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In the chick, polyphasic evoked responses displaying a first negative component have been registered in the superficial part of the "Wulst" after stimulation in the depth of the contra or ipsilateral optic tectum, as early as the first hours following hatching. Moreover, responses on the surface of the tectum have been elicited by contra or ipsilateral stimulation of the Wulst. Latencies of both responses decrease markedly with increasing age but, in the whole, ipsilateral responses remain more latent than contralateral responses.
The influence of X-ray irradiation on the dopamine level in brain and in corpus striatum of male albino rats is studied. The changes in the influence of the dopaminergic agonists apomorphine and L-DOPA, applied independently and in combination, on the dopamine level in brain and striatum, are established comparatively (in non-irradiated rats and in rats on the 72nd hour after irradiation with 900 R). Apomorphine is found to have no significant influence on the dopamine level in brain and striatum of non-irradiated rats, while L-DOPA and its combination with apomorphine raise this level. On the 72nd hour after irradiation with 900 R there is no essential change in the dopamine level in brain and the striatum; apomorphine raises the dopamine level in brain and striatum; the effect of L-DOPA and its combination with apomorphine is potentiated with respect to the increase of the dopamine level in brain and striatum.
The number of nerve cells in two different areas of the corpus striatum (i.e., ventrolateral and dorsomedial) was estimated in rat brain after long-term (36 weeks) treatment with the neuroleptic flupenthixol. Nine rats were given weekly injections of 4 mg/kg flupenthixol dissolved in Viscoleo i.m., and seven rats received Viscoleo alone. Fourteen to 18 weeks after the last drug injection, the animals were decapitated and half of each brain was fixated with formalin for cell-count analysis and the remaining half used for a biochemical analysis (Nielsen, 1977). Separate cell counts in the ventrolateral and dorsomedial corpus striatum yielded a significant cell loss of approximately 10%, but only in the ventrolateral striatum of treated animals. These results suggest at least one concrete anatomical basis for the behavioral and biochemical deficits found in the same animals, as reported earlier. The results further suggest that persistent irreversible anatomical changes can follow long-term neuroleptic treatment. The inconsistencies of results regarding cell loss in the corpus striatum may be due to neglect of dorsal-ventral structural differences in corpus striatum.
Neurotransmitter receptor binding of 5 ligands was examined in the striatum, substantia nigra (SN) and frontal cortex of rats which had received either unilateral 6-hydroxydopamine (6-OHDA) lesions of the nigrostriatal pathway (NSP) or unilateral kainic acid lesions of the striatum. 6-OHDA lesions of the NSP significantly reduced [3H]dihydroalprenolol ([3H]DHA) and [3H]naloxone ([3H]Nal) binding by 31% and 28% respectively, in the denervated striatum compared to the contralateral side. Scatchard analysis revealed that the alteration in [3H]DHA binding was not due to a change in the affinity of the beta-adrenergic receptor for [3H]DHA. In marked contrast to these changes in the striatum, destruction of the NSP resulted in a significant increase in [3H]DHA and [3H]Nal binding by 44% and 26%, respectively, in the frontal cortex of the lesioned compared to the control side. 6-OHDA lesions in the NSP did not alter striatal receptor binding for [3H]quinuclidinyl benzilate ([3H]QNB), [3H]muscimol ([3H]Mus) or [3H]flunitrazepam ([3H]Flu). Similarily, intrastriatal kainic acid injections did not alter striatal receptor binding for [3H]Nal, [3H]Flu or [3H]Mus. Of the various receptor densities measured in the SN after the above lesions the only alteration observed was a 43% increase in [3H]Flu binding following 6-OHDA lesions of the NSP. Scatchard analysis indicated no change in the affinity of the benzodiazepine receptor for [3H]Flu. 6-OHDA lesions of the NSP did not alter [13H]QNB or [3H]Nal binding in the SN. Striatal kainic acid lesions did not alter nigral [3H]QNB or [3H]Flu binding. The results are discussed in terms of neurotransmitter localization and plasticity within the striatum, SN and frontal cortex.
Lesion experiments (in the rat) were designed to elucidate the function of the corpus striatum in neuroleptic- and narcotic-induced catalepsy, respectively. Bilateral lesions of the corpus striatum were observed to attenuate neuroleptic (CPZ)-induced catalepsy. However, analogous lesions of the corpus striatum potentiated narcotic (morphine)-induced catalepsy. These results suggests that (a) the corpus striatum may be a primary site of action of neuroleptic drugs (such as CPZ) in the production of catalepsy, and (b) narcotic (morphine)-induced catalepsy may not be exclusively mediated by the corpus striatum.
Projections to the striatum from the prefrontal cortex, the substantia nigra's pars compacta (SNC), and the ventral tegmental area (AVT) were examined autoradiographically. These projections converge on the striatum in an organized manner such that the prefrontal areas innervated by AVT project to the same part of the striatum as AVT, and prefrontal areas innervated by SNC project to the same part of the striatum as SNC.
The influence of histamine on metabolism of dopamine and serotonin in the rat striatum. Acta Physiol. Pol., 1977, 28 (2): 101--105. Histamine-2HC1 (Hi) given in a dose of 500 micron g did not change DA level in the striatum but HVA was increased by approx. 50%. The Hi-induced rise of HVA level was prevented in animals pretreated with an antihistaminic drug--mepyramine. The pretreatment of rats with atropine reduced significantly the Hi-induced rise of HVA concentration. Hi did not significantly influence 5-HT content in the striatum while the level of 5-HIAA was simultaneously increased by 15%. It is concluded that Hi-induced elevation of HVA content is not a direct effect of Hi on dopaminergic neurons but the Hi action is exerted indirectly through cholinergic system. The increase of serotoninergic activity is probably a consequence of an increased activity of dopaminergic neurons in the striatum.
In rats, a single injection of antipsychotic drugs produced a transitory change in the kinetic state of tyrosine hydroxylase (TH) in striatum and nucleus accumbens. The affinity of TH for 2-amino-4-hydoxy-6,7-dimethyl-5,6,7,8-tetrahydropterine (DMPH4) and the Vmax with respect ot tyrosine were increased. The relative potencies of anti-psychotics to change the kinetics of TH in striatum and nucleus accumbens when injected into rats were measured in the presence of 0.4 mM DMPH4. The doses of methiothepin, pimozide and halopridol which increased the affinity for DMPH4 of striatal TH were lower than those required to produce a similar change in nucleus accumbens. In contrast, thioridazine and clozapine were more effective in nucleus accumbens than in striatum. Chlorpromazine was equally active in these two tissues. Haloperidol increased the turnover rate of dopamine in striatum with doses that are relatively smaller than those required in the nucleus accumbens. Clozapine was more active in increasing turnover rate of dopamine in nucleus accumbens; the activity of chlorpromazine in these two tissues was equal. These results suggest that antipsychotics with high incidence of extrapyramidal side effects affect the nigrostriatal dopaminergic pathway selectively.
It has previously been shown that neuroleptic drugs block an apparently inhibitory influence of dopamine on cholinergic interneurons in striatum, thereby increasing acetylcholine turnover. In this study, systemic administration of the neuroleptic, fluphenazine, decreased the acetylcholine content in the striatum but not the neocortex of rats killed by focussed microwave irradiation. The effect was observed with doses of fluphenazine as low as 0.05 mg/kg, and was also seen after two other neuroleptics, spiroperidol (1 mg/kg) and haloperidol (4 mg/kg). In contrast, neither fluphenazine nor haloperidol pretreatment had any effect on the high affinity accumulation of choline by striatal synaptosomes. These observations suggest that after administration of dopamine receptor antagonists the release and metabolism of acetylcholine in the striatum is increased, but that a compensatory increase in choline uptake does not occur, thereby resulting in a temporary decrease in acetylcholine concentration. On the basis of these findings, we conclude that acetylcholine synthesis is regulated differently in the striatum than in other brain regions.
A H3 proline-leucine mixture was injected into the dorsal ventricular ridge (DVR) and striatum of the Tegu lizard in order to determine their efferent projections. The brains were processed according to standard radioautographic technique, and counterstained with cresyl violet. DVR projections were generally restricted to the telencephalon, while striatal projections were limited to diencephalic and mesencephalic structures. Thus the anterior DVR projects ipsilaterally to nuclei sphericus and lateralis amygdalae, striatum (ipsilateral and contralateral) ventromedial nucleus of the hypothalamus, nucleus accumbens, anterior olfactory nucleus, nucleus of the lateral olfactory tract and lateral pallium. Posterior DVR projections enter ipsilateral anterior olfactory nucleus, lateral and interstitial amygdalar nuclei, olfactory tubercle and bulb, nucleus of the lateral olfactory tract and a zone surrounding the ventromedial hypothalamic nucleus. Labeled axons from striatal injections pass caudally in the lateral forebrain bundle to enter (via dorsal peduncle) nuclei dorsomedialis, medialis posterior, entopeduncularis anterior, and a zone surrounding nucleus rotundus. Others join the ventral peduncle of LFB and enter ventromedial nucleus (thalami), while the remaining fibers continue caudally in the ventral peduncle to the mesencephalic prerubral field, central gray, substantia nigra, nucleus intercollicularis, reticular formation and pretectal nucleus posterodorsalis. These results are discussed in relation to the changing notions regarding terminology, classification and functions of dorsl ventricular ridge and striatum.
The effect of various antipsychotic drugs on the blockade of dopaminergic receptors in striatum and limbic forebrain was examined by establishing dose-response curves for the increase in HVA and for the antagonism of d-amphetamine-induced rotation in rats with unilateral lesions of the substantia nigra. A good quantitative correlation was found between dopaminergic blockade in the striatum as reflected by the ED100 for striatal HVA increase and the ED50 for rotational antagonism and the occurrence of extrapyramidal side effects in man. The ED100 for the increase in HVA in the limbic forebrain showed the same rank order of potency as those in the striatum: Haloperidol greater than primozide greater than chlorpromazine greater than thioridazine greater than clozapine. The results thus demonstrate a very good correlation between the degree of dopaminergic blockade and the increase of extrapyramidal side effects in man, but suggest the possibility of a dissociation between dopaminergic blockade and antipsychotic activity.
The interaction of cortico- and nigrofugal inputs to the striatum of the rat was investigated using the technique of evoked potentials. Repetitive, unilateral stimulation of the substantia nigra inhibited potentials which were evoked from the ipsilateral rostral cortex and recorded from the ipsilateral striatum. The inhibition was antagonized by low doses of various intraperitoneally administered neuroleptics such as: pimozide (0.1 - 0.2 mg/kg), haloperidol (0.1 - 0.5 mg/kg), chlorpromazine (0.5 - 2.0 mg/kg) and thioridazine (0.5 - 4.0 mg/kg). These findings are discussed in view of the existing controversy regarding the mode of action of dopamine in the striatum.
Systemic administration of haloperidol to rats failed to alter the concentration of dopamine but increased the concentration of 3,4-dihydroxy-phenylacetic acid (DOPAC), the major metabolite of dopamine, in both the striatum and substantia nigra. These haloperidol-induced changes in DOPAC were prevented by an intranigral microinjection of baclofen, a drug which reduces nigrostriatal dopaminergic neuronal activity. It has been proposed that nigrostriatal neurons are regulated, in part, by the activation of autoreceptors in substantia nigra. However, intranigral microinjections of high concentrations of several dopaminergic antagonists failed to mimic the biochemical effects resulting from systemic administration of these drugs; instead, they slightly increased the concentrations of both dopamine and DOPAC in the striatum and decreased dopamine in substantia nigra. Intranigral microinjections of the dopamine agonist, apomorphine, failed to alter the concentration of DOPAC in the striatum, but reduced both dopamine and DOPAC in the nigra. If DOPAC concentrations reflect nigrostriatal dopaminergic neuronal activity, the present results suggest that dopaminergic agonists and antagonists acting in substantia nigra do not exert a major influence on the activity of these neurons.
The effect of ionizing radiation on the amount of dopamine in corpus striatum was investigated in rats exposed to 650 or 850 R of X-rays. The amount of dopamine in the corpus striatum was measured fluorimetrically in various periods of time after irradiation. It was found that, irrespective of the dose applied, the ionizing radiation caused a significant depletion of dopamine in the striatum.
Kainic acid (3 nmoles bilaterally) was injected into the dorsal striatum of the rat producing virtually complete destruction of cell bodies in this structure but without directly affecting the dopamine terminals ascending from the substantia nigra and terminating in the striatum. Other fibres of passage, such as the internal capsule, were also spared. The locomotor and stereotypy responses to doses of amphetamine, a dopamine releasing agent, were found to be consistently enhanced after this lesion. The stereotypy and locomotor activity in response to the direct receptor agonist, apomorphine, however were not consistently affected. The results are interpreted in terms of a functional dichotomy between dorsal and ventral striatum and in terms of previously demonstrated electrophysiological alterations in the striatonigral feedback loop after kainic acid injection. Similarities are noted with the effects of these two stimulant drugs in human patients with Huntington's disease, thus strengthening the kainic acid animal model of this disease, first proposed on biochemical grounds.
Knife cuts were made that preferentially interrupted (a) the nigrostriatal pathway; (b) pallidofugal projections to the lower brainstem; (c) caudate-pallidal interconnections; and (d) fibers entering or leaving the striatum ventrally. The effects of these cuts on conditioned (shuttle box) avoidance, passive avoidance, swimming escape, sucrose-rewarded alley running, locomotor activity, and various measures of sensory-motor function were examined. The norepinephrine, dopamine and serotonin content of the striatum, residual forebrain and hypothalamus were determined following the completion of behavioral testing. The pattern of results suggests that striatal functions which are significantly influenced by several afferent and efferent connections are essential for the acquisition and, perhaps, execution of complex behavior in appetitive as well as aversive test paradigms. A special role for the dopaminergic afferents to the striatum was not established in these tests.
In neuronal ceroid lipofuscinosis, the small spinous nerve cells of the striatum show a conspicuous pathological change in that they develop spindle-shaped and pigment-filled appendages of the soma. The axon emerges from the tip of these expansions, the volume of which often exceeds that of the cell body. The aspiny neurons of the striatum do not show this alteration. The pigment-filled expansions close to the axon may be considered an early sign of neuronal degeneration. The small spinous nerve cell is the predominant cell type of the striatum which receives inputs from various sources. Its slowly progressive destruction might account for extra-pyramidal motor disturbances in the course of neuronal ceroid lipofuscinosis.