Entopeduncular Neurons Research Articles

Cocaine and amphetamine regulated transcript peptide (CART) in the tadpole brain: Response to different energy states

Cocaine- and amphetamine-regulated transcript peptide (CART) is an anorexigenic neuropeptide known to play a key role in energy homeostasis across the vertebrate phyla. In the current study, we have investigated the response of the CART immunoreactive system to varying energy states in the brain of a tadpole model. The pro-metamorphic tadpoles of Euphlyctis cyanophlyctis were fasted, or intracranially injected with glucose or 2-deoxy-d-glucose (2DG; an antagonist to glucose inducing glucoprivation) and the response of the CART containing system in various neuroanatomical areas was studied using immunohistochemistry. Glucose administration increased the CART immunoreactivity in the entopeduncular neurons (EN), preoptic area (POA), ventral hypothalamus (vHy) and the Edinger Westphal nucleus (EW) while CART positive cells decrease in response to fasting and glucoprivation. A substantial decrease in CART was noted in the EW nucleus of tadpoles injected with 2DG. These regions might contain the glucose-sensing neurons and regulate food intake in anurans. Therefore, we speculate that the function of central CART and its antagonistic action with NPY in food and feeding circuitry of anurans is evolutionary conserved and might be responsible for glucose homeostasis.

Endocannabinoids and Dopamine Balance Basal Ganglia Output.

The entopeduncular nucleus is one of the basal ganglia's output nuclei, thereby controlling basal ganglia information processing. Entopeduncular nucleus neurons integrate GABAergic inputs from the Striatum and the globus pallidus, together with glutamatergic inputs from the subthalamic nucleus. We show that endocannabinoids and dopamine interact to modulate the long-term plasticity of all these primary afferents to the entopeduncular nucleus. Our results suggest that the interplay between dopamine and endocannabinoids determines the balance between direct pathway (striatum) and indirect pathway (globus pallidus) in entopeduncular nucleus output. Furthermore, we demonstrate that, despite the lack of axon collaterals, information is transferred between neighboring neurons in the entopeduncular nucleus via endocannabinoid diffusion. These results transform the prevailing view of the entopeduncular nucleus as a feedforward “relay” nucleus to an intricate control unit, which may play a vital role in the process of action selection.

Changes in dynorphin immunoreactivity but unaltered density of enkephalin immunoreactive neurons in basal ganglia nuclei of genetically dystonic hamsters

Dystonia is regarded as a basal ganglia disorder. In the dt(sz) hamster, a genetic animal model of paroxysmal dystonia, previous studies demonstrated a reduced density of striatal GABAergic interneurons which inhibit striatal GABAergic projection neurons. Although the disinhibition of striatal GABAergic projection neurons was evidenced in the dt(sz) hamster, alterations in their density have not been elucidated so far. Therefore, in the present study, the density of striatal methionin-(met-) enkephalin (ENK) immunoreactive GABAergic neurons, which project to the globus pallidus (indirect pathway), was determined in dt(sz) and control hamsters to clarify a possible role of an altered ratio between striatal interneurons and projection neurons. Furthermore, the immunoreactivity of dynorphin A (DYN), which is expressed in entopeduncular fibers of striatal neurons of the direct pathway, was verified by gray level measurements to illuminate the functional relevance of an enhanced striato-entopeduncular neuronal activity previously found in dt(sz) hamsters. While the density of striatal ENK immunoreactive (ENK(+) ) neurons did not significantly differ between mutant and control hamsters, there was a significantly enhanced ratio between the DYN immunoreactive area and the whole area of the EPN in dt(sz) hamsters compared to controls. These results support the hypothesis that a disbalance between a reduced density of striatal interneurons and an unchanged density of striatal projection neurons causes imbalances in the basal ganglia network. The consequentially enhanced striato-entopeduncular inhibition leads to an already evidenced reduced activity and an altered firing pattern of entopeduncular neurons in the dt(sz) hamster.

The presence and absence of prosencephalic cell groups relaying striatal information to the medial and lateral thalamus in tenrec

Although there are remarkable differences regarding the output organization of basal ganglia between mammals and non-mammals, mammalian species with poorly differentiated brain have scarcely been investigated in this respect. The aim of the present study was to identify the pallidal neurons giving rise to thalamic projections in the Madagascar lesser hedgehog tenrec (Afrotheria). Following tracer injections into the thalamus, retrogradely labelled neurons were found in the depth of the olfactory tubercle (particularly the hilus of the Callejal islands and the insula magna), in subdivisions of the diagonal band complex, the peripeduncular region and the thalamic reticular nucleus. No labelled cells were seen in the globus pallidus. Pallidal neurons were tentatively identified on the basis of their striatal afferents revealed hodologically using anterograde axonal tracer substances and immunohistochemically with antibodies against enkephalin and substance P. The data showed that the tenrec's medial thalamus received prominent projections from ventral pallidal cells as well as from a few neurons within and ventral to the cerebral peduncle. The only regions projecting to the lateral thalamus appeared to be the thalamic reticular nucleus (RTh) and the dorsal peripeduncular nucleus (PpD). On the basis of immunohistochemical data and the topography of its thalamic projections, the PpD was considered to be an equivalent to the pregeniculate nucleus in other mammals. There was no evidence of entopeduncular (internal pallidal) neurons being present within the RTh/PpD complex, neuropils of which did not stain for enkephalin and substance P. The ventrolateral portion of RTh, the only region eventually receiving a striatal input, projected to the caudolateral rather than the rostrolateral thalamus. Thus, the striatopallidal output organization in the tenrec appeared similar, in many respects, to the output organization in non-mammals. This paper considers the failure to identify entopeduncular neurons projecting to the rostrolateral thalamus in a mammal with a little differentiated cerebral cortex, and also stresses the discrepancy between this absence and the presence of a distinct external pallidal segment (globus pallidus).

Ablation of striatal interneurons influences activities of entopeduncular neurons.

To characterize modulatory effects of striatal interneurons upon the output nucleus of the basal ganglia, we ablated striatal interneurons that express substance P receptors by using local injection of a selective neurotoxin, substance P-saporin, in rats. We then made extracellular recordings of the activity of entopeduncular neurons and examined their responses to stimulation in the motor cortex. In the interneuron-ablated animals, the spontaneous discharge rate of entopeduncular neurons was significantly decreased, and the proportion of entopeduncular neurons showing responses to cortical stimulation was significantly larger, in comparison with intact animals. It is suggested that striatal interneurons expressing substance P receptors are important for motor control mechanisms mediated by the cortico-basal ganglia pathways.

Altered Discharge Pattern of Basal Ganglia Output Neurons in an Animal Model of Idiopathic Dystonia

A decreased activity of basal ganglia output neurons is thought to underlie idiopathic dystonias and other hyperkinetic movement disorders. We found recently a reduced spontaneous discharge rate of entopeduncular neurons (internal globus pallidus in primates) in<i>dt</i>^<i>sz</i> hamsters, an unique model for idiopathic paroxysmal dystonia in which stress-inducible attacks show an age-dependent severity. Otherwise, it has been suggested that an altered discharge pattern may be more important for the occurrence of dystonia than a reduced discharge rate. Based on qualitative and computerized quantitative evaluations of interspike interval histograms and spike trains of extracellularly recorded single neurons, we investigated the spontaneous discharge pattern of GABAergic entopeduncular and nigral neurons in<i>dt^sz</i> hamsters at different ages. The discharge pattern of entopeduncular neurons was highly irregular and showed an altered burst-like firing in<i>dt^sz</i> hamsters at the age of the most marked expression of dystonia when compared with age-matched nondystonic controls. In line with a recently reported normalization of discharge rates after age-dependent disappearance of dystonia, we found an almost complete normalization of the discharge pattern of entopeduncular neurons after remission of dystonia in<i>dt^sz</i> hamsters. Investigations of GABAergic nigral neurons, reported recently to have the same spontaneous discharge rates in dystonic and nondystonic hamsters, did not show an altered firing pattern in<i>dt^sz</i> hamsters. The present data clearly indicate the fundamental importance of an altered discharge pattern of entopeduncular neurons for the expression of paroxysmal dystonia, and probably also for other dyskinesias, and may explain the improvements obtained by pallidotomy in dystonic patients despite an obviously reduced pallidal output.

Altered discharge pattern of basal ganglia output neurons in an animal model of idiopathic dystonia.

A decreased activity of basal ganglia output neurons is thought to underlie idiopathic dystonias and other hyperkinetic movement disorders. We found recently a reduced spontaneous discharge rate of entopeduncular neurons (internal globus pallidus in primates) in dt(sz) hamsters, an unique model for idiopathic paroxysmal dystonia in which stress-inducible attacks show an age-dependent severity. Otherwise, it has been suggested that an altered discharge pattern may be more important for the occurrence of dystonia than a reduced discharge rate. Based on qualitative and computerized quantitative evaluations of interspike interval histograms and spike trains of extracellularly recorded single neurons, we investigated the spontaneous discharge pattern of GABAergic entopeduncular and nigral neurons in dt(sz) hamsters at different ages. The discharge pattern of entopeduncular neurons was highly irregular and showed an altered burst-like firing in dt(sz) hamsters at the age of the most marked expression of dystonia when compared with age-matched nondystonic controls. In line with a recently reported normalization of discharge rates after age-dependent disappearance of dystonia, we found an almost complete normalization of the discharge pattern of entopeduncular neurons after remission of dystonia in dt(sz) hamsters. Investigations of GABAergic nigral neurons, reported recently to have the same spontaneous discharge rates in dystonic and nondystonic hamsters, did not show an altered firing pattern in dt(sz) hamsters. The present data clearly indicate the fundamental importance of an altered discharge pattern of entopeduncular neurons for the expression of paroxysmal dystonia, and probably also for other dyskinesias, and may explain the improvements obtained by pallidotomy in dystonic patients despite an obviously reduced pallidal output.

Nigrostriatal lesion and dopamine agonists affect firing patterns of rodent entopeduncular nucleus neurons.

Altered activity of the entopeduncular nucleus, the rodent homologue of the globus pallidus internal segment in primates, is thought to mediate behavioral consequences of midbrain dopamine depletion in rodents. Few studies, however, have examined dopaminergic modulation of spiking activity in this nucleus. This study characterizes changes in entopeduncular neuronal activity after nigrostriatal dopaminergic lesion and the effects of systemic treatment with selective D(1) (SKF 38393) and D(2) (quinpirole) agonists in lesioned rats. Extracellular single-unit recordings were performed in awake immobilized rats, either in neurologically intact animals (n = 42) or in animals that had received unilateral 6-hydroxydopamine infusion into the medial forebrain bundle several weeks previously (n = 35). Nigrostriatal lesion altered baseline activity of entopeduncular neurons in several ways. Interspike interval distributions had significantly decreased modes and significantly increased coefficient of variation, skewness and kurtosis; yet interspike interval mean (the inverse of firing rate) was not affected. Also, spectral analysis of autocorrelograms indicated that lesion significantly reduced the incidence of regular-spiking neurons and increased the incidence of neurons with 4-18 Hz oscillations. Dopamine agonist treatment reversed some lesion-induced effects: quinpirole reversed changes in interspike interval distribution mode and coefficient of variation, while combined quinpirole and SKF 38393 blocked the appearance of 4-18 Hz oscillations. However, no agonist treatment normalized all aspects of entopeduncular activity. Additionally, inhibition of firing rates by D(1) or combined D(1)/D(2) receptor activation indicated that dopamine agonists affected the overall level of entopeduncular activity in a manner similar to that found in the substantia nigra pars reticulata and globus pallidus internal segment after dopamine neuron lesion. These data demonstrate that lesion of the nigrostriatal tract leads to modifications of several aspects of firing pattern in the rodent entopeduncular nucleus and so expand on similar findings in the rodent substantia nigra pars reticulata and in the globus pallidus internal segment in humans and nonhuman primates. The results support the view that dysfunction in the basal ganglia after midbrain dopamine neuron loss relates more consistently to abnormal activity patterns than to net changes in firing rate in the basal ganglia output nuclei, while overall decreases in firing rate in these structures may play a more important role in adverse motor reactions to dopamine agonist treatments.

Neostriatal and globus pallidus stimulation induced inhibitory postsynaptic potentials in entopeduncular neurons in rat brain slice preparations

Recent anatomical studies revealed that the entopeduncular nucleus of the rat receives GABAergic inputs from both the neostriatum and the globus pallidus. The present study was undertaken to reveal the physiological features of these inputs using the intracellular recording method in rat brain slice preparations. Most of the entopeduncular nucleus neurons generated repetitive firing without spike accommodation with intracellular current stimulation and thus were classified as Type-I. A small number of neurons were classified as Type-II since they generated spikes with pronounced accommodation. Most of the Type-I, but none of Type-II, entopeduncular nucleus neurons exhibited monosynaptic GABAergic inhibitory postsynaptic potentials (IPSPs) after stimulation of the neostriatum and the globus pallidus. Neostriatal stimulation induced long latency IPSPs while pallidal stimulation induced long latency IPSPs compounded with short latency IPSPs. The IPSPs were mediated by GABA A receptors. The unitary IPSPs to striatal stimulation were small while those to pallidal stimulation were large in amplitude and able to reset ongoing rhythmic firing. The short latency IPSPs induced by pallidal stimulation reversed at a somatic membrane potential that was a few millivolts more depolarized than the long latency IPSPs, suggesting that the striatal inputs were evoked in more distal portions of the neurons than the pallidal inputs. Repetitive activation of these inputs resulted in a poor amplitude summation but a prolongation of the duration of the IPSPs. The results of the present study indicate that the pallidal projection to the entopeduncular nucleus is physiologically significant and that the neostriatum and the globus pallidus play important roles in controlling the activity of the entopeduncular nucleus, although in different ways.

Spontaneous Remission of Paroxysmal Dystonia Coincides with Normalization of Entopeduncular Activity indtszMutants

Recent studies have shown a dramatically decreased spontaneous discharge rate of entopeduncular neurons in a unique animal model of idiopathic paroxysmal dystonia, the dt(sz) mutant hamster. These changes were found in animals at the age at which the most marked expression of dystonia is usually observed. In this rodent model, the age-dependent disappearance of stress-inducible dystonic attacks at an age of approximately 10 weeks allows investigations of the relevance of pathophysiological changes for the occurrence of dystonia by ontogenetic studies. Therefore, we examined the entopeduncular activity by extracellular single unit recordings in groups of dt(sz) mutants and nondystonic control hamsters at 17-22 weeks of age. In contrast to recent findings, after the complete remission of dystonia, the mean discharge rate of entopeduncular neurons in dt(sz) mutants (28.1 +/- 1.2 spikes/sec) was similar to that of age-matched nondystonic control hamsters (30.8 +/- 0.9 spikes/sec). Thus, the disappearance of paroxysmal dystonia is accompanied by a normalization of the entopeduncular activity in dt(sz) mutants. The present data clearly demonstrate the fundamental importance of a decreased basal ganglia output for the expression of paroxysmal dystonia.

Study of projections from the entopeduncular nucleus to the thalamus of the rat

The entopeduncular nucleus (EP) is a major outflow nucleus of the basal ganglia and innervates the lateral habenula, parafascicular, pedunculopontine, ventrolateral (VL), ventromedial (VM), and mediodorsal thalamic nuclei. This study investigated the morphology of single axons of entopeduncular neurons projecting to the motor thalamus by placing small injections of dextran biotin into the EP and reconstructing drawings of single axons from serial sections. There were two populations of entopeduncular-thalamic projection axons: those that projected only to the motor thalamus (VL and VM) and those that projected to both the motor thalamus and other nuclei (e.g., the habenula). The neurochemistry of EP neurons projecting to the thalamus was investigated by injecting the retrograde tracer FluoroGold into the VL and VM thalamic nuclei to retrogradely fill entopeduncular projection neurons. These were subsequently immunohistochemically labeled for choline acetyl transferase, γ-aminobutyric acid (GABA), and glutamate. Consistent with previous studies, significant proportions of these neurons were GABA immunoreactive. In addition, approximately half of the entopeduncular-thalamic projecting neurons were found to be cholinergic. This excitatory input is most likely derived from axons that branch as they pass through the motor thalamus to the lateral habenula. J. Comp. Neurol. 426:366–377, 2000. © 2000 Wiley-Liss, Inc.

Deficit of Striatal Parvalbumin-Reactive GABAergic Interneurons and Decreased Basal Ganglia Output in a Genetic Rodent Model of Idiopathic Paroxysmal Dystonia

The underlying mechanisms of various types of hereditary dystonia, a common movement disorder, are still unknown. Recent findings in a genetic model of a type of paroxysmal dystonia, the dt(sz) mutant hamster, pointed to striatal dysfunctions. In the present study, immunhistochemical experiments demonstrated a marked decrease in the number and density of parvalbumin-immunoreactive GABAergic interneurons in all striatal subregions of mutant hamsters. To examine the functional relevance of the reduction of these inhibitory interneurons, the effects of the GABA(A) receptor agonist muscimol on severity of dystonia were examined after microinjections into the striatum and after systemic administrations. Muscimol improved the dystonic syndrome after striatal injections to a similar extent as after systemic treatment, supporting the importance of the deficiency of striatal GABAergic interneurons for the occurrence of the motor disturbances. The disinhibition of striatal GABAergic projection neurons, as suggested by recent extracellular single-unit recordings in dt(sz) hamsters, should lead to an abnormal neuronal activity in the basal ganglia output nuclei. Indeed, a significantly decreased basal discharge rate of entopeduncular neurons was found in dt(sz) hamsters. We conclude that a deficit of striatal GABAergic interneurons leads by disinhibition of striatal GABAergic projection neurons to a reduced activity in the entopeduncular nucleus, i.e., to a decreased basal ganglia output. This finding is in line with the current hypothesis about the pathophysiology of hyperkinesias. The results indicate that striatal interneurons deserve attention in basic and clinical research of those movement disorders.

Study of projections from the entopeduncular nucleus to the thalamus of the rat

The entopeduncular nucleus (EP) is a major outflow nucleus of the basal ganglia and innervates the lateral habenula, parafascicular, pedunculopontine, ventrolateral (VL), ventromedial (VM), and mediodorsal thalamic nuclei. This study investigated the morphology of single axons of entopeduncular neurons projecting to the motor thalamus by placing small injections of dextran biotin into the EP and reconstructing drawings of single axons from serial sections. There were two populations of entopeduncular-thalamic projection axons: those that projected only to the motor thalamus (VL and VM) and those that projected to both the motor thalamus and other nuclei (e.g., the habenula). The neurochemistry of EP neurons projecting to the thalamus was investigated by injecting the retrograde tracer FluoroGold into the VL and VM thalamic nuclei to retrogradely fill entopeduncular projection neurons. These were subsequently immunohistochemically labeled for choline acetyl transferase, gamma-aminobutyric acid (GABA), and glutamate. Consistent with previous studies, significant proportions of these neurons were GABA immunoreactive. In addition, approximately half of the entopeduncular-thalamic projecting neurons were found to be cholinergic. This excitatory input is most likely derived from axons that branch as they pass through the motor thalamus to the lateral habenula.

1628 Inputs from the entopeduncular nucleus and the subthalamus to the VA-Vl nucleus of the thalamus, and projection patterns of entopeduncular neurons in the cat

1628 Inputs from the entopeduncular nucleus and the subthalamus to the VA-Vl nucleus of the thalamus, and projection patterns of entopeduncular neurons in the cat

Neurons projecting from the entopeduncular nucleus to the thalamus receive convergent synaptic inputs from the subthalamic nucleus and the neostriatum in the rat

The two major afferents of the entopeduncular nucleus are the subthalamic nucleus and the neostriatum, which have opposing physiological effects on entopeduncular neurons. Experiments were performed to test the hypothesis that individual entopeduncular neurons that project to the thalamus receive convergent synaptic input from both the subthalamic nucleus and the neostriatum in the rat. This was achieved using double anterograde tracing combined with retrograde tracing. In the electron microscope anterogradely labelled subthalamic (Subthalamic Type 1) and neostriatal terminals were observed to form asymmetrical and symmetrical synaptic contacts respectively, with all parts of entopeduncular neurons. Labelled subthalamic and neostriatal terminals were observed in convergent synaptic contact with entopeduncular neurons, some of which were retrogradely labelled from the thalamus. A second rarer type of terminal was labelled (Subthalamic Type 2) which formed symmetrical synaptic contacts with the proximal regions of unlabelled and retrogradely labelled entopeduncular neurons. These terminals are believed to be derived from the globus pallidus. It is concluded that the topographical and synaptic organization of the so-called direct (neostriatum to entopeduncular nucleus) and indirect pathways (involving the subthalamus and the globus pallidus) is capable of mediating the inhibition and excitation of output neurons in the entopeduncular nucleus that occur following neostriatal stimulation.

Participation of nucleus entopeduncularis in motor instrumental reflex and entopeduncular influences on motor thalamic nuclei in normal and MPTP-treated cats

Activity of entopeduncular neurons was studied in chronic experiments on cats during performance of instrumental movement: pedal pressing and holding. One-hundred and twenty-four neurons were extracellularly investigated in intact animals and 81 neurons in cats treated with N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (5 mg/kg daily, intramuscularly for five days). The mean discharge frequency of nucleus entopeduncularis neurons recorded 48–72 h after the last MPTP injection increased from12.9 ± 1.5 to22.1 ± 1.4impulses/s, but dropped to preinjection values within the next ten days. In intact animals and in MPTP-treated cats 23 and 17%, respectively, of neurons changed their activity before or during the movement performance. Along with nucleus entopeduncularis neurons that changed their activity simultaneously with instrumental movement performance, 16% of nucleus entopeduncularis nerve cells in intact cats and 12% in MPTP-treated cats responded 50–800 ms before the myogramme of working forepaw biceps was started. Excitatory responses associated with movement performance in MPTP-exposed cats were more pronounced, indicating enhancement of nucleus entopeduncularis neuronal activity in animals with injured nigrostriatal system. Since nucleus entopeduncularis neurons are inhibitory cells, the increase in their activity had to be accompanied by reinforcement of inhibitory influence on neurons in motor thalamic nuclei. In order to test this hypothesis, two groups of acute experiments were performed on ketamine-anaesthetized and myorelaxine-immobilized cats. Neuronal responses in ventral anterior and ventral lateral thalamic nuclei to nucleus entopeduncularis stimulation were investigated in normal and MPTP-treated animals in doses that were identical to those administered in chronic experiments. In intact cats, 28% of neurons responded to nucleus entopeduncularis stimulation with the latency shorter than 7 ms. In half of the inhibited neurons after the first phase of inhibition lasting18 ± 2ms, the second inhibitory phase was recorded. The duration of the latter was24 ± 4ms. Although in MPTP-treated cats the number of neurons inhibited by nucleus entopeduncularis stimulation was practically the same as in normal ones (24.5%), the first phase tended to be shorter, and a statistically significant increase of the second inhibitory phase duration (up to50 ± 11ms) was found. It was suggested that changes in the inhibitory processes in motor thalamic neurons receiving afferents from nucleus entopeduncularis could be explained by GABA B-mediated hyperpolarization of the neuronal membrane, evoked by increasing pallidothalamic inhibitory influences.

The coexistence of substance P- and glutamic acid decarboxylase-like immunoreactivity in entopeduncular neurons of the rat

The coexistence of substance P- and glutamic acid decarboxylase-like immunoreactivity in cell bodies was investigated in the entopeduncular neurons of the rat by the double-immunofluorescence method using species-specific antibodies. Over half of the substance P-like immunoreactive cells were GABAergic. Double-labeled neurons were generally seen in the rostral to the middle region of the entopeduncular nucleus. Since the rostral portion of the entopeduncular nucleus mainly projects to the lateral habenular nucleus, it is suggested that double-labeled neurons in the entopeduncular nucleus largely project to the lateral habenular nucleus which is involved in the limbic system.

The functional role of the pedunculopontine nucleus in the regulation of the electrical activity of entopeduncular neurons in the rat.

The purpose of this study was to investigate the influence of the pedunculopontine nucleus (PPN) on the electrical activity of entopeduncular nucleus (EP) in the rat and to analyze the influence of the subthalamic nucleus (STN) on the PPN-evoked responses of EP cells. Most of the EP neurons recorded (65.1%) were identified electrophysiologically as output cells projecting to the lateral habenula while only a minority (3.8%) were output cells to the PPN. Stimulation of the PPN in intact rats caused a short-latency (2.5 +/- 2.0, S.D. ms) activation in 22.6% and suppression of activity in 8.5% of EP neurons recorded. The mean impulse rate of EP neurons in intact rats was 27.0 +/- 5.5, S.D. imp./s and the overall mean interspike interval 36.8 +/- 7.1, S.D. ms. In rats where the PPN had been destroyed 10-12 days before recording by a local microinjection of kainic acid only a few EP neurons were still responsive to stimulation of the PPN showing suppression of activity. In these rats the kainate lesion slowed the impulse spontaneous activity to 14.3 +/- 6.3, S.D. imp./s and markedly altered the distribution of interspike intervals in 62.5% of the EP neurons recorded. The overall mean interspike interval in this group of deregulated neurons was 68.2 +/- 20.1, S.D. ms. A small kainate lesion of the STN placed 4-5 days before recording, on the other hand, did not affect the spontaneous activity of EP cells but increased the percentage of cells which were activated (43.6%) by stimulating the PPN. The present data demonstrate a predominant activatory influence of the PPN on EP cells and suggest that destruction of the STN may affect the responsiveness of entopeduncular cells to stimulation of the PPN possibly through the removal of a tonic inhibitory STN influence on the EP.

Ingestion-related activity of caudate and entopeduncular neurons in the cat

Single-unit activity was recorded in the caudate nucleus and entopeduncular nucleus in cats during ingestion. In both nuclei, ingestion-related neurons were of two types: those with no facial somatosensory receptive field and an ingestion-related response, and those with a facial somatosensory field and an ingestion response. Neurons in both regions contained cells with conditioned responses to the noise produced by the solenoid that delivered milk. No caudate neurons and only 3% of entopeduncular neurons were phasically related to jaw muscle activity. These results indicate that neurons in both input and output regions of the basal ganglia in the cat have complex ingestion-related response characteristics with little relationship to specific orolingual movements.

Postnatal differentiation and growth of cat entopeduncular neurons. A transient spiny period associated with branch elongation

Qualitative and computer-assisted analyses were performed on Golgi-impregnated neurons which were serially reconstructed in 3 dimensions. Analysis of the temporal pattern of growth indicated that the initial outgrowth, formation of the adult number of dendrites and virtually all dendritic branching occurred in the prenatal period. About 40% of the total growth of the dendrites occurred in the postnatal period. Maturation was completed by 90–120 days. Analyses of the mode of dendritic growth and of the morphological changes associated with growth revealed two significant findings. First, the outward expansion of the dendritic tree was not due to the addition of new branches but resulted from the elongation of terminal and non-terminal branches. Thus, growth occurred between branch points as well as on terminal portions of dendrites. Second, a transient population of spines was found during the period of postnatal growth. These spines may play an integral role in synaptogenesis and dendritic branch elongation. We suggest that developing afferent fibers initially contact spines. As spines retract, axon terminals are brought to the shaft of the dendrites. Further, the dendrites elongated because membrane associated with spines is incorporated into the shafts of dendrites. Striopallidal projections and other afferents may provide an important trophic influence for the normal dendritic differentiation of pallidal neurons by inducing the elaboration or retraction of spines.