Optic Tract Stimulation Research Articles

Changes in glutamate receptor function in synaptic input to the superficial superior colliculus (SSC) with aging and in retinal degeneration in the Royal College of Surgeons (RCS) rat

Ionotropic and metabotropic glutamate receptors mediate and modulate retinocollicular transmission. The Royal College of Surgeons (RCS) dystrophic strain of rats suffers from a progressive retinal degeneration with age and hence loss of visual function. We investigated whether this loss of function is accompanied by functional changes in a central target of retinal axons, the superficial superior colliculus (SSC). Field potential recordings were made in SSC slices from RCS rats aged either 4–7 weeks or 33–52 weeks. Blockade of GABAergic transmission revealed a field EPSP in response to optic tract stimulation which was sensitive to the NMDA antagonist AP5. In normal non-dystrophic rats the contribution of NMDA receptors to the fEPSP declined with age, whereas in dystrophic animals no such decline was seen. As mGluR8 may be located on terminals of retinal axons, we also assessed the function of this receptor. The mGluR8 agonist DCPG reduced fEPSPs in normal and dystrophic rats in both age groups to a similar extent, although the effect of DCPG declined with age. These findings indicate that the contribution of NMDA receptors to retinocollicular transmission declines with age in normal rats, but that such a decline is not seen in dystrophic rats which have severely reduced visual function. As NMDA receptors are associated with neural plasticity, it may be that this finding represents an increased residual potential for plasticity in dystrophic rats which may be functionally important.

Activation of Group II and Group III metabotropic glutamate receptors by endogenous ligand(s) and the modulation of synaptic transmission in the superficial superior colliculus

Previous work from this laboratory indicates that Group II/III metabotropic glutamate (mGlu) receptors modulate responses of SC neurones to visual stimuli in vivo. It is thought that tonic levels of glutamate may be sufficient to activate some mGlu receptors. We wished to investigate if these receptors are activated under ambient conditions in SC. Field excitatory postsynaptic potentials (fEPSPs) evoked by optic tract stimulation were recorded from 300 μm slices of the adult pigmented rat superior colliculus at 34 °C. The Group II receptor selective agonist LY354740 (100–300 nM) had no significant effect on the peak amplitude of the fEPSP, although it did enhance the late phase of the fEPSP. In order to test for activation of Group II receptors by endogenous ligand, the selective antagonists LY341495 (50 nM) or EGLU (200 μM) were applied: these either enhanced or reduced the fEPSP amplitude. In similar experiments carried out at 22 °C, no effect was seen. The fEPSP enhancements, but not the fEPSP reductions, could be occluded by GABA antagonists. Application of higher concentrations of LY341495 (300, 600 nM—known to also affect Group III receptors, particularly mGlu8), or co-application of 50 nM LY341495 and the Group III-selective antagonist CPPG (100 μM) produced enhancements of responses, or counteracted response reductions over those seen with 50 nM LY341495 alone. The predominant Group II receptor in SC is mGlu3. It is known that this can be located presynaptically on GABAergic and glutamatergic terminals, postsynaptically, and on glia. Our results indicate that such receptors are tonically activated by endogenous transmitter, have distinct effects, and influence retino-collicular transmission. Furthermore, there is a segregation of effects where receptors exert some of their effects via modulation of GABAergic circuitry.

Synaptic Activation of Metabotropic Glutamate Receptors Regulates Dendritic Outputs of Thalamic Interneurons

Information gating through the thalamus is dependent on the output of thalamic relay neurons. These relay neurons receive convergent innervation from a number of sources, including GABA-containing interneurons that provide feed-forward inhibition. These interneurons are unique in that they have two distinct outputs: axonal and dendritic. In addition to conventional axonal outputs, these interneurons have presynaptic dendrites that may provide localized inhibitory influences. Our study indicates that synaptic activation of metabotropic glutamate receptors (mGluRs) increases inhibitory activity in relay neurons by increasing output of presynaptic dendrites of interneurons. Optic tract stimulation increases inhibitory activity in thalamic relay neurons in a frequency- and intensity-dependent manner and is attenuated by mGluR antagonists. Our data suggest that synaptic activation of mGluRs selectively alters dendritic output but not axonal output of thalamic interneurons. This mechanism could serve an important role in focal, feed-forward information processing in addition to dynamic information processing in thalamocortical circuits.

Reduction of excitatory transmission in the retino-collicular pathway via selective activation of mGlu8 receptors by DCPG

We have previously shown that activation of Group III metabotropic glutamate (mGlu) receptors modulates synaptic transmission in the superior colliculus. We thus investigated the effect of the selective mGlu8 receptor agonist (S)-3,4-dicarboxyphenylglycine (DCPG) on excitatory synaptic transmission in the superficial superior colliculus (SC) using an in vitro slice preparation of the rat SC. Field EPSPs evoked by optic tract stimulation under conditions of GABA receptor blockade were reduced by DCPG by up to 67.8±5.46% (EC 50 1.25±0.56 μM), and this effect could be antagonised by LY341495 at a concentration (300nM) known to be effective at mGlu8 receptors but not at mGlu4 or mGlu7 receptors. The broad-spectrum (mGlu4/mGlu7/mGlu8) agonist L-2-amino-4- phosphonobutyric acid (L-AP4) produced similar reductions of synaptic transmission (maximal reduction 68.6±2.33%; EC 50 5.7±2.61 μM). These data are consistent with previous results which show that mGlu8 receptor activation can reduce synaptic transmission in the spinal cord, and indicate that similar mechanisms operate in other brain areas. Furthermore, this indicates that the mGlu8 receptor may have a role in the modulation of visual transmission in the superior colliculus.

Synaptic Mechanisms Regulating the Activation of a Ca2+-Mediated Plateau Potential in Developing Relay Cells of the LGN

Using intracellular recordings in an isolated (in vitro) rat brain stem preparation, we examined the synaptic responses of developing relay neurons in the dorsal lateral geniculate nucleus (LGN). In newborn rats, strong stimulation of the optic tract (OT) evoked excitatory postsynaptic potentials (EPSPs) that gave rise to a sustained (300-1,300 ms), slow-decaying (<0.01 mV/s), depolarization (25-40 mV). Riding atop this response was a train of spikes of variable amplitude. We refer to this synaptically evoked event as a plateau potential. Pharmacology experiments indicate the plateau potential was mediated by the activation of high-threshold L-type Ca(2+) channels. Synaptic activation of the plateau potential relied on N-methyl-D-aspartate (NMDA) receptor-mediated activity and the spatial and/or temporal summation of retinally evoked EPSPs. Inhibitory postsynaptic responses (IPSPs) did not prevent the expression of the plateau potential. However, GABA(A) receptor activity modulated the intensity of optic tract stimulation needed to evoke the plateau potential, while GABA(B) receptor activity affected its duration. Expression of the plateau potential was developmentally regulated, showing a much higher incidence at P1-2 (90%) than at P19-20 (1%). This was in part due to the fact that developing relay cells show a greater degree of spatial summation than their mature counterparts, receiving input from as many as 7-12 retinal ganglion cells. Early spontaneous retinal activity is also likely to trigger the plateau potential. Repetitive stimulation of optic tract in a manner that approximated the high-frequency discharge of retinal ganglion cells led to a massive temporal summation of EPSPs and the activation of a sustained depolarization (>1 min) that was blocked by L-type Ca(2+) channel antagonists. These age-related changes in Ca(2+) signaling may contribute to the activity-dependent refinement of retinogeniculate connections.

AMPA receptor properties at the synapse between retinal afferents and thalamocortical cells in the dorsal lateral geniculate nucleus of the rat

The thalamocortical (TC) cells in dorsal lateral geniculate nucleus transfer signals from retinal afferents to the primary visual cortex. The excitatory retinal input to the TC cells is mediated by ionotropic receptors of the N-methyl- d-aspartate (NMDA) and non-NMDA type. In the present study the excitatory postsynaptic current (EPSC) mediated by non-NMDA receptors in this synapse was characterised by means of voltage-clamp recordings from TC neurons in rat thalamic slices. The specific alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor antagonist GYKI-53655 fully blocked the non-NMDA meditated EPSC, evoked by optic tract stimulation. The EPSC peak amplitudes were linearly related to the command voltage, suggesting that the receptor complex includes the GluR2 subunit. The EPSC amplitude and decay time increased during application of the desensitisation blocker, cyclothiazide, showing that the EPSC was partly controlled by fast desensitisation.

Three GABA Receptor-Mediated Postsynaptic Potentials in Interneurons in the Rat Lateral Geniculate Nucleus

Inhibition is crucial for the thalamus to relay sensory information from the periphery to the cortex and to participate in thalamocortical oscillations. However, the properties of inhibitory synaptic events in interneurons are poorly defined because in part of the technical difficulty of obtaining stable recording from these small cells. With the whole-cell recording technique, we obtained stable recordings from local interneurons in the lateral geniculate nucleus and studied their inhibitory synaptic properties. We found that interneurons expressed three different types of GABA receptors: bicuculline-sensitive GABA(A) receptors, bicuculline-insensitive GABA(A) receptors, and GABA(B) receptors. The reversal potentials of GABA responses were estimated by polarizing the membrane potential. The GABA(A) receptor-mediated responses had a reversal potential of approximately -82 mV, consistent with mediation via Cl(-) channels. The reversal potential for the GABA(B) response was -97 mV, consistent with it being a K(+) conductance. The roles of these GABA receptors in postsynaptic responses were also examined in interneurons. Optic tract stimulation evoked a disynaptic IPSP that was mediated by all three types of GABA receptors and depended on activation of geniculate interneurons. Stimulation of the thalamic reticular nucleus evoked an IPSP, which appeared to be mediated exclusively by bicuculline-sensitive GABA(A) receptors and depended on the activation of reticular cells. The results indicate that geniculate interneurons form a complex neuronal circuitry with thalamocortical and reticular cells via feed-forward and feedback circuits, suggesting that they play a more important role in thalamic function than thought previously.

Retinal input induces three firing patterns in neurons of the superficial superior colliculus of neonatal rats.

By using an in vitro isolated brain stem preparation, we recorded extracellular responses to electrical stimulation of the optic tract (OT) from 71 neurons in the superficial superior colliculus (SC) of neonatal rats (P1-13). At postnatal day 1 (P1), all tested neurons (n = 10) already received excitatory input from the retina. Sixty-nine (97%) superficial SC neurons of neonatal rats showed three response patterns to OT stimulation, which depended on stimulus intensity. A weak stimulus evoked only one spike that was caused by activation of non-N-methyl-D-aspartate (NMDA) glutamate receptors. A moderate stimulus elicited a short train (<250 ms) of spikes, which was induced by activation of both NMDA and non-NMDA receptors. A strong stimulus gave rise to a long train (>300 ms) of spikes, which was associated with additional activation of L-type high-threshold calcium channels. The long train firing pattern could also be induced either by temporal summation of retinal inputs or by blocking gamma-aminobutyric acid-A receptors. Because retinal ganglion cells show synchronous bursting activity before eye opening at P14, the retinotectal inputs appear to be sufficient to activate L-type calcium channels in the absence of pattern vision. Therefore activation of L-type calcium channels is likely to be an important source for calcium influx into SC neurons in neonatal rats.

Electrophysiological and neurochemical study of the rat geniculo-cortical pathway. Evidence for glutamatergic neurotransmission.

The projection from the dorsal lateral geniculate nucleus to the primary visual cortex of the rat was studied electrophysiologically. Electrical stimulation of the dorsal lateral geniculate nucleus and the optic tract produced three types of responses on neurons of area 17: excitation followed by inhibition, excitation and inhibition. These results extend and confirm, in adult rats, previous studies done in rat geniculate-visual cortex cocultures preparations in vitro. The role of glutamate in the neurotransmission of the rat geniculo-cortical pathway was also investigated. In a first set of experiments, the effects of kynurenate, an antagonist of glutamate receptors, on visual cortex neurons with a monosynaptic excitatory response to dorsal lateral geniculate nucleus stimulation were studied. Microiontophoresis of kynurenate in area 17 neurons selectively suppressed the excitatory response to dorsal lateral geniculate nucleus and optic tract stimulation. In a second set of experiments, the effects of electrical stimulation of the dorsal lateral geniculate nucleus and the optic tract on the release of amino acids in the rat visual cortex in vivo were studied. Using the push-pull method, we perfused a discrete region of the visual cortex with artificial cerebrospinal fluid (CSF), and the amino acid content of the perfusates was analysed by high performance liquid chromatography (HPLC). Stimulation of either the dorsal lateral geniculate nucleus or the optic tract significantly increased glutamate release in area 17. The rest of the amino acids studied did not show significant changes. The results provide evidence for the participation of glutamate in the neurotransmission of the geniculo-cortical pathway in the rat.

Physiological properties of neurons in the optic layer of the rat's superior colliculus.

We made intracellular recordings from 74 neurons in the optic layer of the rat superior colliculus (SC). Resting membrane potentials were -62.3 +/- 6.2 (SD) mV, and input resistances were 37.9 +/- 10.1 MOmega. Optic layer neurons had large sodium spikes (74.2 +/- 12.3 mV) with an overshoot of 12 mV and a half-amplitude duration of 0.75 +/- 0.2 ms. Each sodium spike was followed by two afterhyperpolarizations (AHPs), one of short duration and one of longer duration, which were mediated by tetraethylammonium (TEA)-sensitive (IC) or apamin-sensitive (IAHP) calcium-activated potassium currents, respectively. Sodium spikes were also followed by an afterdepolarization (ADP), which was only revealed when the AHPs were blocked by TEA or apamin. In response to hyperpolarizing current pulses, optic layer neurons showed an inward rectification mediated by H channels. At the break of the current pulse, there was a rebound low-threshold spike (LTS) with a short duration of <25 ms. The LTS usually induced two sodium spikes (doublet). Most optic layer neurons (84%) behaved as intrinsically bursting cells. They responded to suprathreshold depolarization with an initial burst (or doublet) followed by a train of regular single spikes. The remaining 16% of cells acted as chattering cells with high-frequency gamma (20-80 Hz) rhythmic burst firing within a narrow range of depolarized potentials. The interburst frequency was voltage dependent and also time dependent, i.e., showed frequency adaptation. Unmasking the ADP with either TEA or apamin converted all of the tested intrinsically bursting cells into chattering cells, indicating that the ADP played a crucial role in the generation of rhythmic burst firing. Optic layer neurons receive direct retinal excitation mediated by both N-methyl--aspartate (NMDA) and non-NMDA receptors. Optic tract (OT) stimulation also led to gamma-aminobutyric acid-A (GABAA) receptor-mediated inhibition, the main effect of which was to curtail the excitatory response to retinal inputs by shunting the excitatory postsynaptic current. Intracellular staining with biocytin showed that the optic layer neurons that we recorded from were mostly either wide-field vertical neurons or other cells with predominately superficially projecting dendrites. These cells were similar to calbindin immunoreactive cells seen in the optic layer. The characteristics of these optic layer neurons, such as prominent AHPs, strong shunting effect of inhibition, and short-lasting LTS, suggest that they respond transiently to retinal inputs. This is consistent with a function for these cells as the first relay station in the extrageniculate visual pathway.

Endogenous adenosine facilitates neurotransmission via A 2A adenosine receptors in the rat superior colliculus in vivo

The concentration of endogenous adenosine in the cerebrospinal fluid increased 2–3-fold of the original level in the area of rat superior colliculus after the intraperitoneal administration of an adenosine deaminase inhibitor, EHNA (erythro-9-(2-hydroxy-3-nonyl)adenosine, 10 mg/kg). Potentials evoked in the superior colliculus by optic tract stimulation were also facilitated by 120–160% of their initial amplitudes. A selective A 1 adenosine receptor antagonist, DPCPX (8-cyclopentyl-1,3-dipropylxanthine), failed to reduce such EHNA-induced facilitation. However, a selective A 2A adenosine receptor antagonist, KF17837 (8(3,4-dimethoxystyryl)-1,3-dipropyl-7-methylxanthine) completely eliminated the facilitatory effects of EHNA. Northern blot analysis demonstrated abundant expression of A 1 adenosine receptor mRNA in the superior colliculus. RT-PCR analysis was able to detect the concomitant expression of A 2A adenosine receptor mRNA, but at levels lower than one-tenth of the striatal expression. In the superior colliculus, A 2A adenosine receptors function predominantly on the facilitatory effects of adenosine, irrespective of the ubiquitous expression of A 1 adenosine receptors.

The modulatory cholinergic system in goldfish tectum may be necessary for retinotopic sharpening.

The cholinergic circuit within the tectum and the cholinergic input from the nucleus isthmi mediate a presynaptic augmentation of retinotectal transmitter release via nicotinic receptors. In this study, the cholinergic systems were either eliminated using the cholinergic neurotoxin AF64A or blocked using nicotinic antagonists to test for effects on the activity-driven sharpening of the regenerating retinotectal projection. The effectiveness of the AF64A was verified by recording field potentials elicited by optic tract stimulation and by immunohistochemical staining for choline acetyltransferase (ChAT). At 1 week after intracranial (IC) injection of AF64A (12 to 144 nmoles) into the fluid above the tectum, field potentials showed a selective dose-dependent decrement of the cholinergic polysynaptic component with no effect on the amplitude of the glutamatergic monosynaptic component. The decrement was only partially recovered in recordings at 2 and 6 weeks. In normal fish, the ChAT antibody stains a population of periventricular neurons, their apical dendrites, and a dense plexus within the optic terminal lamina that consists of their local axons and fine dendrites and of input fibers from the nucleus isthmi. One week after IC AF64A injection (48-72 nmoles), most immunostaining in superficial tectum was lost but most neuronal somas in the deep tectum could still be seen, and staining in the tegmentum below the tectum was completely intact. At 2 weeks and later, the staining of neuronal somata largely recovered, but staining of the superficial plexus did not. AF64A treatment at 18 days after nerve crush, when regenerating retinal fibers are beginning to form synapses, prevented retinotopic sharpening of the projection. Recordings showed a rough retinotopic map on the tectum but the multiunit receptive fields (MURFs) at each tectal point averaged 34 deg vs. 11 deg in vehicle-injected control regenerates. AF64A treatment before nerve crush also blocked sharpening, ruling out a direct effect on retinal growth cones or retinal fibers, as AF64A rapidly decomposes, whereas its effect on the cholinergic fibers is long-lasting. IC injection or minipump infusion of the nicotine antagonists alpha-bungarotoxin (alpha BTX), neuronal bungarotoxin (nBTX), and pancuronium during regeneration also prevented sharpening (MURFs averaging 29.4 deg, 33.0 deg, and 31.4 deg, respectively). Control Ringer's solution infusions or injections over the same period (19-37 days postcrush) had no effect on regenerated MURF size (11.7 deg). The results show that the cholinergic innervation, which modulates transmitter release, is required for activity-driven retinotopic sharpening, thought to be triggered by NMDA receptor activation.

Excitatory and inhibitory transmission from the optic tectum to nucleus isthmi and its vicinity in amphibians.

Intracellular recordings were made from nucleus isthmi (NI) and its vicinity in toads (Bufo bufo gargarizans) in response to electrical stimulation of the bilateral optic tract. The results suggest that NI mainly receives its excitatory input from the ipsilateral tectum and its inhibitory input from the contralateral tectum. Tegmental cells in a region medioventral to NI were usually characterized by strong spontaneous activity and an excitatory-inhibitory sequence of postsynaptic potentials in response to stimulation of either side of the bilateral optic tract. Sixty of the recorded cells were stained with Lucifer yellow to show their morphological features and anatomical positions within NI and its vicinity.

Enhanced activation of NMDA receptor responses at the immature retinogeniculate synapse

The maturation of retinogeniculate excitatory transmission and intrathalamic inhibition was studied in slices of the dorsal LGN obtained from ferrets during the first 2 postnatal months. Response to optic tract stimulation at neonatal ages consisted of slow EPSPs lasting several hundred milliseconds. Application of the NMDA receptor antagonist D-(-)-2-amino-5-phosphonovaleric acid (D-APV) during the first 2 postnatal weeks resulted in EPSPs that were reduced in peak amplitude and dramatically curtailed in duration, indicating that NMDA receptors participate strongly in retinogeniculate transmission at the immature synapse. Gradually, EPSPs became shorter in duration such that after the second postnatal week, the retinogeniculate EPSPs were only a few milliseconds in duration. At this late stage of development responses were remarkably less affected by application of D-APV. These changes in contribution of NMDA receptors to retinogeniculate transmission were found to be due to the development of strong IPSPs, the result of gradual maturation of activation of GABAergic inhibition. Indeed, application of bicuculline methiodide to block GABAA receptor-mediated IPSPs strongly enhanced the NMDA component of the EPSPs in more mature cells. The voltage dependence and kinetics of NMDA-induced excitatory postsynaptic currents (NMDA EPSCs) were characterized by voltage-clamp recordings after blocking AMPA/kainate receptors with 6-cyano-7-nitroquinoxaline-2,3-dione and GABAA receptors wit' bicuculline methiodide. The voltage dependence of the NMDA EPSCs remained unaltered with age. During the first postnatal month the kinetic properties of the NMDA EPSCs also remained unaltered, but a reduction in EPSC duration was observed within the following weeks, well after the critical period of anatomical reorganization.(ABSTRACT TRUNCATED AT 250 WORDS)

Membrane and synaptic properties of developing lateral geniculate nucleus neurons during retinogeniculate axon segregation.

During the first postnatal month in the ferret (Mustela putorius furo), the projections from the retina to the lateral geniculate nucleus (LGN) become segregated into eye-specific layers and ON and OFF sublayers, a process that is thought to depend in part on neuronal activity. Remarkably, virtually nothing is known about the physiological features of LGN neurons during this period. We have recorded intracellularly from 46 A-layer neurons in slices of the ferret LGN between the ages of postnatal days 7 and 33. The passive membrane properties and current-voltage relationships of the developing neurons were similar in many, though not all, respects to those of adult LGN neurons. Action potentials in younger animals were smaller in amplitude and longer in duration than in older animals, but cells at all ages were capable of producing spike trains whose latency and spike number varied with stimulus intensity. In addition, cells at all ages responded with low-threshold potentials upon release from hyperpolarization. Slightly more than half of the LGN neurons responded to optic tract stimulation with excitatory postsynaptic potentials (EPSPs), inhibitory postsynaptic potentials (IPSPs), or EPSP-IPSP pairs, beginning with the youngest ages. Thus, as early as the second postnatal week, and much before the onset of pattern vision, LGN neurons have many of the membrane and synaptic properties of adult thalamic neurons. These data are consistent with LGN cells playing a significant role in activity-dependent reshaping of the retinogeniculate pathway.

Retinogeniculate EPSPs recorded intracellularly in the ferret lateral geniculate nucleus in vitro: role of NMDA receptors.

We used an in vitro preparation of the ferret lateral geniculate nucleus (LGN) to examine the role of the NMDA class of excitatory amino acid (EAA) receptors in retinogeniculate transmission. Intracellular recordings revealed that blockade of NMDA receptors both shortened the time course and reduced the amplitude of fast and slow components of excitatory postsynaptic potentials (EPSPs) evoked by optic tract stimulation. The amplitude and width of the EPSPs mediated by NMDA receptors increased as membrane potential was depolarized towards spike threshold. Individual LGN cells were influenced to varying extents by blockade of NMDA receptors; NMDA and non-NMDA receptor blockade together attenuated severely the entire retinogeniculate EPSP. The dependence of all components of retinogeniculate EPSPs (and action potentials) on NMDA receptor activation supports the hypothesis that the NMDA receptor participates in fast (less than 10 ms) synaptic events underlying conventional retinogeniculate transmission. The voltage dependence of the NMDA receptor-gated conductance suggests strongly that the transmission of retinal information through the LGN is subject to modulation by extraretinal inputs that affect the membrane potential of LGN neurons.

Visual input to commissural neurons of the cat's superior colliculus

Cells projecting into the commissure of the cat's superior colliculus were identified during extracellular recording by antidromic activation. Electrical stimulation of the ipsilateral optic tract evoked action potentials in the majority of commissural neurons. Response latencies of 1.4 +/- .5 ms (mean +/- S.D.) in a few cells indicated that some commissural neurons receive direct input from the axons of retinal Y-cells. Most commissural cells responded 5.9 +/- 1.9 ms (mean +/- S.D.) following optic tract shock, implying that the responsible pathway was composed of more slowly conducting axons or did not proceed directly to the colliculus. Results of previous studies of retinal inputs to cells in the deep tectal layers suggest that the later responses were mediated by an indirect Y pathway through the visual cortex.

Postsynaptic potentials and morphology of tectal cells responding to electrical stimulation of the bullfrog nucleus isthmi

Postsynaptic responses of tectal cells in the bullfrog (Rana catesbeiana) were intracellularly recorded following electrical stimulation of the optic tract and the nucleus isthmi, and fluorescent dye, Lucifer yellow, was injected into some of the impaled cells to show their morphologies. Two main response types were found: The first type was an EPSP followed by an IPSP, and the second type was single IPSP. The first type predominates in cells responding to the optic tract stimulation and the second type prevails in cells responding to the isthmic stimulation. Fifteen cells stained with Lucifer yellow were localized in layer 6 (11 cells), layer 7 (1 cell), and layer 8 (3 cells). They were mainly identified as pear-shaped cells, large ganglionic cells, and stellate cells. Three injections demonstrated "dye-coupling," which labeled up to six cells following one injection. Comparisons of postsynaptic potentials with cellular morphologies suggested that the nucleus isthmi could directly excite large ganglionic neurons in layer 6. Synaptic mechanisms for strong isthmic inhibition on the tectal neurons remain unknown.

Optic tract stimulation evokes GABA A but not GABA B IPSPs in the rat ventral lateral geniculate nucleus

The inhibitory postsynaptic potentials (IPSPs) evoked in neurons of the rat ventral lateral geniculate nucleus (vLGN) by electrical stimulation of the optic tract and the action of GABA and baclofen on the same cells were studied using intracellular recording techniques in an in vitro slice preparation. A short latency short duration IPSP always followed the monosynaptic excitatory postsynaptic potential (EPSP). This IPSP reversed in polarity at about -65mV and was reversibly blocked by bicuculline (50 μM) thus indicating that it represents a GABA A receptor-mediated IPSP. No long-lasting IPSP was evoked in vLGN cells by stimulation of the optic tract, while in the same slice, long-lasting GABA B IPSPs were routinely recorded in the dorsal lateral geniculate nucleus. GABA applied by ionophoresis evoked a hyperpolarization that had a reversal potential close to -70 mV and was antagonized by bicuculline. Baclofen hyperpolarized vLGN neurons and its action was reversibly blocked by the selective GABA B antagonist phaclofen (1 mM). In the presence of bicuculline GABA also produced a hyperpolarization that had properties similar to that evoked by baclofen. These results indicate that, although functional GABA A and GABA B receptors are present on vLGN neurons, stimulation of the optic tract evokes only GABA A but not GABA B mediated IPSPs. The lack of long-lasting GABA B IPSPs could explain the absence of long-lasting inhibition observed in vLGN neurons in vivo following stimulation of the optic tract.

Two types of thalamic reticular cells in relation to the two visual thalamocortical systems in the rat

We found in urethane-anesthetized rats that thalamic reticular (TR) cells responding to an electrical stimulus of the optic tract (OT) can be further subdivided into two types, viz. S- and L-type cells. S-type cells, which were selectively excited from area 17 of the visual cortex, were characterized by short latency responses (2.3–6.1 ms) to OT stimulation. TR cells activated antidromically from the dorsal lateral geniculate nucleus were all classified as S-type. Long OT latencies (5.2–15.3 ms) and selective excitation from area 18a were peculiar to L-type cells, which showed antidromic responses to the lateral posterior nucleus stimulation. Mapping studies documented that cells belonging to each type were segregated in the thalamic reticular nucleus; L-type cells were located in the most posterior part. It is suggested that S- and L-type are inhibitory interneurons modulating activity of geniculocortical and extrageniculocortical projection cells, respectively.