Intracellular study of rat globus pallidus neurons: membrane properties and responses to neostriatal, subthalamic and nigral stimulation.

Physiological properties of globus pallidus (GP) neurons were studied intracellularly in anesthetized rats. More than 70% of the neurons exhibited continuous repetitive firing of 2-40 Hz, while others exhibited periodic burst firing or no firing. The repetitively firing neurons exhibited the following properties: spike accommodation; spike frequency adaptation; continuous firing with a frequency of about 100 Hz generated by intracellular current injections; fast anomalous rectification; ramp-shaped depolarization upon injection of depolarizing current; and post-active hyperpolarization. The burst firing neurons evoked a large depolarization with multiple spikes in response to depolarizing current, and a similar response was observed after the termination of hyperpolarizing current. The few neurons which did not fire spontaneous spikes exhibited strong spike accommodation when they were stimulated by current injections. The continuously firing neurons were antidromically activated by stimulation of the neostriatum (Str) (23 of 68), the subthalamic nucleus (STh) (55 of 75), and the substantia nigra (SN) (25 of 46). The antidromic latencies of the 3 stimulus sites were very similar (about 1 ms). None of the burst firing neurons were antidromically activated. Three non-firing neurons evoked antidromic responses only after Str stimulation. Only repetitively firing neurons evoked postsynaptic responses following stimulation of the Str and the STh. Stimulation of the Str evoked initial small EPSPs with latencies of 2-4 ms and strong, short duration IPSPs with latencies of 2-12 ms. Stimulation of the STh evoked short latency EPSPs overlapped with IPSPs. Frequently, these responses induced by Str and STh stimulation were followed by other EPSPs lasting 50-100 ms. These results indicated: (1) that the GP contains at least 3 electrophysiologically different types of neurons; (2) that GP projections to the Str, the STh, and the SN are of short latency pathways; (3) that Str stimulation evokes short latency EPSPs followed by IPSPs and late EPSPs in GP neurons; and (4) that STh stimulation evokes short latency EPSPs overlapped with short latency IPSPs and late EPSPs in GP neurons.     

Postsynaptic potentials evoked in spiny neostriatal projection neurons by stimulation of ipsilateral and contralateral neocortex

Postsynaptic potentials were evoked in neostriatal neurons by stimulation of the ipsilateral and contralateral medial agranular frontal cortical field (AGm) in the rat. This cortical region is known to project bilaterally to the dorsal lateral head of the caudate-putamen of rats. Ipsilateral stimulation of AGm should excite all types of corticostriatal neurons projecting to neostriatal neurons in the corresponding area in neostriatum, while stimulation of the same cortical area on the side contralateral to the recording should evoke synaptic potentials from a more restricted subpopulation of crossed corticostriatal neurons. Neostriatal neuronal responses were recorded intracellularly and spiny projection neurons identified by intracellular staining with horseradish peroxidase. The initial EPSP response to contralateral stimulation was similar to that evoked from the ipsilateral side, except for the absence of a relatively small short latency component responsible for the earliest part of the response to ipsilateral cortical stimulation. Comparison with previous findings indicated that this earliest EPSP component was due to activation of fast-conducting descending cortical efferents with collateral projections exclusively to the ipsilateral neostriatum. Stimulation of contralateral neostriatum evoked responses identical to those obtained using stimulation of contralateral neocortex. Analyses of these responses indicated that both EPSPs arise from activation of the same population of fibers. Stimulation of the contralateral internal capsule just caudal to neostriatum was not effective in evoking the EPSP. Chronic hemidecortication did not change the shape of the EPSP evoked from the intact contralateral side, but reduced its amplitude by approximately one half. These observations indicate that contralaterally projecting corticostriatal neurons in the rat project bilaterally in neostriatum, have axonal branches to the contralateral cerebral cortex as well as neostriatum, and converge onto neostriatal neurons that also receive input from the corresponding cortical region on the ipsilateral side.     

Corticofugal influences on the reticulospinal neurons of gigantocellular nucleus in cats]

Stimulation of the motor cortex evoked excitatory and inhibitory PSP in reticulospinal neurons of the cat gigantocellular nucleus. EPSP were recorded in 94.3% of the investigated neurons and IPSP in 5.7%. Analysis of the presynaptic pathways showed that 77.4% of EPSPs appeared through monosynaptic and 22.6% through polysynaptic corticoreticular connections. According to latency, duration and rise time all monosynaptic EPSP were divided into two groups (fast and slow). Obviously, fast EPSPs are generated by fast corticobulbar fibres and slow ones by slow fibres. IPSP were recorded in neurons which were also inhibited by stimulation of the ventral funiculi of the spinal cord. It is suggested that motor cortical signals can be transmitted to the spinal cord through both mono- and polysynaptic connections of the fast and slow pyramidal neurons with reticulospinal neurons.     

Responses of the vibrissal projection zone of the cat somatosensory projection zone to afferent activation]

Responses of 375 neurons of SI cortex region in the vibrissae projection zone were recorded in unanesthetized cats: responses to electrical stimulation of infraorbital nerve and mechanical stimulation of vibrissae were studied. Nerve and vibrissae stimulation evoked complex synaptic potentials (short EPSPs followed by IPSPs) in most neurons primary IPSPs were found in other units. The corresponding changes of impulse activity could be recorded in many neurons extracellularly. Initial inhibition was evoked by vibrissae stimulation more frequently (in 45% units comparing to 16% when the nerve was stimulated). Difference of minimal EPSP and IPSP latencies during intraorbital nerve stimulation was 0.8 ms, difference of mean values--1.4 ms. Directional sensitivity of cortical neurons (to the changes in direction of vibrissae deflection) is demonstrated. Neurons located in the close proximity may possess different pattern of directional sensitivity. It is supposed that short latency neuronal inhibition in SI cortical zone is mainly afferent (not recurrent). Probable mechanisms of directional sensitivity of the studied neurons are discussed.     

Hippocampal inputs to identified neurons in an in vitro slice preparation of the rat nucleus accumbens: evidence for feed-forward inhibition.

The aim of the present study was to analyze responses of nucleus accumbens neurons to stimulation of the fornix. The recorded neurons were labeled with biocytin and identified as medium spiny neurons. A large majority of cells generated a depolarizing postsynaptic potential in response to stimulation of the fornix. Using intracellular current injection, this depolarizing response was dissociated into an EPSP reversing at -6 +/- 6 mV and an IPSP reversing at -71 +/- 4 mV. Both the EPSP and IPSP were abolished by 6-cyano-7-nitroquinoxaline-2,3-dione. In addition, the IPSP was blocked by bicuculline and picrotoxin. The onset latency of the EPSP was constant in spite of varying stimulus intensities. In contrast, the onset latency of the IPSP increased with decreasing stimulus intensity. Notably, the stimulus threshold for evoking IPSPs was generally lower than for EPSPs. At stimulus intensities well above threshold, the IPSP onset was only slightly delayed with respect to the EPSP onset. These results indicate that the EPSP can be characterized as a monosynaptic and glutamate-mediated synaptic response. The IPSP, however, appears to be mediated by a disynaptic feed-forward pathway involving both glutamate and GABAA receptors. Recurrent and lateral inhibitory interactions have previously been proposed to be predominant organizational principles in the caudate-putamen and nucleus accumbens. This study indicates that feed-forward inhibition is an additional principle governing the activities of striatal neural networks.     

Electrophysiology of rat thalamo-cortical relay neurons: an in vivo intracellular recordingf and labeling study

Membrane properties and responses to frontal cortical stimulation were studied on electrophysiologically and morphologically identified thalamo-cortical neurons in anesthetized rats. Those neurons generated membrane responses resembling the low-threshold Ca-spike, g_K(Ca) and I_A that have been previously demonstrated in in vitro studies of thalamic neurons. Stimulation of the frontal cortex evoked a sequence of responses; antidromic spike, initial depolarization, long duration hyperpolarization and a short period of depolarization. The initial depolarization was considered to be a monosynaptic excitatory postsynaptic potential (EPSP) which overlapped with an inhibitory postsynaptic potential (IPSP). Major constituents of the long duration hyperpolarization were considered to be short duration IPSPs and long duration disfacilitations of cortical inputs.     

A short duration GABAergic inhibition in identified neostriatal medium spiny neurons: in vitro slice study

Inhibition in the neostriatum was investigated in rat in vitro slice preparation using intracellular recording and labeling technique. The initial response recorded following local stimulation is a monosynaptically activated EPSP. In 17% of the neurons tested, IPSPs were observed following EPSPs evoked by local stimulation. In paired shock experiments reduction of test EPSP amplitude or action potentials occurred over interstimulus intervals (ISIs) of 3-38 msec. In some neurons, a pulse injection of depolarizing current was used to trigger an action potential which was in a paired shock, used to condition a test monosynaptically induced EPSP. Test EPSPs were shunted over ISIs less than 45 msec. Paired shock performed on the slices perfused with the medium containing GABA antagonists (e.g., bicuculline methiodide, picrotoxin, or penicillin-G) resulted invariably in potentiation of test EPSPs. Inhibition in the neostriatum in vitro is demonstrated as reduction in test amplitude in paired shock tests, by the presence of IPSPs and by the shunting of EPSPs conditioned by an action potential triggered by direct depolarization. Neurons exhibiting these forms of inhibition were intracellularly labelled with HRP and identified as medium spiny neurons. These results indicate that striatal GABAergic medium spiny neurons which are known to have an extensive axon collateral plexus play in a role in a short lasting inhibition observed in the striatum.     

Pallidal inputs to subthalamus: Intracellular analysis

Neuronal responses of the subthalamic nucleus (STH) to stimulation of the globus pallidus (GP) and the substantia nigra (SN) were studied by intracellular recording in the decorticated rat. (1) GP and SN stimulation evoked antidromic spikes in STH neurons with a mean latency of 1.2 ms and 1.1 ms, respectively. Based on the above latencies, the mean conduction velocity of the STH neurons projecting toward GP was estimated to be 2.5 m/s, and that toward SN was 1.4 m/s. Many STH neurons could be activated following stimulation of both GP and SN, indicating that single STH neurons project to two diversely distant areas. In spite of differences in conduction distance of GP and SN from STH, differences in the conduction velocities of bifurcating axons make it possible for a simultaneous arrival of impulses in the target areas to which these STH neurons project. (2) GP stimulation evoked short duration (5-24 ms) hyperpolarizing potentials which were usually followed by depolarizing potentials with durations of 10-20 ms. These potentials were tested by intracellular current applications and intracellular injections of chloride ions. The results indicated that the hyper- and depolarizing potentials were IPSPs and EPSPs respectively. These IPSPs were considered to be monosynaptic in nature since changes in the stimulus intensities of GP did not alter the latency of IPSPs. The mean latency of the IPSPs was 1.3 ms. Based on the above mean latency the mean conduction velocity of GP axons projecting to STH was estimated to be 3.8 m/s. (3) Analysis of electrical properties of STH neurons indicated that: (i) input resistance estimated by a current-voltage relationship ranged from 9 to 28 M omega; (ii) the membrane showed rectification in the hyperpolarizing direction; (iii) direct stimulation of neurons by depolarizing current pulses produced repetitive firings with frequencies up to 500 Hz. (4) Morphology of the recorded STH neurons was identified by intracellular labeling of neurons with horseradish peroxidase. Light microscopic analysis indicated that the recorded neurons were Golgi type I neurons with bifurcating axons projecting toward GP and SN.     

Convergence of projections from the rat hippocampal formation, medial geniculate and basal forebrain onto single amygdaloid neurons: an in vivo extra- and intracellular electrophysiological study.

We recorded extra- and intracellular responses from rat amygdaloid neurons in vivo after electrical stimulation of the hippocampal formation (dentate gyrus, hippocampal fields CA3 and CA4, entorhinal cortex, subicular complex); medial geniculate; and basal forebrain (diagonal band, ventral pallidum, olfactory tubercle, nucleus accumbens, bed nucleus of stria terminalis, lateral preoptic area, substantia innominata). Stimulation of hippocampal formation structures evoked IPSPs or EPSP-IPSP sequences in which the IPSP had a lower threshold than the EPSP. Recordings from candidate inhibitory neurons in the amygdala indicated that excitatory afferents from the hippocampal formation contact both amygdaloid inhibitory and principal neurons (feedforward inhibition), and that the inhibitory neurons have a lower threshold of activation. Medial geniculate stimulation also evoked EPSP-IPSP sequences. In marked contrast to these results, stimulation of basal forebrain structures evoked short latency IPSPs in amygdaloid neurons. This provides the first physiological evidence for direct inhibition of the amygdala by the basal forebrain. Basal forebrain stimulation also evoked EPSP-IPSP sequences in amygdaloid neurons. Individual amygdaloid neurons could show responses to stimulation of the hippocampal formation, basal forebrain, and medial geniculate, indicating that synaptic input from these areas converges onto single amygdaloid cells. The findings provide further information about the synaptic organization of afferents to the amygdala, and indicate that single amygdaloid neurons play a role in the synaptic integration of input from these diverse sources.     

Ascending and descending convergent inputs to neurons in the nucleus parabrachialis of the rat: an intracellular study

Responses of the nucleus parabrachialis neurons (PBN) to electrical stimulation of the lateral hypothalamus (HL), central nucleus of the amygdala (Ac), dorsolateral funicullus in the spinal cord (SC), mediocaudal nucleus tractus solitarius (NTS), and substantia nigra (SN) were investigated in anesthetized rats by intracellular recording technique. Convergent excitatory postsynaptic potentials (EPSPs) were evoked on 8 of 36 neurons tested by both HL and NTS stimulation. The EPSPs evoked by HL stimulation were characterized as monosynaptic in 4 neurons. The EPSPs evoked by SC stimulation were characterized as monosynaptic in 2 of 36 neurons, moreover, these neurons were also antidromically activated by HL stimulation. Stimulation of Ac evoked EPSPs on 10 of 36 cells tested; 8 demonstrated to be monosynaptic. In addition, IPSP evoked by SN stimulation and EPSP evoked by NTS stimulation converged on three neurons. The results indicate that ascending and descending inputs converge on lateral PBN neurons.     

Orientation selectivity of synaptic potentials in neurons of cat primary visual cortex

Neurons of the visual cortex of the cat were penetrated with intracellular electrodes and postsynaptic potentials evoked by visual stimuli recorded. By alternately polarizing the cell with steady current injected through the recording electrode, IPSPs and EPSPs could be recorded and analyzed independently. Hyperpolarizing current suppressed IPSPs and enhanced EPSPs by moving the membrane potential toward the IPSP equilibrium potential. Depolarizing the cell toward the EPSP equilibrium potential enhanced IPSP. The responses to electrical stimulation of the LGN, where EPSPs and IPSPs could be distinguished easily by virtue of their characteristic latencies and shapes, were used to set the current injection to the appropriate level to view the two types of synaptic potential. EPSPs were found to be well oriented in that maximal depolarizing responses could be evoked at only one stimulus orientation; rotating the stimulus orientation in either direction produced a fall in the EPSP response. IPSPs were also well tuned to orientation, and invariably the preferred orientations of EPSPs and IPSPs in any one cell were identical. In addition, no systematic difference in the width of tuning of the two types of potential was seen. This result has been obtained from penetrations of over 30 cortical cells, including those with simple and complex receptive fields. It is concluded that orientation of cortical receptive fields is neither created nor sharpened by inhibition between neurons with different orientation preference. The function of inhibition evoked simultaneously with excitation by optimally oriented stimuli has yet to be determined, though it is likely to be the mechanism underlying other cortical receptive field properties, such as direction selectivity and end-stopping.     

Excitatory and inhibitory transmission from dorsal root afferents to neonate rat motoneurons in vitro

Intracellular recordings were made from antidromically identified motoneurons in neonate (12-22 days) rat transverse spinal cord slices and the transmitters and receptors probably involved in initiating the excitatory (EPSP) and inhibitory (IPSP) postsynaptic potentials were investigated. Stimulation of dorsal roots elicited in motoneurons an EPSP, an IPSP, or an EPSP followed by an IPSP. EPSPs in 70% of motoneurons had a short latency (less than or equal to 1 ms) and in the remaining cells a latency longer than 1 ms. The IPSPs had a long latency (greater than or equal to 1 ms). Short- and long-latency EPSPs were enhanced by the acidic amino acid uptake inhibitor L-aspartic acid-beta-hydroxamate (AAH) and depressed by the non-selective glutamate receptor antagonists gamma-D-glutamylglycine (DGG) and kynurenic acid. Short-latency EPSPs were suppressed by the quisqualate/kainate (QA/KA) receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX) but not by the N-methyl-D-aspartate (NMDA) receptor antagonists D-(-)-2-amino-5-phosphonovaleric acid (APV) and ketamine. Long-latency EPSPs were reduced by DNQX as well as by APV and ketamine. Superfusion of the slices with a Mg-free solution increased the EPSPs and unmasked a late, APV-sensitive component. The IPSP was reduced by the glycine antagonist strychnine as well as by APV and ketamine but resistant to DNQX. The results indicate that stimulation of dorsal roots elicited in motoneurons a monosynaptic EPSP mediated by glutamate/aspartate acting predominantly on the QA/KA subtype of glutamate receptors; an NMDA component can be unveiled in Mg-free solution.(ABSTRACT TRUNCATED AT 250 WORDS)     

Intracellular responses of caudate neurons to temporally and spatially combined stimuli

Intracellular recordings of caudate neuronal responses evoked by temporally combined stimulations of cortex, thalamus, and substantia nigra were made in the cat. Excitatory postsynaptic potentials (EPSPs) which temporally coincided were additive. EPSPs which coincided with an inhibitory postsynaptic potential (IPSP) previously evoked from the same stimulus site were enhanced. The cortical stimulus was prepotent in the sense that EPSPs evoked from thalamic or nigral stimulation were inhibited by the cortical IPSP. The cortical EPSP was enhanced if it was evoked during a nigral or thalamic IPSP. These results are discussed in the context of recent reports concerning the fine structure of synaptic contacts of input fibers to the caudate nucleus.     

Response characteristics of subthalamic neurons to the stimulation of the sensorimotor cortex in the rat

Responses of the subthalamic nucleus (STH) neurons to the stimulation of the sensorimotor cortex (Cx) were recorded in intact rats and in those which received lesions in the pallidum, the neostriatum, the brainstem, or the corpus callosum. Most of the STH units (78%) exhibited two excitatory peaks which were interrupted by a brief period of inhibition. Some of units which were located in the peripheral part of the STH tended to lack the brief inhibitory component and exhibited a long period of excitation. These excitations were followed by a long-lasting inhibitory period. Intracellular recording indicated that these responses were EPSPs interrupted by a short IPSP and a long period of disfacilitation of Cx inputs. A quinolinic acid lesion of the neostriatum and a knife cut of the brainstem failed to alter these responses, while an ibotenic acid lesion of the globus pallidus abolished the short inhibition seen in the midst on the excitation. Stimulation of contralateral Cx also evoked excitatory responses in the STH. The responses were completely eliminated by a parasagittal knife cut of the rostral part of the corpus callosum.     

Inhibition of protein kinase activity enhances long-term potentiation of hippocampal IPSPs.

In this study on guinea pig hippocampal slices, protein kinase C (PKC) involvement in long-term potentiation (LTP) of GABAA and GABAB receptor-mediated fast and slow IPSPs, respectively, was examined. Stimulation of the stratum radiatum induced EPSPs followed by fast and slow IPSPs in the CA1 neurons. Tetanic stimulation of the stratum caused a marginal LTP of the fast IPSP but not of the slow IPSP. When K-252b, a potent inhibitor of PKC, was injected into CA1 neurons, LTP of fast and slow IPSPs was observed. These results indicate that PKC activation in CA1 neurons is involved in minimizing, rather than inducing, LTP of the IPSPs so that the EPSP is not distorted.     

Synaptic potentials of hypoglossal motoneurons and a common inhibitory interneuron in the trigemino-hypoglossal reflex

The responses of the hypoglossal motoneurons to stimulation of the inferior alveolar nerve (IAN) and the masseter nerve (MN) have been studied in cats anesthetized with sodium pentobarbital or decerebrated. On the basis of intracellulary recorded responses, hypoglossal motoneurons could be divided into 3 types. (1) DD type, in which a depolarizing-hyperpolarizing (EPSP-IPSP) potential was evoked by stimulation of IAN and MN. (2) DH type, in which a depolarizing-hyperpolarizing (EPSP-IPSP) potential was evoked by IAN stimulation and a hyperpolarizing potential (IPSP) was evoked by MN stimulation. (3) HH type, in which a hyperpolarizing potential (IPSP) was evoked by both stimuli.In the vicinity of the hypoglossal nucleus, intracellular and extracellular recordings were made from a group of neurons which could not be antidromically activated by stimulation of the hypoglossal nerve. These neurons fired in regular bursts of 3–18 spikes, with frequencies of up to 900/sec following stimulation of the ipsi-IAN, the contra-IAN, the ipsi-MN and the ipsilateral hypoglossal nerve. With a single shock to the ipsi-IAN, the mean latency of the peak of the initial spikes was 0.56 msec shorter than that of the onset of IPSPs of hypoglossal motoneurons. There was a correlation between the number of spikes of these neurons and the amplitude of IPSPs of the hypoglossal motoneuron evoked by varied stimulus intensities applied to the ipsi-IAN and the ipsi-MN. Electrophoretic injection of dye (fast green FCF) through the recording microelectrode revealed that all these neurons were located in the region ventral to the hypoglossal nucleus around the radix of the hypoglossal nerve. These results suggest that these perihypoglossal neurons are inhibitory interneurons which synapse on the hypoglossal motoneurons in the trigemino-hypoglossal reflex.     

Excitatory projection of the rat subicular complex to the cingulate cortex and synaptic integration with thalamic afferents

We studied the responses of rat cingulate cortex neurons to electrical stimulation of the subicular complex. Intracellular and 'quasi-intracellular' recordings from layer V posterior cingulate neurons showed that stimulation of the presubiculum or postsubiculum evoked EPSPs and action potentials. These were usually followed by shallow IPSPs averaging 122 ms in duration. Frequency potentiation of an EPSP was demonstrated in one case. Laminar analysis of field potentials provided evidence for a source of excitatory synaptic drive in layer II-III of the posterior cingulate cortex, where the subicular projections terminate, presumably on apical dendrites of layer V pyramids. Intracellular HRP injection of neurons showing EPSPs after subicular complex stimulation established that these responsive neurons were layer V pyramids. One cell with physiological properties characteristic of inhibitory interneurons was recorded in layer V. Stimulation of the thalamic nuclei lateralis and anterior ventralis also evoked EPSPs and action potentials in layer V cingulate neurons. In one cell it was possible to show that EPSPs evoked by presubicular stimulation and by nucleus anterior ventralis summed. These results indicate that subicular and thalamic afferents make excitatory synaptic contact onto dendrites of the same layer V cingulate neurons; that spatial summation can integrate the input from these two sources; and that inhibition from local interneurons limits the duration of this excitatory influence.     

Opposing effects of striatonigral feedback pathways on midbrain dopamine cell activity

The existence of a striatonigral GABAergic pathway has been well established both anatomically and biochemically. During intracellular recording from identified DA neurons in vivo, stimulation of the striatum (100 microA, 50 microseconds pulses) elicits an inhibitory postsynaptic potential (IPSP) and a rebound depolarization. The IPSP is a short latency (1.8-2.2 ms) conductance increase to chloride, since: the reversal potential is near the chloride reversal potential reported for other cells (-68 mV); intracellular chloride injection progressively reverses the IPSP into a depolarization with a similar time course; and the response of DA cells to systemic injection of the chloride channel blocker, picrotoxin, also exhibits a similar reversal potential. In contrast, during extracellular recording, stimulation of the striatum at low levels of intensity (e.g. 20 microA at 10 Hz) increases the firing rate of DA cells. Stimulation of the striatum will, in addition, elicit IPSPs in a subclass of substantia nigra zona reticulata neurons at the same latency as the IPSPs triggered in DA cells. These IPSPs also reverse with intracellular chloride injection. However, their amplitude is larger and their duration longer than observed in DA cells, and there is no depolarizing rebound. The late component of the IPSP in the zona reticulata neurons corresponds temporally to the rebound depolarization seen in DA cells in response to striatal stimulation. In addition, when recorded extracellularly, striatal stimulation will inhibit the firing of this class of zona reticulata interneurons at the same stimulation parameters that will excite DA cells. These data suggest that striatal cells may send branched fast-conducting GABAergic projections to zona reticulata cells and DA cells. Furthermore, low levels of striatal stimulation can excite DA cells by preferentially inhibiting interneurons in the zona reticulata which are more sensitive to the inhibitory effects of GABA than are DA neurons.     

Inhibitory interaction between X and Y units in the cat lateral geniculate nucleus

Intracellular and extracellular recordings were obtained from X and Y type relay neurons in the cat lateral geniculate nucleus (LGN). In both cell populations, unit responses to visual and electrical stimuli were studied. Stimulation electrodes were placed in the optic chiasm (OX), the optic radiation (OR), the homolateral superior colliculus (SC) and the homolateral mesencephalic reticular formation (MRF).X neurons have a different response to certain visual stimuli than Y neurons; when the visual stimulus exceeds the receptive field center (RFC) X neurons show a delayed response more often than do Y neurons. This differential delay between X and Y responses is partly because of short latency postsynaptic inhibition in the LGN. For fast, moving visual stimuli, Y cells respond with a brisk burst at stimulus velocities of 300°/sec; X cells are inhibited by such stimuli.The EPSP threshold for OX stimuli is higher in X cells than in Y cells. At stimulus intensities close to the EPSP threshold, X cells show a near maximal IPSP whereas in Y cells, the IPSP is minimal. The IPSP latency to OX stimulation is between 1.8 and 2.5 msec in X and Y cells; because the EPSP latency in X cells is significantly longer than in Y cells, X cell EPSPs frequently start at the same time as the IPSP.75% of the Y cells could be orthodromically driven from both the OX and SC stimuli. Analysis of the EPSP shape and correlation of the latencies suggests that the activation from SC is mediated via bifurcating optic tract fibers which project to both SC and LGN. X cells were never activated from SC; however, there was an IPSP in X and Y cells after stimulation of the SC. IPSP amplitude increased with the eccentricity of the neuron's RFC and was comparable to the IPSP that followed an OX stimulus set at the estimated threshold of the Y fibers.These results suggest an inhibitory convergence of the X and Y system in the LGN. The analysis of EPSPs shows that quite frequently several OT fibers converge onto a single X or Y relay cell; often, however, one fiber appears to provide the dominant input. With a few exceptions, the converging fibers have similar conduction velocities.     

Tectal afferents monosynaptically activate neurons in the pigeon isthmo-optic nucleus

Postsynaptic responses of 105 neurons in brain slices were intracellularly recorded from the isthmo-optic nucleus (ION) in pigeons, and 18 of these neurons were labeled with Lucifer yellow. Excitatory postsynaptic potentials (EPSPs) or spikes were produced in 93 cells, inhibitory postsynaptic potentials (IPSPs) in 10 cells, and EPSPs followed by IPSPs in two cells following electrical stimulation of the tecto-isthmooptic tract. The EPSPs occurred in an all-or-none fashion, with short latencies (1.3 +/- 0.6 ms). Repetitive stimulation increased their amplitude and duration, demonstrating that temporal summation was involved. Neurons producing excitatory responses were distributed throughout cellular layers of the nucleus. Pure IPSPs had a latency of 3.9 +/- 2.3 ms, and cells that responded in this manner were only distributed in the rostral portion of the nucleus. In the remaining two cells with EPSP-IPSP responses, the latency of excitatory responses was 1.5 ms in one cell and 1.4 ms in the other, and that of inhibitory responses was, respectively, 5.1 and 4.1 ms. Thus, it appeared that excitation was monosynaptic, whereas inhibition may be polysynaptic. Four single injections resulted in dye-coupled labeling, and two pairs of closely apposed cells fired spikes, probably resulting from spatial summation of their excitatory responses. The present study suggests that tectal cells directly activate ION neurons and that tectal fibers contact isthmo-optic neurons in a one-to-one fashion. Taken together with previous studies, it appears that the entire tecto-ION-retinal pathway is excitatory.