Search PubMed⌕ Search

Biomedical subjects

G Paxinos

Publications and source records attributed to G Paxinos.

At least 55 records · Page 3Linked to original sources
PubMed1991

Distribution of catecholamine uptake sites in human brain as determined by quantitative [3H] mazindol autoradiography.

Because of the importance of the catecholamine system in Parkinson's disease and its relevance to a variety of clinical movement disorders, catecholamine uptake sites were mapped in the human brain using [3H] mazindol autoradiography. Displacement studies with known dopamine (DA) and noradrenaline (NA) uptake blockers showed that binding in the striatum was to dopamine uptake sites; binding in the locus coeruleus was to noradrenergic uptake sites. By using the selective noradrenergic uptake blocker desmethylimipramine (DMI), a comprehensive map of both DA and NA uptake sites was generated. In general, catecholamine uptake sites were better seen in terminals than in cells of origin or axonal projections. In some areas, such as the locus coeruleus, punctate binding could be seen over individual pigmented cells. A variegated pattern of binding was seen in caudate nucleus and putamen and some correspondence of patches of low binding with striosomes was observed in the caudate. The highest levels of binding to DA uptake sites was observed in the striatum, where regional differences in binding occurred. The most dense binding was seen in the ventral striatum, and a rostral-to-caudal decrement in binding levels in caudate nucleus and putamen was evident. Binding was more intense in the putamen compared to the caudate and within the caudate lower values were seen laterally. The highest levels of binding to noradrenergic uptake sites were in the locus coeruleus and dorsal raphé, although these sites may be on terminals from other projections. Whereas uptake sites were more often evident in known catecholamine pathways, [3H] mazindol binding was seen in some areas where catecholamine neurons or terminals had not been identified previously. These maps of the catecholamine uptake system add further information concerning the nature of the distribution of catecholamines in human brain and provide an important baseline for the study of disease and ageing processes.

Aged↗
PubMed1991

Evidence for plasticity of the dopaminergic system in parkinsonism.

A series of compensatory mechanisms within the dopaminergic system have been shown to maintain clinical function in the presence of dopamine loss. Experimental evidence for increased presynaptic dopamine turnover owing to increased dopamine synthesis, release, and reduced reuptake exists. Direct evidence that these mechanisms maintain extracellular dopamine levels is provided by intracerebral microdialysis techniques. Postsynaptic denervation supersensitivity clearly occurs with D2 dopamine receptors, although this is less evident with D1 receptors. Similarly, mechanisms of plasticity have been shown to be relevant in human postmortem and Positron Emission Tomographic studies of patients with Parkinson's disease. However, although presynaptic increases in dopamine turnover are well documented, postsynaptic D1 and D2 receptor changes have been more difficult to establish, mainly because of methodological difficulties. D2, but not D1, receptor increases have been documented in drug naive Parkinsonian patients with PET techniques. In transplantation of adrenal gland to striatum in animal models and patients with Parkinsonism where clinical improvement occurs, plasticity of host response may be as important as plasticity of the graft. Although some elements of the compensatory mechanism of dopamine plasticity may be deleterious, such as dyskinesias owing to dopamine receptor supersensitivity, the overall effect of delay and minimization of the clinical expression of disease is advantageous. An even greater understanding of the mechanisms involved may assist in developing future therapeutic strategies.

Adrenal Glands↗
PubMed1991

Localization and characterization of endothelin receptor binding sites in the rat brain visualized by in vitro autoradiography.

Endothelin binding sites in rat brain were mapped by quantitative in vitro autoradiography employing [125I]endothelin-1 as radioligand. [125I]Endothelin-1 bound with high affinity and specificity to rat cerebellar sections and was potently displaced by unlabelled endothelins (endothelin-1 greater than endothelin-2 = endothelin-3) and sarafotoxin 6B. The highest densities of endothelin binding sites were found in the cerebellum (especially Purkinje cell layer), choroid plexus and median eminence. High densities were found in the supraoptic and paraventricular hypothalamic nuclei, anterior hypothalamic area, ventromedial hypothalamic nucleus, mammillary nuclei and glomerular layer of olfactory bulb. Moderate densities were found in many thalamic nuclei, the pretectal region, interpeduncular nucleus, suprachiasmatic nucleus, raphe nuclei, tegmental nuclei, olfactory ventricle, red nucleus, subthalamic nucleus, central gray, reticular nuclei, vestibular nuclei, oculomotor and trochlear nuclei, hypoglossal nucleus, motor trigeminal nucleus, nucleus of the trapezoid body and lateral cerebellar nucleus. Low but detectable densities of endothelin binding sites were found in medial geniculate nucleus, fields of Ammon's horn, caudate-putamen, globus pallidus, entopeduncular nucleus, substantia nigra, anterior commissure, internal capsule, anterior pituitary, median preoptic nucleus, septohypothalamic nucleus, superior colliculus and area postrema. These patterns were completely abolished by 1 microM unlabelled endothelin-1, -2 and -3 and sarafotoxin S6B. Brain endothelin binding sites show high affinity for endothelin-1, -2 and -3 and sarafotoxin 6B with highest affinity for endothelin-1. Endothelin binding sites show a non-vascular pattern of distribution in the brain, suggesting that the peptide may have widespread functions as a modulator of neuronal function.

Animals↗
PubMed1991

Angiotensin converting enzyme in the monkey (Macaca fascicularis) brain visualized by in vitro autoradiography.

Angiotensin converting enzyme is localized in the monkey (Macaca fascicularis) brain by in vitro autoradiography using the radiolabelled inhibitor, [125I]351A. This radioligand binds with high affinity and specificity to monkey cortical sections. Specific inhibitors of converting enzyme, lisinopril and perindoprilat complete for the radioligand binding to monkey cortex sections with inhibitory constants of 10 nM. High concentrations of angiotensin converting enzyme occur in most components of the basal ganglia including the caudate nucleus, putamen, the internal and external globus pallidus, nucleus accumbens, ventral pallidum and the reticular part of the substantia nigra. The distribution of converting enzyme in the caudate nucleus and putamen is heterogeneous, with prominent patches of higher activity. The patches in the caudate nucleus correspond closely with the acetylcholinesterase-poor striosomes. In the hypothalamus, very high levels of angiotensin converting enzyme occur in the median eminence and the pituitary stalk and high concentrations occur in the supraoptic and suprachiasmatic nuclei. Moderate, diffuse binding is observed in the median preoptic nucleus, the medial preoptic area, and in the anterior, lateral, ventromedial, posterior and arcuate nuclei. In the circumventricular organs, the subcommissural and subfornical organs exhibit high levels of angiotensin converting enzyme. The organum vasculosum of the lamina terminalis and the pineal body display moderate enzyme activities whereas the area postrema is devoid of labelling. The interpeduncular nucleus and, in the hippocampal formation, the molecular layer of the dentate gyrus are also intensely labelled. High levels of angiotensin converting enzyme activity are also detected throughout the cerebral cortex with laminations of higher activity corresponding to cell dense layers of the cortex. Layered binding is also present in the cerebellar cortex, with the most intense labelling in the molecular layer. Moderate concentrations of converting enzyme also occur in the paraventricular, medial habenula, lateral habenula and central median nuclei of the thalamus, the amygdala, the central gray, the locus coeruleus, the parabrachial nucleus and dorsal tegmental nucleus. The dorsal vagal complex, inferior olivary nucleus and the caudal subnucleus of the spinal trigeminal nucleus all display high levels of binding. Moderate, diffuse labelling is found throughout the reticular region and is also present in the gracile and cuneate nuclei. Although the overall distribution of angiotensin converting enzyme in the monkey brain resembles that in the rat, there are some striking differences. These include the high levels of binding throughout the monkey cerebral cortex and in the interpeduncular and suprachiasmatic nuclei.

Acetylcholinesterase↗
PubMed1991

Angiotensin II receptor subtypes in rat brain.

1. Angiotensin II (AII) receptor binding was localized in the rat brain by in vitro autoradiography using the antagonist analogue, 125I-[Sar1, Ile8] AII. AII receptor binding was then differentiated into type I and type II subtypes by displacement with unlabelled non-peptide antagonists specific for AII subtypes. 2. Type I binding was determined as that inhibited by Dup753 (10 mumol/L) and type II binding as that inhibited by XD329-1 (10 mumol/L). The reducing agent dithiothreitol (DTT) decreased the binding to type I receptors and enhanced the binding to type II receptors. 3. Structures such as the vascular organ of the lamina terminalis, subfornical organ, median preoptic nucleus, area postrema, nucleus of the solitary tract, which are known to be related to some central actions of AII, contain exclusively type I AII receptors. 4. In contrast, the locus coeruleus, ventral and dorsal parts of lateral septum, superior colliculus, subthalamic nucleus, some nuclei of the thalamus, and the nuclei of the inferior olive contain predominantly type II AII receptors. 5. These results reveal important pharmacological heterogeneity of brain AII receptors which suggest different regional functions and are relevant to the central actions of emerging classes of new non-peptide AII receptor antagonists.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1991

Angiotensin II receptor subtypes in rat brain and peripheral tissues.

Angiotensin II (Ang II) receptor binding was localized in rat adrenal gland, kidney, and brain by in vitro autoradiography using the antagonist analogue 125I-[Sar1, Ile8]Ang II and differentiated into type I (AT-1) and type II (AT-2) subtypes using unlabelled non-peptide antagonists specific for Ang II subtypes. AT-1 binding was determined as that remaining in the presence of an excess of the AT-2 antagonist, PD 123177 (10 microM), and AT-2 binding as that remaining in the presence of an excess of the AT-1 antagonist, DUP753 (10 microM). The reducing agent dithiothreitol decreased the binding to AT-1 receptors and enhanced the binding to AT-2 receptors. The rat adrenal gland contains both AT-1 and AT-2 receptors in the ratio of approximately 3:2 in the cortex and 1:9 in the medulla. By contrast, in the kidney only AT-1 receptors were evident in glomeruli, proximal tubule, and inner stripe of the outer medulla. In the brain, the pattern of Ang II receptor subtypes varies greatly from region to region. Many brain structures known to be involved in blood pressure regulation and fluid and electrolyte balance, such as circumventricular organs (including vascular organ of the lamina terminalis, subfornical organ, median eminence, and area postrema), median preoptic nucleus, hypothalamic paraventricular nucleus, and regions in the medulla oblongata involved in autonomic control (nucleus of the solitary tract, dorsal motor nucleus of the vagus, and intermediate reticular nucleus), contain exclusively AT-1 receptors. By contrast, locus coeruleus, lateral septal nuclei, superior colliculus, subthalamic nucleus, many nuclei of the thalamus, and nuclei of the inferior olive contain predominantly AT-2 receptors. The detailed binding characteristics of each subtype were determined by competition studies with a series of antagonists. The pharmacological specificity obtained in kidney, adrenal cortex and adrenal medulla, superior colliculus, and nucleus of the solitary tract produces specificity patterns which confirm the assignments of AT-1 and AT-2 receptors described above. The present study reveals important pharmacological heterogeneity of Ang II receptors in key target organs. The subtype-specific receptor mapping described here is relevant to the understanding of the role of angiotensin peptides in peripheral organs and in the central nervous system and is relevant to the actions of non-peptide Ang II receptor antagonists.

Adrenal Glands↗
PubMed1990

Corticotropin-releasing factor receptors in the rabbit brain visualized by in vitro autoradiography.

Corticotropin-releasing factor (CRF) binding sites were visualized in the rabbit brain by in vitro autoradiography using the radioligand 125I-[Tyr0]ovine CRF. The radioligand binding to sections of rabbit cingulate cortex were competed for by ovine and rat CRF with inhibitory constants (Ki) of 26 and 37 nM, respectively, whereas sauvagine and alpha-helical CRF9-41 were approximately 10-fold less potent. In the rabbit brain, the highest densities of binding sites for CRF are found in the pineal gland and the choroid plexus. The cerebral cortex is labelled throughout, with the highest concentration of binding sites in the piriform and primary olfactory divisions. In the cerebellar cortex, the granular layer is more intensely labelled than the molecular layer. The distribution of CRF binding sites in the hippocampus follows a laminar pattern; the molecular layer of the dentate gyrus is intensely labelled, the oriens, radiatum and lacunosum moleculare layers of Ammon's horn contain moderate densities of binding and no binding is observed in the granular layer of the dentate gyrus and the pyramidal cell layer. The ventral subnucleus of the lateral septum, the zonal and superficial layers of the superior colliculus contain high densities of receptors. A moderate concentration of binding sites is observed in the caudate nucleus, putamen, bed nucleus of the stria terminalis, paraventricular, anterodorsal and anteroventral thalamic nuclei and the medial nucleus of the mammillary body.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Developmental expression of proenkephalin mRNA and peptides in rat striatum.

The development of proenkephalin (PE) gene expression in the rat striatum was examined at the mRNA and peptide levels. Immunocytochemistry was performed with antisera generated to the PE-specific peptide product Met-enkephalin-Arg-Gly-Leu (MERGL). The distribution of immunostaining was compared with the distribution of PE mRNA, determined by in situ hybridization with an oligonucleotide probe. PE mRNA first appeared at E16 in the caudal ventrolateral striatum, followed at E17-18 by the appearance of MERGL immunoreactivity in a similar distribution. The anatomical gradients of PE gene expression were similar to the pattern of histogenesis of striatal neurons, suggesting that the timing of PE gene expression is related to the time of neuronal withdrawal from the mitotic cycle. The relation of the development of PE gene expression to the known patterns of striatal histogenesis, neurochemical compartmentalization and dopaminergic innervation is discussed.

Animals↗
PubMed1988

The effects of various lesions and knife-cuts on septal and amygdala kindling in the rat.

Large bilateral aspiration lesions of the hippocampus had no significant effect on septal kindling, whereas large bilateral DC lesions of the pyriform lobe resulted in a small but significant increase in the number of septal stimulations required to complete kindling. Bilateral aspiration lesions of the dorsal hippocampus or large bilateral DC lesions of the ventral hippocampus had no effect on amygdala kindling. Small DC lesions of the stria terminalis significantly facilitated amygdala kindling. Unilateral or bilateral ventral knife-cuts delivered in a coronal plane anterior to the amygdala, disrupting communication with anterior pyriform structures, produced a small but nearly significant increase in the number of stimulations required for amygdala kindling. Similar cuts placed posterior to the amygdala, disrupting communication with the hippocampus, significantly facilitated kindling. Cuts that were medially placed, to disrupt the ventral amygdala-fugal pathway, had no effect on amygdala kindling. These results show that the hippocampus is not critical for either septal or amygdala kindling. The pyriform lobe structures appear to play a facilitatory role in kindling, but none of the lesions or knife-cuts were capable of blocking or even severely retarding kindling.

Amygdala↗
PubMed1988

Localization and characterization of angiotensin II receptor binding and angiotensin converting enzyme in the human medulla oblongata.

Angiotensin II receptor and angiotensin converting enzyme distributions in the human medulla oblongata were localised by quantitative in vitro autoradiography. Angiotensin II receptors were labelled with the antagonist analogue 125I-[Sar1, Ile8] AII while angiotensin converting enzyme was labelled with 125I-351A, a derivative of the specific converting enzyme inhibitor, lisinopril. Angiotensin II receptor binding and angiotensin converting enzyme are present in high concentrations in the nucleus of the solitary tract, the dorsal motor nucleus of vagus, the rostral and caudal ventrolateral reticular nucleus, and in a band connecting the dorsal and ventral regions. In the rostral and caudal ventrolateral reticular nucleus, angiotensin II receptors are distributed in a punctate pattern that registers with neuronal cell bodies. The distribution and density of these cell bodies closely resemble those of catecholamine-containing neurones mapped by others. In view of the known interactions of angiotensin II with both central and peripheral catecholamine-containing neurons of laboratory animals, the current anatomical findings suggest similar interactions between these neuroactive compounds in the human central nervous system. The presence of angiotensin II receptors and angiotensin converting enzyme in the nucleus of the solitary tract, dorsal motor nucleus of vagus, and rostral and caudal ventrolateral reticular nucleus demonstrates sites for central angiotensin II to exert its known actions on vasopressin release and autonomic functions including blood pressure control. These data also suggest a possible interaction between angiotensin II and central catecholeminergic systems.

Aged↗
PubMed1988

Localization of vasopressin binding sites in rat brain by in vitro autoradiography using a radioiodinated V1 receptor antagonist.

Vasopressin may act in the brain as a neurotransmitter or neuromodulator to influence blood pressure, memory, body temperature and brain development. In order to localize probable central nervous system sites for these actions, we have used 125I-labelled 1-d(CH2)5, 7-sarcosine-8-arginine vasopressin, a specific V1-receptor antagonist, and in vitro autoradiography to map brain vasopressin binding sites. High levels of binding were found in the choroid plexus, blood vessels, lateral septum, bed nucleus of stria terminalis, accumbens nucleus, central nucleus of amygdala, stigmoid hypothalamic nucleus, suprachiasmatic nucleus, arcuate nucleus, nucleus of the solitary tract, area postrema and parts of the hippocampus, thalamus, superior colliculus, and inferior olivary nuclei. Many of these regions are known to be vasopressin-sensitive and to contain vasopressin fibres. Significantly there was no binding to the paraventricular nor the supraoptic nuclei. Displacement of the radioligand from the lateral septum with unlabelled vasopressin analogues gave a rank order of potencies: d(CH2)5-D-Tyr2(Et)Val4-desGly9-arginine-vasopressin approximately equal to d(CH2)5-Tyr2-(Me)arginine-vasopressin approximately equal to arginine-vasopressin approximately equal to d(CH2)5-Sar7-arginine-vasopressin greater than [1-deamino, 8-D-arginine]-vasopressin approximately equal to oxytocin much greater than vasopressin4-9, consistent with binding to V1 receptor subtype. These studies confirm and extend previous findings of V1 receptors in the rat brain. In particular, several new regions of vasopressin receptor binding have been identified, possibly due to the advantages of a radioiodinated ligand with high receptor affinity without binding to neurophysins. Future study of these regions may prove fruitful in elucidating the central actions of vasopressin.

Animals↗
PubMed1988

Vasopressin receptors in rat brain and kidney: studies using a radio-iodinated V1 receptor antagonist.

Arginine8-vasopressin (AVP) acts via V1 receptors (blood vessels, liver and brain) and V2 receptors (renal collecting duct). To study brain and kidney V1 receptors selectively, a specific V1 receptor antagonist [d(CH2)5,Sar7]AVP was radio-iodinated and purified by high performance liquid chromatography. Iodine-125[d(CH2)5,Sar7]AVP bound to single classes of rat liver and kidney V1 receptors with high affinity (liver: Kd = 3.0 +/- 0.9 mol/l and Bmax = 530 +/- 10 fmol/mg protein; kidney: Kd = 0.5 +/- 0.9 nmol/l and Bmax = 11 +/- 8 fmol/mg protein) in a time-dependent and saturable manner. Displacement of the radioligand from liver and renal medulla membranes and sections of the brain and kidneys by unlabelled AVP analogues was consistent with that expected for binding to V1 receptors. In vitro autoradiography of rat brain revealed areas of specific receptor binding in many regions, including regions involved in central cardiovascular regulation, such as the nucleus of the solitary tract and area postrema, as well as choroid plexus and large blood vessels. Binding was observed in several regions not previously observed to contain AVP receptors. In the kidney [3H]AVP bound to the inner and outer medulla, probably to vascular V1 and collecting duct V2 receptors. In contrast, [125I][d(CH2)5,Sar7]AVP binding was only in the inner medulla, possibly to vasa recta. These findings support a functional role for V1 receptors in the brain and kidney.

Animals↗
PubMed1987

Angiotensin receptor binding in human hypothalamus: autoradiographic localization.

Binding of 125I-[Sar1,Ile8]angiotensin II in the human hypothalamus was mapped by in vitro autoradiography carried out on frozen sections of hypothalamus from two human brains. Regions showing the greatest specific binding of this radioligand were the organum vasculosum of the lamina terminalis, median preoptic nucleus, subfornical organ, median eminence, arcuate nucleus and paraventricular nucleus. These regions may be sites of angiotensin II receptors involved in the regulation of blood pressure, fluid balance and pituitary hormone secretion.

Aged↗
PubMed1987

Angiotensin converting enzyme in rat brain visualized by quantitative in vitro autoradiography.

Angiotensin converting enzyme was localized in rat brain by quantitative in vitro autoradiography using an [125I]labelled converting enzyme inhibitor called "351A". This radioligand was found to bind with high affinity and specificity to angiotensin converting enzyme. Very high levels of converting enzyme were observed in the ventricular choroid plexus, ependyma of all ventricles and large and medium blood vessels, subfornical organ, and organum vasculosum of the lamina terminalis. High levels of converting enzyme were found in the basal ganglia including caudate putamen, nucleus accumbens, globus pallidus, entopenduncular nucleus and substantia nigra pars reticulata. The neurosecretory nuclei, paraventricular nucleus and supraoptic nucleus, as well as the median eminence and posterior pituitary displayed high levels of the enzyme. In the amygdala, basolateral, lateral, basomedial, medial and anterior cortical nuclei showed moderate converting enzyme activity. The medial habenula and molecular layer of the dentate gyrus showed high levels of activity. In the cerebellum, dense labelling was observed in the Purkinje cell layer. Moderate levels of converting enzyme occurred in the gelatinosus subnucleus of the caudal part of the nucleus of the spinal tract of the trigeminal. There was a close correspondence between the distribution of angiotensin converting enzyme and angiotensin II in the neurosecretory nuclei (paraventricular and supraoptic nuclei) and median eminence and this suggests a role of angiotensin converting enzyme in the production of angiotensin II in this system. There was also a good correspondence between the distribution of angiotensin converting enzyme and angiotensin II in the subfornical organ, median preoptic nucleus, and organum vasculosum of the lamina terminalis, structures abutting the anterior wall of the third ventricle which are implicated in fluid and electrolyte homeostasis. A striking discrepancy occurs in the basal ganglia which is reported to contain very little angiotensin II or angiotensin II receptors but is very rich in angiotensin converting enzyme. It is concluded that the enzyme may act to convert circulating angiotensin I to angiotensin II in circumventricular organs; generate intraneuronal angiotensin II in pathways such as the hypothalamic-hypophyseal tract; and process neuropeptides other than angiotensin II in regions such as basal ganglia.

Afferent Pathways↗
PubMed1987

Angiotensin II receptors and angiotensin converting enzyme in the medulla oblongata.

Quantitative in vitro autoradiography was used to map angiotensin II (ANG II) receptors and angiotensin converting enzyme (ACE) in sections from rat, rabbit, sheep, and human medulla oblongata and to follow changes in receptor and ACE density after disruption of vagal projections by nodose ganglionectomy in the rat. ANG II receptors and ACE are both concentrated in the nucleus of the solitary tract and dorsal motor nucleus of vagus of the rat, rabbit, sheep, and human. An ANG II receptor-containing band connecting the nucleus of the solitary tract with the dorsolateral medulla was seen in rabbit and human tissue, providing evidence for association of ANG II receptors with vagal afferent fibers. ANG II receptors were found to be concentrated in the rostral and caudal ventrolateral medulla, which corresponded to the region of C1 and A1 catecholamine-containing cell groups in the rabbit. This localization was also evident in rat and human tissue. In all four species, a prominent, ANG II receptor-rich band in the intermediate reticular nucleus was found to connect the ventrolateral medulla and the dorsal vagal complex. In humans and sheep, this band contains puncta that overlie cell bodies. One week after nodose ganglionectomy in the rat, the density of ANG II receptors in the ipsilateral dorsal vagal complex fell markedly. This fall was most prominent in the rostral dorsal motor nucleus of vagus (to 46% of control density) and in the nucleus of the solitary tract (to 56% of control). ACE levels and calcitonin gene-related peptide receptor density were unchanged in both nuclei after ganglionectomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1985

Bregma, lambda and the interaural midpoint in stereotaxic surgery with rats of different sex, strain and weight.

Craniometric and stereotaxic data from rats of different sex, strain and weight were compared. It was found that stereotaxic atlases can be used with rats of different sex and strain provided that the weights of the rats conform to those used in the reference atlas. If rats of different weights are used, greater accuracy can be achieved if bregma is used as the reference point for work with rostral structures and the interaural line for work with caudal structures.

Animals↗
PubMed1982

Neostriatal enkephalin-immunoreactive neurones project to the globus pallidus.

The origin of enkephalin-immunoreactive nerve terminals in the globus pallidus was investigated by combining immunocytochemistry with stereotaxic injection of neurotoxic agents (colchicine and kainic acid) and microknife deafferentations. The intracerebral administration of colchicine, irrespective of whether in the caudate putamen or in globus pallidus, induces the appearance of enkephalin-immunoreactive cell bodies and fibres in the caudate putamen. No immunoreactive cell bodies were depicted in the globus pallidus after this treatment. Kainic acid injections in the caudate putamen produced topographic depletions of enkephalin-immunoreactive terminals in the globus pallidus. The more anterior injections produced medial-anterior depletions, while posterior injections gave latero-posterior depletions. Injections in the globus pallidus produced only a non-specific loss of fluorescence restricted to the tip of the cannula. Coronal microknife cuts produced a combination of build-up and depletion of enkephalin immunofluorescence according to the position of the cut. The build-up of immunoreactive materials was always observed in the caudate-putamen side of the cut while depletions observed in the globus pallidus were related to the extent of deafferentation of this nucleus from the caudate putamen. All these observations confirmed the neostriatal origin (caudate putamen) of the enkephalinergic fibres present in the paleostriatum (globus pallidus).

Animals↗