differed from those of physiological locomotion, whereas in STIM ON the gait loop tended to resume features closer to the control. Switching the electrodes on and off in patients with GPi electrodes resulted in quasi-parallel changes of the trunk inclination and of the planar gait loop. The bulk of the data suggest that the basal-ganglia circuitry may be relevant in locomotion by providing an appropriate spatio-temporal framework for the control of posture and movement in a gravity-based body-centered frame of reference. Pallido-thalamic and/or pallido-mesencephalic pathways may influence the timing of the inter-segmental coordination for gait.

Aged↗

Short-term memory for reaching to visual targets: psychophysical evidence for body-centered reference frames.

Pointing to a remembered visual target involves the transformation of visual information into an appropriate motor output, with a passage through short-term memory storage. In an attempt to identify the reference frames used to represent the target position during the memory period, we measured errors in pointing to remembered three-dimensional (3D) targets. Subjects pointed after a fixed delay to remembered targets distributed within a 22 mm radius volume. Conditions varied in terms of lighting (dim light or total darkness), delay duration (0.5, 5.0, and 8.0 sec), effector hand (left or right), and workspace location. Pointing errors were quantified by 3D constant and variable errors and by a novel measure of local distortion in the mapping from target to endpoint positions. The orientation of variable errors differed significantly between light and dark conditions. Increasing the memory delay in darkness evoked a reorientation of variable errors, whereas in the light, the viewer-centered variability changed only in magnitude. Local distortion measurements revealed an anisotropic contraction of endpoint positions toward an "average" response along an axis that points between the eyes and the effector arm. This local contraction was present in both lighting conditions. The magnitude of the contraction remained constant for the two memory delays in the light but increased significantly for the longer delays in darkness. These data argue for the separate storage of distance and direction information within short-term memory, in a reference frame tied to the eyes and the effector arm.

Anisotropy↗

Viewer-centered frame of reference for pointing to memorized targets in three-dimensional space.

Pointing to a remembered visual target involves the transformation of binocular visual information into an appropriate motor output. Errors generated during pointing tasks may indicate the reference frames used by the CNS for the transformation and storage of the target position. Previous studies have proposed eye-, shoulder-, or hand-centered reference frames for various pointing tasks, depending on visual conditions. We asked subjects to perform pointing movements to remembered three-dimensional targets after a fixed memory delay. Pointing movements were executed under dim lighting conditions, allowing vision of the fingertip against a uniform black background. Subjects performed repeated movements to targets distributed uniformly within a small (radius 25 mm) workspace volume. In separate blocks of trials, subjects pointed to different workspace regions that varied in terms of distance and direction from the head and shoulder. Additional blocks were performed that differed in terms of starting position, effector hand, head rotation, and memory delay duration. Final pointing positions were quantified in terms of the constant and variable errors in three dimensions. The orientation of these errors was examined as a function of workspace location to identify the underlying reference frames. Subjects produced anisotropic patterns of variable error, with greater variability for endpoint distances from the body. The major axes of the variable-error tolerance ellipsoids pointed toward the eyes of the subject, independent of workspace region, effector hand (left or right), initial hand position, and head rotations. Constant errors were less consistent across subjects, but also tended to point toward the head and body. Both overshoots and undershoots of the target position were observed. Increasing the duration of the memory delay period increased the size but did not alter the orientation of the variable-error ellipsoids. Variability of the endpoint positions increased equally in all three Cartesian directions as the memory delay increased from 0.5 to 8.0 s. The anisotropy of variable errors indicates a viewer-centered reference frame for pointing to remembered visual targets with vision of the finger. The anisotropy of pointing variability stems from variability in egocentric binocular cues as opposed to reliance on allocentric visual references or to specific approximations in the sensorimotor transformation. Nevertheless, observed increases in variability with longer memory delays indicate that the short-term storage of the target position does not simply mirror the retinal and ocular sensory signals of the visually acquired target location. Thus spatial memory is carried out in an internal representation that is viewer-centered but that may be isotropic with respect to Cartesian space.

Adult↗

Outward potassium currents activated by depolarization in rat globus pallidus.

Voltage-dependent potassium currents play a key role in shaping the firing pattern of central neurons. Their pharmacological and physiological identification is rather important in the structures which are involved in the filtering of input/output messages. In this regard, globus pallidus external segment (GPe) is indicated as a crucial station in the well-known indirect pathway of the basal ganglia. Among the potassium conductances which have been indicated to condition the firing behavior and the neuronal integrative properties in many central neurons, we analysed the depolarization-activated ones by means of patch-clamp recordings in the whole-cell configuration. Two main families of calcium-independent outward potassium currents are activated by depolarization in GPe neurons acutely isolated from the adult rat. From depolarized holding potentials (-50/-45 mV), a slowly-activating, sustained current is evoked; it manifests very little inactivation and it is available at rather depolarized potentials (-30 mV/-20 mV). This current is relatively resistant to 4-aminopyridine (4-AP) but it is blocked by tetraethilammonium ions (TEA) and consequently it resembles delayed rectifier current (Ik). From negative holding potentials (-80/-100 mV), on the other hand, A-like conductances are activated. Together with a fast-inactivating transient current, another component is observed in a significant proportion of recordings (45%). This current shows half-inactivation voltage around -90 mV, peculiar sensitivity to micromolar doses of 4-AP and a slow rate of recovery from inactivation. The presence and the modulation of these A-like currents may be a very critical aspect in the membrane physiology of pallidal neurons.

4-Aminopyridine↗

Electrophysiology of dopamine D-1 receptors in the basal ganglia: old facts and new perspectives.

1. The dopamine (DA) D1-receptor family is highly represented in the mammalian brain and particularly in the nigrostriatal system, whose integrity is crucial for the execution of motor performances. 2. In the last decade, our understanding of the electrophysiology of D1 receptors on caudate-putamen neurons has greatly improved. The effects of the activation of striatal D1 receptors were studied by extracellular single unit recordings in the intact animal as well as by intracellular recordings in rat brain slice preparation. More recently, whole-cell recordings on isolated striatal neurons have further addressed this issue and confirmed the inhibitory modulatory role of D1 receptor on the electrical activity of striatal neurons. 3. Several important questions, however, concerning the functional effects of D1 receptor activation in the basal ganglia are still debated: the cellular segregation of the distribution of D1-D2-like receptors, their synergistic or opposite functional roles at the second messenger level, the effects of D1 receptor activation on the transmitter release and the modifications of D1 receptor pharmacology in dopamine-denervated striata. 4. A different perspective will also be discussed: the involvement of D1 receptors in long-term changes of synaptic efficacy in the striatum as a possible correlate of motor learning.

Animals↗

Activation of metabotropic glutamate receptors increase the frequency of spontaneous GABAergic currents through protein kinase A in neonatal rat hippocampal neurons.

1. The tight-seal whole cell recording technique was used to study the effects of the metabotropic glutamate receptor (mGluR) agonist, trans-1-aminocyclopentane-1,3-dicarboxylic acid (t-ACPD) on spontaneous gamma-aminobutyric acid (GABA)-mediated synaptic currents in neonatal rat CA1 hippocampal neurons in slices obtained from postnatal (P) days P6-P12. 2. Bath application of t-ACPD (3-30 microM), in the presence of kynurenic acid, induced a concentration-dependent increase in frequency but not in amplitude of spontaneous GABAergic currents. The mean frequency ratio (t-ACPD 10 microM over control) was 2.6 +/- 1 (mean +/- SD), whereas the mean amplitude ratio was 1.1 +/- 0.3. 3. The effect of t-ACPD was partially antagonized by the mGluR antagonist (RS)-alpha-methyl-4-carboxyphenylglycine (MCPG, 1 mM). 4. t-ACPD (10-30 microM) did not modify the frequency of miniature GABAergic synaptic currents recorded in tetrodotoxin (the mean frequency ratio of t-ACPD over control was 0.7 +/- 0.3). 5. Forskolin (30 microM), but not its analogue 1,9 dideoxyforskolin (30 microM), mimicked the effect of t-ACPD. Similar effects were obtained with 3-isobutyl-1-methylxanthine (IBMX, 200 microM). 6. The potentiating effect of t-ACPD on spontaneous GABAergic currents was prevented by Rp-cAMPS (30 microM), a specific antagonist of protein kinase A. This suggests that mGluRs localized at the soma-dendritic level of GABAergic interneurons and positively coupled to cyclic AMP may modulate GABA release during a critical period of postnatal development.

Animals↗

The modulation of dopamine receptors in rat striatum.

In the last decades, the contribution given by basic electrophysiology to the understanding of the nigrostriatal pathway in mammals has been rather important. The main results obtained by our group will be revised in this short review. The most common responses produced by dopamine (DA) on the principal striatal cells (the medium spiny neurons) are the modulation of the corticostriatal synaptic transmission and the decrease of voltage-dependent inward conductances. After blockade of DA transmission, both spontaneous and cortically driven glutamatergic postsynaptic potentials were inhibited by the selective activation of DA D2 receptors. In naive animals, the DA-mediated inhibition of postsynaptic firing activity was mediated by D1 receptor activation. Nevertheless, the two main subclasses of DA receptors seemed to cooperate in the formation of the long-term depression (LTD) of excitatory synaptic transmission in the striatum. The excitotoxic hypothesis of neurodegeneration has further stimulated our interest towards the study of the interactions between DA and other neurotransmitters into the basal ganglia.

Animals↗

Developmental changes in spontaneous GABAA-mediated synaptic events in rat hippocampal CA3 neurons.

Ongoing spontaneous postsynaptic potentials (SPSPs) were intracellularly recorded at 34-36 degrees C from hippocampal CA3 neurons in slices obtained from postnatal days (P) 0-6 and 7-31. SPSPs occurred randomly, and their frequency distribution was fitted by a single exponential function. They were little affected by kynurenic acid, but were reversibly blocked by bicuculline, implying that they were mediated by GABAA receptors. The mean amplitude was 4.53 +/- 0.89 mV in control conditions and 4.07 +/- 0.79 mV in kynurenic acid. In kynurenic acid (with CsCl-filled microelectrodes), SPSPs reversed polarity at 2.4 +/- 2 mV. When tetrodotoxin (1 microM) was added to kynurenic acid solution, GABAA-mediated miniature postsynaptic potentials (MPSPs) were recorded. Under these conditions large events disappeared. The mean amplitude of MPSPs was 2.51 +/- 0.43 mV. The mean frequency decreased from 2.96 +/- 1.04 Hz in kynurenic acid to 0.4 +/- 0.15 Hz in kynurenic acid plus tetrodotoxin. In contrast with P0-P6, at P7-P31 SPSPs were significantly affected by kynurenic acid. The mean amplitude of SPSPs shifted from 4.71 +/- 0.82 mV in control conditions to 3.79 +/- 0.76 mV in kynurenic acid. At this developmental stage, the reversal potential of GABAA-mediated SPSPs shifted towards more negative values (-23.7 +/- 1.3 mV). Addition of tetrodotoxin to kynurenic acid solution abolished larger events and revealed GABAergic MPSPs. The mean amplitude of MPSPs was 2.72 +/- 0.5 mV, a value very close to that observed at P0-P6. Synaptic currents were recorded at 22-24 degrees C from voltage-clamped CA3 pyramidal neurons (at P6) using the tight-seal whole-cell recording technique.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

Responses of rat mesencephalic dopaminergic neurons to a prolonged period of oxygen deprivation.

We employed intracellular electrophysiological techniques to examine the effects of a prolonged anoxia (more than 7 min superfusion with artificial cerebrospinal fluid saturated with 95% N2-5% O2) on dopaminergic neurons of the rat ventral mesencephalon maintained in vitro. A prolonged anoxia caused an inhibition of the spontaneous firing and a sustained (mean 16 min) and slowing declining hyperpolarization of the membrane in 30 dopaminergic cells. This was associated with a decrease of the apparent input resistance at 5, 10, 15 and 20 min of O2 deprivation by 38% (n = 18), 42% (n = 8), 48% (n = 18) and 54% (n = 8) of control, respectively. The continuation of anoxia, 1-4 min after the hyperpolarizing period, induced an irreversible depolarization (n = 8). More than 50% of the cells (17 of 30) fully recovered their electrophysiological properties after 15 min of O2 deprivation. Since the intracellular diffusion of cesium (a potassium channel blocker) was able to block the hyperpolarization and to reveal a depolarization caused by anoxia, we tested whether the blockade of the hyperpolarization modified the resistance of the cells to O2 deprivation. We observed that the cells loaded with cesium were depolarized and damaged in a period of O2 deprivation less than 10 min. The apparent input resistance of these neurons was irreversibly reduced by 36% of the control at 5 min of anoxia (n = 6). Furthermore, in order to ascertain whether an impairment of the sodium/potassium pump due to energy failure is involved in the anoxia-induced depolarization, we blocked the Na+/K+ ATPase pump with the inhibitor ouabain.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effects of dihydropyridine calcium antagonists on rat midbrain dopaminergic neurones.

1. The effects of the dihydropyridine calcium channel antagonists, nifedepine and nimodipine (300 nM-30 microM) were tested in vitro on intracellularly recorded dopaminergic neurones in the rat ventral mesencephalon. 2. Bath applied nifedipine and nimodipine inhibited in a concentration-dependent manner the spontaneous firing discharge of the action potentials, whereas, the dihydropyridine calcium channel agonist, Bay K 8644 increased the firing rate. 3. Pacemaker oscillations and bursts of action potentials were produced by loading the cells with caesium. Nifedipine and nimodipine reduced the rate and the duration of the caesium-induced membrane oscillations and decreased the number of action potentials in a burst. During the blockade of potassium currents the dopaminergic neurones often developed a prolonged (100-800 ms) afterdepolarization that was also inhibited by dihydropyridines. 4. The spontaneous discharge of calcium spikes was also inhibited by both dihydropyridine calcium antagonists. The apparent input resistance and the level of membrane potential were not affected by the dihydropyridine calcium antagonists. 5. If the action potential duration was less than 150 ms the shape of the spike was not clearly influenced by both calcium antagonists. However, when the duration of the action potential was longer than 150-200 ms due to the intracellular injection of caesium ions plus the extracellular application of tetraethylammonium (10-50 mM), both nifedipine and nimodipine reversibly shortened the plateau potential. 6. It is suggested that nifedipine and nimodipine depress the rhythmic and bursting activity of the dopaminergic cells and shorten the calcium action potential by blocking dihydropyridine-sensitive high-threshold calcium currents.

Action Potentials↗

Effects of anoxia on rat midbrain dopamine neurons.

1. Dopamine-containing neurons of the rat midbrain were recorded intracellularly in vitro. Anoxia (2-5 min) caused reversible membrane hyperpolarization (4-25 mV), which blocked spontaneous firing of action potentials. Under voltage clamp, anoxia produced an outward current (100-1,000 pA) associated with an increase in the apparent input conductance. 2. The mean reversal potential of the anoxia-induced response at 2.5 and 12.5 mM [K+] was -86 and -66 mV, respectively. 3. The effect of anoxia was not blocked by tetrodotoxin (TTX), saclofen, (-)sulpiride, or strychnine. Superfusate containing low calcium (0.5 mM CaCl2 and 10 mM MgCl2 or 0.5-1 mM CaCl2 and 1 mM CoCl2) or low sodium (25-40% of control) reduced the anoxia-induced outward current. 4. Extracellular barium (0.1-1 mM) blocked the anoxia-induced hyperpolarization/outward current. Other K+ channel blockers (tetraethylammonium, apamin, quinine, and glibenclamide) failed to reduce anoxia-induced current. 5. When the dopamine-containing neurons were loaded with cesium (1-2 mM), anoxia caused a reversible membrane depolarization and a block of the firing activity. This depolarization was voltage dependent; it was decreased or blocked by the hyperpolarization of the membrane. 6. Perfusion of the cells with 0.5-1 microM TTX did not affect the membrane depolarization/inward current caused by anoxia. These were also present when the cells were treated with the excitatory amino acid receptor antagonists D,L-2-amino-5-phosphonovalerate (APV) (30 microM) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) (10 microM). 7. The exposure of the neurons with low-sodium, low-calcium solutions reversibly reduced the depolarizing/inward effects of anoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

Neurotensin induces an inward current in rat mesencephalic dopaminergic neurons.

Neurotensin (0.3-3 microM) depolarized the membrane and increased the firing discharge of dopaminergic cells in slices of the rat mesencephalon. Under voltage-clamp, at holding potentials from -50 to -60 mV (near the resting membrane potential), neurotensin produced a sustained inward shift in the holding current. This inward current was reduced with the hyperpolarization of the membrane to -125 mV. It was resistant to tetrodotoxin, but it was diminished following the perfusion with low sodium (choline chloride substitution) solution. It persisted in low calcium (0-0.5 mM). Changes in the intracellular concentration of chloride did not affect neurotensin-induced current. The neurotensin-induced inward current did not reverse at hyperpolarized potentials in 10.5 mM extracellular K+. It was also seen in the presence of the potassium channel blockers tetraethylammonium (10-20 mM), barium (1 mM), apamine (1 microM) and 4-aminopyridine (1-1.5 mM). Also the extracellular application of cesium (1-5 mM) had no effect on the cellular responsiveness to neurotensin. The action of neurotensin appears to be mediated, at least partially, by a TTX-insensitive but voltage-dependent inward current carried by sodium. The non-dopaminergic cells of the substantia nigra and ventral tegmental area were not affected by neurotensin.

Animals↗

Activation of metabotropic glutamate receptors induces an inward current in rat dopamine mesencephalic neurons.

To investigate the electrophysiological effects of the stimulation of the metabotropic excitatory amino acid receptors, we applied trans-1-amino-cyclopentane-1,3-dicarboxylate, an agonist of this type of receptors, on presumed rat dopamine cells intracellularly recorded in vitro. Trans-1-amino-cyclopentane-1,3-dicarboxylate (3-30 microM, t-ACPD) caused a sustained increase of the spontaneous firing rate and a depolarization. When the membrane potential was held at about the resting level (-50, -60 mV), by the single-electrode voltage-clamp technique, t-ACPD induced an inward current. In 57% of the tested cells the inward current was associated with a decrease of the apparent input conductance. In the remaining cells no obvious changes in membrane conductance were observed. The active form of t-ACPD, (1S,3R)-1-amino-cyclopentane-1,3-dicarboxylate [3-50 microM, (1S,3R)-ACPD] also produced a reversible inward current on the dopaminergic cells and this was antagonized by (S)-4-carboxy-3-hydroxyphenylglycine (300 microM), a selective antagonist of the (1S,3R)-ACPD-induced depolarization on central neurons. The (1S,3R)-ACPD-induced inward current was not antagonized by L-2-amino-3-phosphonopropionic acid (100 microM), an antagonist of the t-ACPD-induced activation of inositide synthesis. 6-cyano-7-nitroquinoxaline-2,3-dione (10 microM), an alfa-amino-3-hydroxy-5- methyl-isoxazole propionic acid/kainate antagonist, DL-amino-5-phosphonopentanoic acid (30 microM), an N-methyl-D-aspartate antagonist, and scopolamine (10 microM), a muscarinic antagonist, did not significantly affect the actions of t-ACPD. A block of synaptic transmission obtained by applying tetrodotoxin failed to prevent the action of t-ACPD.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Cyano-7-nitroquinoxaline-2,3-dione↗

l-deprenyl test in migraine: neuroendocrinological aspects.

We evaluated the effect of l-deprenyl, a drug that increases the availability of endogenous dopamine, on the plasma levels of prolactin and growth hormone in 10 female patients with migraine and in 10 control subjects matched for age and menstrual phase. The patients showed a significant decrease in prolactin levels at 30, 60 and 120 min after the oral administration of 5 mg of l-deprenyl when compared with the values obtained in controls (p < 0.001). The effects of l-deprenyl on growth hormone plasma levels were not significantly different between patients and controls. These data suggest that l-deprenyl inhibits prolactin release in migraine patients, but not in control subjects. This differential sensitivity could be explained by dopamine receptor supersensitivity in migraine patients.

Adult↗

A voltage-clamp analysis of NMDA-induced responses on dopaminergic neurons of the rat substantia nigra zona compacta and ventral tegmental area.

The effects of NMDA-receptor activation on dopaminergic neurons of the rat substantia nigra zona compacta and ventral tegmental area were studied by using in vitro intracellular electrophysiological recordings (current and voltage-clamp). NMDA depolarized the membrane and increased the firing activity. A voltage-dependent inward current and a reduction of the apparent input conductance were observed in voltage-clamp experiments. Interestingly, the peak amplitude of the inward current occurred at approximately -60 mV. The NMDA-induced responses were reduced by the application of DL-2-amino-5-phosphonovaleric acid (APV). The NMDA-induced current was unaffected by potassium channel blockers, was present in low-sodium solutions or in solutions treated with TTX; but was reduced or blocked in low-calcium solutions containing cobalt. In addition, no reduction of the apparent input conductance was observed either in the solutions without magnesium or in those with low-sodium. Our data indicate that the activation of NMDA receptors produces a powerful excitatory stimulus on the dopaminergic neurons of the ventral mesencephalon and this may be primarily the result of a voltage-dependent influx of calcium ions. The degeneration of the dopaminergic cells after application of neurotoxins may be explained by their peculiar response to NMDA.

2-Amino-5-phosphonovalerate↗