engages the totality of spiny striatal axons. estimated numbers are 110 million in man, 40 in chimpanzees and 12 in macaques. the striato-pallido-nigral bundle is made up of thin, poorly myelinated axons from the striatal spiny neurons grouped into pencils "converging like the spokes of a wheel" (papez, 1941). it gives its "pale" aspect to the receiving areas. the bundle strongly stains for iron using perls' prussian blue (in addition to iron it contains many heavy metals including cobalt, copper, magnesium and lead). convergence and focusing after the huge reduction in number of neurons between the cortex and the striatum (see corticostriate connection), the striatopallido-nigral connection is a further reduction in the number of transmitting compared to receiving neurons. numbers indicate that, for 31 million striatal spiny neurons in macaques, there are only 166000 lateral pallidal neurons, 63000 medial pallidal, 18000 lateral nigral and 35000 in the pars reticulata. if the number of striatal neurons is divided by their total number, as an average, each target neuron may receive information from 117 striatal neurons. (numbers in man lead to about the same ratio). a different approach starts from the mean surface of the pallidonigral target neurons and the number of synapses that they may receive. each pallidonigral neuron may receive 70000 synapses. each striatal neuron may contribute 680 synapses. this leads again to an approximation of 100 striatal neurons for one target neuron. this represents a huge, infrequent, reduction in neuronal connections. the consecutive compression of maps cannot preserve finely distributed maps (as in the case for instance of sensory systems). the fact that a strong anatomical possibility of convergence exists does not means that this is constantly used. a recent modeling study starting from entirely 3-d reconstructed pallidal neurons showed that their morphology alone is able to create a center-surround pattern of activity. physiological analyses have shown a central inhibition/peripheral excitation pattern, able of focusing the pallidal response in normal conditions. percheron and filion (1991) thus argued for a "dynamically focused convergence". disease, is able to alter the normal focusing. in monkeys intoxicated by mptp, striatal stimulations lead to a large convergence on pallidal neurons and a less precise mapping. focusing is not a property of the striatopallidal system. but, the very particular and contrasted geometry of the connection between striatal axons and pallidonigral dendrites offers particular conditions (the possibility for a very large number of combinations through local additions of simultaneous inputs to one tree or to several distant foci for instance). the disfocusing of the system is thought to be responsible for most of the parkinsonian series symptoms. the mechanism of focusing is not known yet. the structure of the dopaminergic innervation does not seem to allow it to operate for this function. more likely focusing is regulated by the upstream striatopallidal and corticostriatal systems. synaptology and combinatory the synaptology of the striato- pallidonigral connection is so peculiar as to be recognized easily. pallidonigral dendrites are entirely covered with synapses without any apposition of glia. this gives in sections characteristic images of "pallissades" or of "rosettes". more than 90% of these synapses are of striatal origin. the few other synapses such as the dopaminergic or the cholinergic are interspersed among the gabaergic striatonigral synapses. the way striatal axons distribute their synapses is a disputed point. the fact that striatal axons are seen parallel to dendrites as "woolly fibers" has led to exaggerate the distances along which dendrites and axons are parallel. striatal axons may in fact simply cross the dendrite and give a single synapse. more frequently the striatal axon curves its course and follow the dendrite forming "parallel contacts" for a rather short distance. the average length of parallel contacts was found to be 55 micrometres with 3 to 10 boutons (synapses). in another type of axonal pattern the afferent axon bifurcates and gives two or more branches, parallel to the dendrite, thus increasing the number of synapses given by one striatal axon. the same axon may reach other parts of the same dendritic arborisation (forming "random cascades") with this pattern, it is more than likely that 1 or even 5 striatal axons are not able to influence (to inhibit) the activity of one pallidal neuron. certain spatio-temporal conditions would be necessary for this, implying more afferent axons. pallidonigral outmaps what is described above concerned the input map or "inmap" (corresponding to the spatial distribution of the afferent axons from one source to one target). this does not correspond necessarily to the output map or outmap (corresponding to the distribution of the neurons in relation to their axonal targets). physiological studies and transsynaptic viral markers have shown that islands of pallidal neurons (only their cell bodies or somata, or trigger points) sending their axons through their particular thalamic territories (or nuclei) to one determined cortical target are organized into radial bands. these were assessed to be totally representative of the pallidal organisation. this is certainly not the case. pallidum is precisely one cerebral place where there is a dramatic change between one afferent geometry and a completely different efferent one. the inmap and the outmap are totally different. this is an indication of the fundamental role of the pallidonigral set: the spatial reorganisation of information for a particular "function", which is predictably a particular reorganisation within the thalamus preparing a distribution to the cortex. the outmap of the nigra (lateralis reticulata) is less differentiated. pars compacta and nearby dopaminergic elements in strict sense, the pars compacta is a part of the core of basal ganglia core since it directly receives synapses from striatal axons through the striatopallidonigral bundle. the long ventral dendrites of the pars compacta indeed plunge deep in the pars reticulata where they receive synapses from the bundle. however, its constitution, physiology and mediator contrast with the rest of the nigra. this explains why it is analysed here between the elements of the core and the regulators. ageing leads to the blackening of its cell bodies, by deposit of melanin, visible by naked eye. this is the origin of the name of the ensemble, first "locus niger" (vicq d'azyr), meaning black place, and then "substantia nigra" (sömmerring), meaning black substance. structure the densely distributed neurons of the pars compacta have larger and thicker dendritic arborizations than those of the pars reticulata and lateralis. the ventral dendrites descending in the pars reticulata receives inhibitory synapses from the initial axonal collaterals of pars reticulata neurons (hajos and greefield, 1994). groups of dopaminergic neurons located more dorsally and posteriorly in the tegmentum are of the same type without forming true nuclei. the "cell groups a8 and a10" are spread inside the cerebral peduncule. they are not known to receive striatal afferences and are not in a topographical position to do so. the dopaminergic ensemble is thus also on this point inhomogeneous. this is another major difference with the pallidonigral ensemble. the axons of the dopaminergic neurons, that are thin and varicose, leave the nigra dorsally. they turn round the medial border of the subthalamic nucleus, enter the h2 field above the subthalamic nucleus, then cross the internal capsule to reach the upper part of the medial pallidum where they enter the pallidal laminae, from which they enter the striatum. they end intensively but inhomogeneously in the striatum, rather in the matrix of the anterior part and rather in the striosomes dorsalwards. these authors insit on the extrastriatal dopaminergic innervation of other elements of the basal ganglia system: pallidum and subthalamic nucleus. physiology contrarily to the neurons of the pars reticulata-lateralis, dopaminergic neurons are "low-spiking pacemakers", spiking at low frequency (0,2 to 10 hz) (below 8, schultz). the role of the dopaminergic neurons has been the source of a considerable literature. as the pathological disappearance of the black neurons was linked to the appearance of parkinson's disease, their activity was thought to be "motor" . a major discovery has been that the stimulation of the black neurons had no motor effect. their activity is in fact linked to reward and prediction of reward. in a recent review (schultz 2007), it is demonstrated that phasic responses to reward-related events, notably reward-prediction errors, ...lead to ..dopamine release..." while it is thought that there could be different behavioral processes including long time regulation. due to its widespread distribution, the dopaminergic system may regulate the basal ganglia system in many places. regulators of the basal ganglia core subthalamic nucleus as indicated by its name, the subthalamic nucleus is located below the thalamus; dorsally to the substantia nigra and medial to the internal capsule. the subthalamic nucleus is lenticular in form and of homogeneous aspect. it is made up of a particular neuronal species having rather long ellipsoid dendritic arborisations, devoid of spines, mimicking the shape of the whole nucleus. the subthalamic neurons are "fast-spiking pacemakers" spiking at 80 to 90 hz. there are also about 7,5% of gaba microneurons participating in the local circuitry. the subthalamic nucleus receives its main afference from the lateral pallidum. another afference comes from the cerebral cortex (glutamatergic), particularly from the motor cortex, which is too much neglected in models. a cortical excitation, via the subthalamic nucleus provokes an early short latency excitation leading to an inhibition in pallidal neurons. subthalamic axons leave the nucleus dorsally. except for the connection to the striatum (17.3% in macaques), most of the principal neurons are multitargets and feed axons to the other elements of the core of the basal ganglia. some send axons to the substantia nigra medially and the medial and lateral nuclei of the pallidum laterally (3-target 21.3%). some are 2-target with the lateral pallidum and the substantia nigra (2.7%) or the lateral pallidum and the medial(48%). fewer are single target for the lateral pallidum. if one adds all those reaching this target, the main afference of the subthalamic nucleus is, in 82.7% of the cases, the lateral pallidum (external segment of the globus pallidus. while striatopallidal and the pallido-subthalamic connections are inhibitory (gaba), the subthalamic nucleus utilises the excitatory neurotransmitter glutamate. its lesion resulting in hemiballismus is known for long. deep brain stimulation of the nucleus suppress most of the symptoms of the parkinson' syndrome, particularly dyskinesia induced by dopamine therapy. subthalamo-lateropallidal pacemaker as said before, the lateral pallidum has purely intrinsic basal ganglia targets. it is particularly linked to the subthalamic nucleus by two-way connections. contrary to the two output sources (medial pallidum and nigra reticulata), neither the lateral pallidum nor the subthalmic nucleus send axons to the thalamus. the subthalamic nucleus and lateral pallidum are both fast-firing pacemakers. together they constitute the "central pacemaker of the basal ganglia" with synchronous bursts. the pallido-subthalamic connection is inhibitory, the subthalamo-pallidal is excitatory. they are coupled regulators or coupled autonomous oscillators, the analysis of which has been insufficiently deepened. the lateral pallidum receives a lot of striatal axons, the subthalamic nucleus not. the subthalamic nucleus receives cortical axons, the pallidum not. the subsystem they make with their inputs and outputs corresponds to a classical systemic feedback circuit but it is evidently more complex. central region of the thalamus the centromedian nucleus is in the central region of the thalamus. in upper primates it has three parts instead of two, with their own types of neuron. output from here goes to the subthalamic nucleus and the putamen. its input includes fibers from the cortex and globus pallidus. pedunculopontine complex the pedunculopontine nucleus is a part of the reticular formation in the brainstem and a main component of the reticular activating system, and gives a major input to the basal ganglia. as indicated by its name, it is located at the junction between the pons and the cerebral peduncle, and near the substantia nigra. the axons are either excitatory or inhibitory and mainly target the substantia nigra. another strong input is to the subthalamic nucleus. other targets are the gpi and the striatum. the complex receives direct afferences from the cortex and above all abundant direct afferences from the medial pallidum (inhibitory). it sends axons to the pallidal territory of the vl. the activity of the neurons is modified by movement, and precede it. all this led mena-segovia et al. (2004) to propose that the complex be linked in a way or another to the basal ganglia system. a review on its role in the system and in