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Dorsal root ganglia development in chicks following partial ablation of the neural crest.

To assess the effects of reduced competition for peripheral targets on developing brachial dorsal root ganglia (DRG), chick embryos were subjected to partial ablations of the brachial neural crest at stages 13 or 14 (Hamburger, V., and H.L. Hamilton (1951) J. Morphol. 88: 49-92), using an ophthalmological cauterization unit. In the initial studies reported here, ganglia developing from the remaining crest material were examined for ganglionic volume and neuronal size, neuronal number, and degenerative activity at stage 35. Results showed that the lesion procedure resulted in the reduction or absence of one or two ganglia on each side at the level of DRG 15 to DRG 17. Hypertrophies occurred in other ganglia remaining at these and at more rostral levels and ranged up to 220%. These hypertrophies were most pronounced, however, not in the ganglia adjacent to those lesioned but rather in more remote ganglia, including those at cervical levels. Accompanying these ganglionic changes were significant alterations in all three neuronal parameters examined. The findings clearly demonstrate a responsiveness of chick brachial DRG to reduced competition resulting from neural crest ablations and that such responsiveness occurs along several axial segments.

Animals↗

Three-dimensional analysis of the intrinsic cardiac ganglia in a young dog.

The intrinsic ganglia of the heart of a young dog were studied by computer graphic reconstruction to determine the accurate location. The heart was embedded in celloidin, and transverse sections were cut. Using every third 60 microns section, a series of 49 sections was mapped. Three-dimensional (3D) images were constructed by a personal computer. Numerous intrinsic ganglia, most of which were located in the epicardiun, were observed. The intrinsic ganglia were found in the base of the aorta and pulmonary vessels and from the base of the superior vena cava to the right atrium, i.e., the sinoatrial nodal region. Using the 3D reconstruction technique, the locations of the intrinsic ganglia could be accurately identified. Furthermore, it was demonstrated that these ganglia formed several groups which formed a continuity. This study suggested that it was necessary to consider the existence of the numerous intrinsic ganglia, when we studied the cardiac innervation.

Animals↗

[Informational analysis of the basal ganglia related system].

This paper describes a major cerebral system whose contours are only emerging: the "basal ganglia related system". This is made up of the "system of the basal ganglia" itself plus its inputs and outputs. The system of the basal ganglia may be divided into the "basal ganglia core" comprising the striatum and its pallidal and nigral targets and the "regulators of the core". Distinguishable include regulators of the striatum (the dopaminergic pars compacta and the central complex of the thalamus or centre median-parafascicularis), regulators of the pallidonigrum (the subthalamic nucleus and the pedunculopontine complex) and internal regulators (at first the lateral nucleus of the pallidum). The main input to this system comes from the cerebral cortex. The main output is the thalamus and from it to the cortex. The whole "basal ganglia related system" may thus be seen as a cortico-cortical circuit passing through the basal ganglia. Information processing in the system is very complex. New data presented here emphasize two connections: cortico-striate and striato-pallidonigral connections. It is stressed that the first uses complex combinations of confluence or difluence on small matricial islands. This step could be a selection and reorganisation of cortical information. The second process is a strong "dynamically focused convergence" combining information from different upstream sources in order to derive an adequate informational product for the production of harmonious and adapted motricity.

Basal Ganglia↗

Metabotropic glutamate receptor mRNA expression in the basal ganglia of the rat.

Metabotropic glutamate receptors (mGluRs) couple the actions of glutamate to intracellular second messenger systems through G-proteins. The mGluRs play an important role in the regulation of basal ganglia function. Ligand binding studies have revealed that the basal ganglia contain at least two pharmacological types of metabotropic binding sites. Agonists of mGluRs can affect both in vitro electrophysiologic responses of striatal neurons and motor behavior in vivo. Recently, cDNAs encoding five mGluRs have been cloned, each with distinct structural and pharmacological properties. In order to elucidate the function of these receptors in the biology of the extrapyramidal motor system, we have used in situ hybridization to examine the regional and cellular expression patterns of mGluR1-mGluR5 in the adult rat basal ganglia. In the striatum, all of these mGluRs were present in widely varying relative densities and cellular patterns. MGluR5 was particularly prominent, and exhibited a heterogeneous cellular distribution, with labeled and unlabeled populations of neurons. MGluR2 was expressed in a small population of large polygonal striatal neurons. The subthalamic nucleus was the only other basal ganglia structure that expressed mGluR2. Distinct cellular distributions of mGluR expression were also observed within the nucleus accumbens, globus pallidus, ventral pallidum, and substantia nigra pars reticulata. MGluR3 was expressed in glia in all basal ganglia structures, but was observed in neurons only in the striatum, substantia nigra pars reticulata, and very weakly in the subthalamic nucleus. Comparison of the restricted mGluR2 and mGluR3 mRNA distributions with that of metabotropic ligand binding sites supports a possible presynaptic location for these receptors in the basal ganglia. MGluR1 was the only mGluR message prominently expressed in the dopaminergic neurons of the substantia nigra pars compacta, suggesting the involvement of this receptor in the regulation of dopamine release from nigrostriatal terminals.

Animals↗

Consequences of nigrostriatal denervation on the functioning of the basal ganglia in human and nonhuman primates: an in situ hybridization study of cytochrome oxidase subunit I mRNA.

To examine the consequences of nigrostriatal denervation and chronic levodopa (L-DOPA) treatment on functional activity of the basal ganglia, we analyzed, using in situ hybridization, the cellular expression of the mRNA encoding for cytochrome oxidase subunit I (COI mRNA), a molecular marker for functional neuronal activity, in the basal ganglia. This analysis was performed in monkeys rendered parkinsonian by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) Intoxication, some of which had been receiving L-DOPA, and in patients with Parkinson's disease (PD). In MPTP-intoxicated monkeys compared with control animals, COI mRNA expression was increased in the subthalamic nucleus (STN) and in the output nuclei of the basal ganglia, i.e., the internal segment of the globus pallidus and the substantia nigra pars reticulata. This increase was partially reversed by L-DOPA treatment. COI mRNA expression remained unchanged in the external segment of the globus pallidus (GPe). In PD patients, all of whom had been treated chronically by L-DOPA, COI mRNA expression in the analyzed basal ganglia structures was similar to that in control subjects. These results are in agreement with the accepted model of basal ganglia organization, to the extent that the output nuclei of the basal ganglia are considered to be overactive after nigrostriatal denervation, partly because of increased activity of excitatory afferents from the STN. Yet, our results would also seem to contradict this model, because the overactivity of the STN does not seem to be attributable to a hypoactivation of the GPe.

Aged↗

Basal ganglia organization in amphibians: chemoarchitecture.

Recent studies dealing with the investigation of the afferent and efferent connections of the basal ganglia of amphibians have revealed many similarities with basal ganglia structures of amniotes. In a further step, the chemoarchitecture of basal ganglia of the frog Rana perezi has been investigated. For use as main markers of amphibian basal ganglia structures, antibodies against tyrosine hydroxylase, substance P, and enkephalin were selected. Moreover, the distributions of nitric oxide synthase (nicotinamide adenine dinucleotide phosphate-diaphorase histochemistry), calretinin, dopamine-beta-hydroxylase, choline acetyltransferase, mesotocin, vasotocin, somatostatin, neuropeptide Y, neuropeptide FF, and serotonin were studied to corroborate a comparison with both basal ganglia and amygdaloid structures of amniotes. On the basis of connections and chemoarchitecture, a striatum proper, nucleus accumbens, dorsal and ventral pallidum, bed nucleus of the stria terminalis, and amygdaloid complex have been identified. Accordingly, a new terminology is proposed that is in line with our current understanding of basal ganglia organization in amphibians.

Amygdala↗

Effects of adenosine on cholinergic transmission in mammalian vesical parasympathetic ganglia.

Intracellular recordings were made from mammalian vesical parasympathetic ganglia. A fast excitatory postsynaptic potential (EPSP) was abolished by hexamethonium (200 microM) in rabbit and feline ganglia. A slow inhibitory postsynaptic potential (IPSP) and a following slow EPSP were abolished by atropine (1 microM) in the feline ganglia. Bath application of adenosine (300 microM) depressed the amplitude of nicotinic fast EPSP by 48 +/- 4% in the rabbit ganglia. The action of adenosine was dose-dependent. An antagonist of A1-purinoceptors, 8-cyclopentyltheophylline (1-10 microM), inhibited the adenosine-induced depression but not the amplitude of fast EPSP. Adenosine (2-3 mM) did not significantly affect either the muscarinic slow IPSP, or the slow EPSP, in the feline ganglia. Adenosine also caused a hyperpolarization (1-5 mV) in 40% of the rabbit neurons and 66% of the feline neurons. However a purinergic IPSP was not recorded from either species. These data suggest diverse actions of adenosine in modulating cholinergic transmission in rabbit and feline vesical ganglia.

Adenosine↗

Origin of neuronal nitric oxide synthase (NOS)-immunoreactive fibers in guinea pig parasympathetic cardiac ganglia.

This study was conducted to determine the origin(s) of neuronal nitric oxide synthase-immunoreactive (NOS-IR) fibers within guinea pig atrial whole-mount preparations containing the cardiac ganglia. Intrinsic NOS-IR cardiac neurons exhibited choline acetyltransferase (ChAT) immunoreactivity, indicating that they were cholinergic as well as nitrergic. Comparison of control versus 72-hour explant culture preparations indicated that most of the nitrergic fibers within cardiac ganglia were extrinsic. The extrinsic NOS-IR fibers were not IR for ChAT (marker of preganglionic parasympathetic neurons), tyrosine hydroxylase (marker of catecholaminergic sympathetic postganglionic axons), or calcitonin gene-related peptide (CGRP) (marker of afferent fibers). Separate NOS-IR and ChAT-IR neurons were present within medullary regions containing the cardiovascular regulatory nuclei (nucleus ambiguus and dorsal motor nucleus of the vagus), but no cells were found that exhibited both NOS immunoreactivity and ChAT immunoreactivity. The small size and location of the medullary NOS-IR neurons suggested they were probably interneurons. Only an occasional sympathetic postganglionic cell in the stellate ganglion complex exhibited NOS immunoreactivity. NOS-IR cells were present in dorsal root ganglia (thoracic 1-5), but these typically also exhibited CGRP immunoreactivity. NOS-IR cells were also present in the nodose ganglia, but only some exhibited CGRP immunoreactivity. We concluded that virtually all the extrinsic NOS-IR nerve fibers represented an afferent fiber input that was separate from the substance P (SP)/CGRP-containing population of sensory fibers. Furthermore, much of this NOS innervation is probably derived from the nodose ganglia.

Afferent Pathways↗

A tissue-culture of nerve cells from adult mammalian ganglia and some electrophysiological properties of the nerve cells in vitro.

A new technique for primary culture of nerve cells isolated from peripheral ganglia of adult mammals has been developed. Nerve cells were isolated from trigeminal ganglia, nodose ganglia, sympathetic ganglia or dorsal root ganglia of adult guinea pigs by collagenase or dispase, and then were grown on collagen-coated plastic dishes for more than 4 weeks. Intracellular recording with a glass microelectrode reveals that the nerve cells in vitro generate not only Na spikes but also tetrodotoxin-resistant Na and Ca spikes. An exception was that the sympathetic ganglion cells in vitro failed to generate tetrodotoxin-resistant Na spikes. Difference in values of the Vmax of these spike components is observed among nerve cells (3-8 days in vitro) of different origin, suggesting that distribution of ionic channels on the plasma membrane may be different among species of nerve cells.

Animals↗

Substance P in the vagal sensory ganglia: localization in cell bodies and pericellular arborizations.

The distribution of Substance P-like immunoreactivity in the jugular and nodose ganglia of rabbits and pigeons has been studied using immunocytochemical staining techniques. Substance P-like immunoreactivity is localized to neuronal cell bodies and processes in the jugular and nodose ganglia, and to pericellular fiber plexi in the nodose ganglia of both species. The numbers and sizes of cells which exhibited Substance P-like immunoreactivity in each ganglion were determined using quantitative morphometric techniques. The distribution of Substance P-like immunoreactivity in the rabbit and pigeon vagal sensory ganglia is characterized by several general features. In most of the ganglia, immunoreactive neurons factor into discrete types which can be distinguished from one another, and from non-immunoreactive neurons, by size. In addition, immunoreactive nodose and jugular ganglion cells, respectively, are distinguishable on the basis of size. Finally, a considerably high percentage of immunoreactive neurons is found in the jugular ganglion than in the nodose ganglion. Substance P-like immunoreactivity was also seen in pericellular fiber plexi which encircle individual neurons in the nodose ganglion of rabbits and pigeons. These plexi are composed of varicose fibers which appear to terminate as boutons on the surface of the cells which they encircle. The distribution of Substance P-like immunoreactivity within the vagal sensory ganglia is discussed with respect to the possible peripheral targets and functions of Substance P-containing vagal afferents. Our findings suggest that Substance P-containing vagal sensory neurons are involved in a variety of visceral and somatic afferent functions.

Animals↗

Complement-mediated lesion of sympathetic ganglia in vitro with acetylcholinesterase antibodies.

When administered to rats, antibodies against acetylcholinesterase (AChE) selectively destroy presynaptic inputs to sympathetic ganglia. To investigate the mechanism of this immunolesion, we created an in vitro system in which relevant components could be manipulated. Freshly dissected rat superior cervical ganglia (SCG) were incubated 15-20 h at 37 degrees C in fresh human serum (a potent source of complement) with continuous oxygenation. More than 96% of neurons in six control ganglia retained synaptic inputs, as defined by action potentials or excitatory postsynaptic potentials (EPSP) upon stimulation of the preganglionic trunk. However, when anti-AChE antibodies were present (0.16 mg/ml), none of 61 neurons from six incubated ganglia showed synaptic responses although membrane potential and input resistance remained normal. Staining for AChE and synaptophysin (a synaptic vesicle marker) was also disrupted in ganglia exposed to AChE antibodies in complement-sufficient serum. When complement was eliminated by substituting serum that was heat-inactivated or deficient in C3, synaptic input was retained in 60-90% of neurons incubated with AChE antibodies. Choline acetyltransferase activity (ChAT), an enzymatic marker of cholinergic cytoplasm in sympathetic ganglia, was largely lost after incubation with AChE antibodies and serum. However, incubation with AChE antibodies in heat-inactivated serum, or serum that was deficient in C3 or C8, caused no measurable loss of ganglionic ChAT activity. These findings strongly implicate the complement cascade in the destruction of preganglionic sympathetic terminals that follows binding of AChE antibodies.

Acetylcholinesterase↗

The early expression of VAChT and VIP in mouse sympathetic ganglia is not induced by cytokines acting through LIFRbeta or CNTFRalpha.

Sympathetic ganglia consist of noradrenergic and cholinergic neurons. The cholinergic marker protein vesicular acetylcholine transporter (VAChT) and the neuropeptide vasoactive intestinal peptide (VIP), co-expressed in mature cholinergic sympathetic neurons, are first detectable during embryonic development of rat sympathetic ganglia. However, the subpopulation of cholinergic sympathetic neurons which innervates sweat glands in mammalian footpads starts to express VAChT and VIP during the first postnatal weeks, under the influence of sweat gland-derived signals. In vitro evidence suggests that the sweat gland-derived cholinergic differentiation factor belongs to a group of neuropoietic cytokines, including LIF, CNTF and CT-1, that act through a LIFRbeta-containing cytokine receptor. To investigate whether the embryonic expression of cholinergic properties is elicited by a related cytokine, the expression of VAChT and VIP was analyzed in stellate ganglia of mice deficient for the cytokine receptor subunits LIFRbeta or CNTFRalpha. The density of VAChT- and VIP-immunoreactive cells in stellate ganglia of new-born animals was not different in LIFRbeta(-/-) and CNTFRalpha(-/-) ganglia as compared to ganglia from wild-type mice. These results demonstrate that the early, embryonic expression of VAChT and VIP is not induced by cytokines acting through LIFRbeta- or CNTFRalpha-containing receptors.

Animals↗

Denervation of vagal cardiopulmonary receptors by injection of kainic acid into the nodose ganglia in dogs.

We determined if kainic acid, a neuroexcitotoxin, could be used to denervate the cell bodies of cardiopulmonary vagal sensory neurons. Kainic acid (5 microg) was injected into the nodose ganglion of five dogs. Ten to fourteen days following this procedure, these kainic acid-injected dogs were anesthetized and tested for the extent of the deafferentation. Five additional dogs were used as the control group. Heart rate and mean arterial pressure were measured, and a Swan-Ganz catheter was advanced into a branch of the pulmonary artery to measure pulmonary capillary wedge pressure. We recorded renal sympathetic nerve activity from branches of the left renal nerves. Bilateral carotid occlusion increased heart rate and mean arterial pressure in only the denervated group, but sympathetic nerve activity increased significantly in both groups. This demonstrates that the carotid baroreflex is preserved after kainic acid is injected into the nodose ganglia. Volume expansion by use of warmed saline (15 ml kg(-1)) increased pulmonary capillary wedge pressure 5 mm Hg in control and 14 mm Hg in denervated dogs. In control dogs, sympathetic nerve activity decreased by 10% per mm Hg increase in pulmonary capillary wedge pressure while in denervated dogs, it decreased by 2% per mm Hg. This demonstrates that the vagal cardiopulmonary baroreflex is essentially abolished after injection of kainic acid into the nodose ganglia. After opening the chest, acetylstrophanthidin 100 microg was applied directly to the epicardial surface of the left ventricle to activate cardiac vagal afferents. Epicardial acetylstrophanthidin decreased sympathetic nerve activity by 28% in the control group, but resulted in no change in the kainic-acid-injected dogs. This demonstrates that vagal cardiac chemosensitive reflexes are abolished after bilateral injection of kainic acid into the nodose ganglia. At the end of these experiments, we removed the nodose ganglia for histological evaluation. The vast majority of cell bodies in the ganglia from the denervated group appeared injured compared to cell bodies in ganglia that had not been injected, suggesting that the destruction of cell bodies of vagal afferents was responsible for the functional denervation. Our findings are consistent with the interpretation that kainic acid treatment interrupts vagal afferents that meditate reflex responses to epicardial acetylstrophanthidin and to volume expansion.

Adrenergic Fibers↗

The hypogastric and thirteenth thoracic ganglia of the rat: effects of age on the neurons and their extracellular environment.

Morphometric analyses of the neurons and microvessels of perfusion-fixed hypogastric (HG) and 13th thoracic (T13) ganglia have been performed in male Wistar rats aged 4, 24 and 30 mo. Estimations of HG volume employing the Cavalieri principle have also been performed and showed that the size of the aged HG is increased by 42%. Routine histological staining of the ganglia with Masson's trichrome indicated that this may be due to the increased amount of interstitial connective tissue which was apparent in the aged animals. The number of neurons per unit area progressively decreased by 38% between ages 4 and 24 mo and by 16% between ages 24 and 30 mo in the HG and by 25% (4 and 24 mo) and 2% (24 and 30 mo) in the T13 ganglion. The total number of neurons in the HG however, estimated by a physical disector analysis, was constant with age. The number of microvessels per unit area, microvessel diameter, neuronal and nuclear areas did not differ significantly between the 3 age groups studied. This observed increase in ganglionic volume and decrease in neuronal packing density may be associated with changes in the extracellular matrix, in particular in glycosaminoglycans whose presence was indicated by metachromasia of the ganglia with toluidine blue. The extracellular matrix was therefore characterised using a panel of monoclonal antibodies against glycosaminoglycans and laminin. Chondroitin-6 sulphate and chondroitin-4 sulphate were present in the interstitial connective tissue, and there was an increase in the expression of both these epitopes at 24 mo, noteably surrounding neuron cell bodies. The expression of chondroitin-4 sulphate/dermatan sulphate was unchanged, thus implying a decreased expression of dermatan sulphate with age. Keratan sulphate and the native chondroitin sulphate epitopes were absent from the ganglia at both ages. Laminin expression was increased in the aged ganglia. It is therefore clear that the constituents of the extracellular matrix are not constant throughout the adult lifespan and that the extracellular matrix may influence neuronal survival in old age. This is the first report characterising age-related changes in the extracellular matrix of autonomic ganglia.

Aging↗

Ultrastructure of intramural ganglia in the striated muscle portions of the guinea pig oesophagus.

The ultrastructure of the myenteric plexus located in the striated muscle portion of the guinea pig oesophagus was examined and compared with that of the plexus associated with the smooth muscle portion of the rest of the digestive tract. The oesophageal ganglia had essentially the same architecture as those of the smooth muscle portion, such as a compact neuropil without the intervention of connective tissue and blood vessels. Some features, however, were particular to the striated muscle part of the oesophagus. It was clearly demonstrated that myelinated fibres, probably sensory terminals of vagal origin, join the myenteric ganglia. Synapses and terminal varicosities are sparsely distributed within the ganglia and fewer morphological types of axon varicosities could be distinguished compared with other regions. Glial cells are well developed in the oesophageal myenteric ganglia. These cells outnumber the ganglion cells, having a higher ratio than in the lower digestive tract, and form numerous cytoplasmic lamellar processes. The lamellar processes, located at the surface of the ganglia, considerably reduce the area of neuronal membrane which directly contacts the basal lamina. The role of these lamellar processes in the oesophageal ganglia is discussed.

Animals↗

Tibial intraneural ganglia in the tarsal tunnel: Is there a joint connection?

Intraneural ganglia are rare entities, and, as such, their pathogenesis has been extremely controversial. Recent evidence from intraneural ganglia occurring at more proximal sites-the peroneal nerve at the fibular neck (the most common site) and the tibial nerve at the knee-has suggested an articular origin rather than de novo formation. To our knowledge, of the 10 previous reports of tibial intraneural ganglia within the tarsal tunnel by others, a joint connection to the ankle joint was only identified in 2 cases. To support a hypothesis that tibial intraneural ganglia occurring within the tarsal tunnel region arise from neighboring joints, we analyzed 3 patients retrospectively, all of whom had magnetic resonance (MR) imaging and operative intervention. One of these patients was treated by a peripheral nerve surgeon specializing in foot and ankle surgery. The other 2 patients were the only ones previously published in the literature who had MR images available for reinterpretation. In none of these cases was a joint communication appreciated by radiologists interpreting the MR images preoperatively or by surgeons intraoperatively. Our review of these same cases demonstrated radiographic evidence of joint communications with the subtalar joints. Based on our findings in this article and our knowledge of intraneural ganglia occurring at more proximal sites, we believe that tibial intraneural ganglia within the tarsal tunnel originate from neighboring joints and that their connections to the joints (pedicles) are through articular branches. The importance of these connections is 2-fold: first, for their role in the pathogenesis of this entity, and second, for their potential therapeutic implications. As is highlighted by the clinical and radiographic follow-up in the 1 patient in this article and in many previously reported at other sites, intraneural cyst recurrence can occur if surgeons do not specifically address the articular connection.

Ankle↗

Latent herpes simplex virus in human trigeminal ganglia. Detection of an immediate early gene "anti-sense" transcript by in situ hybridization.

We used in situ hybridization to study the expression of herpes simplex virus type 1 genes during latent infections of human sensory ganglia. Trigeminal ganglia were recovered at autopsy from 24 subjects with no evidence of an active herpetic infection. These ganglia were hybridized to 35S-labeled single-stranded RNA probes spanning 72 percent of the herpes simplex genome. In the ganglia of 16 subjects, 0.2 to 4.3 percent of the neuronal cells contained abundant nuclear signals for viral RNA. Ganglia from three patients with low or undetectable levels of antibodies to herpes simplex type 1 lacked viral RNA signals, whereas the ganglia from all of six patients with elevated antibody titers showed viral RNA signals. Transcription was detected only from the region of the viral genome containing a gene that encodes an immediate early protein known as the infected-cell protein number zero (ICP0). However, normal ("sense") transcripts of this gene, which are prominent in an acute infection, were not detected. In contrast, a novel transcript was found overlapping with, but opposite in direction to, the ICP0 transcript (and was therefore "anti-sense"). Although this transcript has been only partially characterized, we believe that it may have a role in maintaining the latency of herpes simplex virus.

Adolescent↗

Providing explicit information disrupts implicit motor learning after basal ganglia stroke.

Despite their purported neuroanatomic and functional isolation, empirical evidence suggests that sometimes conscious explicit processes can influence implicit motor skill learning. Our goal was to determine if the provision of explicit information affected implicit motor-sequence learning after damage to the basal ganglia. Individuals with stroke affecting the basal ganglia (BG) and healthy controls (HC) practiced a continuous implicit motor-sequencing task; half were provided with explicit information (EI) and half were not (No-EI). The focus of brain damage for both BG groups was in the putamen. All of the EI participants were at least explicitly aware of the repeating sequence. Across three days of practice, explicit information had a differential effect on the groups. Explicit information disrupted acquisition performance in participants with basal ganglia stroke but not healthy controls. By retention (day 4), a dissociation was apparent--explicit information hindered implicit learning in participants with basal ganglia lesions but aided healthy controls. It appears that after basal ganglia stroke explicit information is less helpful in the development of the motor plan than is discovering a motor solution using the implicit system alone. This may be due to the increased demand placed on working memory by explicit information. Thus, basal ganglia integrity may be a crucial factor in determining the efficacy of explicit information for implicit motor-sequence learning.

Adult↗