The Prospective and Retrospective Memory Questionnaire: a population-based random sampling study.

The Prospective and Retrospective Memory Questionnaire (PRMQ) has been shown to have acceptable reliability and factorial, predictive, and concurrent validity. However, the PRMQ has never been administered to a probability sample survey representative of all ages in adulthood, nor have previous studies controlled for factors that are known to influence metamemory, such as affective status. Here, the PRMQ was applied in a survey adopting a probabilistic three-stage cluster sample representative of the population of Sao Paulo, Brazil, according to gender, age (20-80 years), and economic status (n=1042). After excluding participants who had conditions that impair memory (depression, anxiety, used psychotropics, and/or had neurological/psychiatric disorders), in the remaining 664 individuals we (a) used confirmatory factor analyses to test competing models of the latent structure of the PRMQ, and (b) studied effects of gender, age, schooling, and economic status on prospective and retrospective memory complaints. The model with the best fit confirmed the same tripartite structure (general memory factor and two orthogonal prospective and retrospective memory factors) previously reported. Women complained more of general memory slips, especially those in the first 5 years after menopause, and there were more complaints of prospective than retrospective memory, except in participants with lower family income.

Effect of antidepressants on melatonin metabolite in depressed patients.

Antidepressants increase melatonin levels, but it is still unclear whether this effect is related to the improvement of depressive symptoms or to unrelated pharmacological action of antidepressants. To answer this question, the effect of antidepressants on 6-sulphatoxymelatonin (aMT6s), the main melatonin urinary metabolite, was examined in drug-free depressed patients - most of them antidepressant-naive. aMT6s was evaluated in 34 depressed patients, before and after 8 weeks of placebo (n = 12) or antidepressant (n = 22; fluoxetine, duloxetine or Hypericum perforatum). Both groups showed an improvement of depressive symptoms after treatment compared to baseline (Hamilton Depression scores): 17.0 +/- 1.4 vs. 9.0 +/- 2.8, P = 0.007 for placebo, and 18.6 +/- 1.1 vs. 11.8 +/- 1.6, P < 0.001 for antidepressants). After treatment, aMT6s levels increased after antidepressants (P < 0.01), but not after placebo (P > 0.05). As depressive symptoms improved both in patients taking antidepressant and in those taking placebo, but an effect of antidepressants could only be seen in those taking antidepressants, we suggest that melatonin changes after antidepressants are more likely due to a pharmacological action of these drugs on melatonin secretion.

Dimensionality of the premenstrual syndrome: confirmatory factor analysis of premenstrual dysphoric symptoms among college students.

Premenstrual syndrome and premenstrual dysphoric disorder (PMDD) seem to form a severity continuum with no clear-cut boundary. However, since the American Psychiatric Association proposed the research criteria for PMDD in 1994, there has been no agreement about the symptomatic constellation that constitutes this syndrome. The objective of the present study was to establish the core latent structure of PMDD symptoms in a non-clinical sample. Data concerning PMDD symptoms were obtained from 632 regularly menstruating college students (mean age 24.4 years, SD 5.9, range 17 to 49). For the first random half (N = 316), we performed principal component analysis (PCA) and for the remaining half (N = 316), we tested three theory-derived competing models of PMDD by confirmatory factor analysis. PCA allowed us to extract two correlated factors, i.e., dysphoric-somatic and behavioral-impairment factors. The two-dimensional latent model derived from PCA showed the best overall fit among three models tested by confirmatory factor analysis (chi(2)53 = 64.39, P = 0.13; goodness-of-fit indices = 0.96; adjusted goodness-of-fit indices = 0.95; root mean square residual = 0.05; root mean square error of approximation = 0.03; 90%CI = 0.00 to 0.05; Akaike's information criterion = -41.61). The items "out of control" and "physical symptoms" loaded conspicuously on the first factor and "interpersonal impairment" loaded higher on the second factor. The construct validity for PMDD was accounted for by two highly correlated dimensions. These results support the argument for focusing on the core psychopathological dimension of PMDD in future studies.

Validation of the Beck Depression Inventory for a Portuguese-speaking Chinese community in Brazil.

The objective of the present study was to investigate the psychometric properties and cross-cultural validity of the Beck Depression Inventory (BDI) among ethnic Chinese living in the city of São Paulo, Brazil. The study was conducted on 208 community individuals. Reliability and discriminant analysis were used to test the psychometric properties and validity of the BDI. Principal component analysis was performed to assess the BDI's factor structure for the total sample and by gender. The mean BDI score was lower (6.74, SD = 5.98) than observed in Western counterparts and showed no gender difference, good internal consistency (Cronbach's alpha 0.82), and high discrimination of depressive symptoms (75-100%). Factor analysis extracted two factors for the total sample and each gender: cognitive-affective dimension and somatic dimension. We conclude that depressive symptoms can be reliably assessed by the BDI in the Brazilian Chinese population, with a validity comparable to that for international studies. Indeed, cultural and measurement biases might have influenced the response of Chinese subjects.

Fluorescent histochemical localization of neutral endopeptidase-24.11 (enkephalinase) in the rat brainstem.

Characterization of the distribution of the peptide-degrading enzyme neutral endopeptidase-24.11 (E.C. 3.4.24.11; NEP; enkephalinase) in the rat brainstem was examined by means of a unique fluorescent histochemical method. Enzyme staining was completely blocked by three potent NEP inhibitors (thiorphan, phosphoramidon, and JHF-26) at a concentration of 50 nM, supporting the specificity of this method to visualize sites of NEP activity selectively. At all levels of the brainstem, NEP was localized to cell bodies, cell processes or terminal-like fields and was localized to more than 90 distinct nuclei or subnuclei. In the mesencephalon these included the central gray, cuneiform n., dorsal and lateral tegmental n., inferior colliculus, interpeduncular n., lateral and medial geniculate n., central linear raphe n., mesencephalic n. of the trigeminal nerve, mammillary nuclei, occulomotor n., red n., superior colliculus, ventral n. of the lateral lemniscus, substantia nigra-ventral tegmental area, and the zona incerta. In the pons, NEP staining was restricted to fewer regions or nuclei, including the dorsal and ventral cochlear n., facial n., motor trigeminal n., principal sensory trigeminal n., parabrachial nuclei, pontine n., the oral and caudal pontine reticular n., pontine olivary nuclei, several pontine tegmental nuclei, pontine raphe nuclei, and the trapezoid n. In the cerebellum, staining was localized largely to the granule cell layer of the cerebellar cortex. Scattered staining was observed in the molecular cell layer. The medulla contained extensive NEP staining localized to nuclei that included the ambiguous n., dorsal motor n. of the vagus, hypoglossal n., inferior olivary n., prepositus hypoglossus n., solitary tract n., nuclei of the spinal tract of the trigeminal n., and the lateral, medial, and superior vestibular nuclei. Nuclei of the medullary reticular formation that were also richly stained for NEP included the raphe magnus n., raphe obscurus n., raphe pallidus n., dorsal, lateral, and ventral reticular nuclei of the medulla, and the gigantocellular, lateral paragigantocellular, linear, paramedian and parvicellular reticular nuclei. The widespread distribution of NEP in the brainstem suggests the existence of a number of functional systems, including the pathways involved in the mechanisms of pain and analgesia, which are potential targets of NEP inhibitors. In most regions, the distribution of NEP closely overlapped with that reported for the enkephalins, and showed a more restricted overlap with the reported distribution of substance P.

Fluorescent histochemical localization of neutral endopeptidase-24.11 (enkephalinase) in the rat spinal cord.

The localization of neutral endopeptidase-24.11 (E.C. 3.4.24.11; enkephalinase) in rat spinal cord was investigated by a novel fluorescent histochemical method. Enkephalinase was localized by using a coupled enzyme assay based upon the sequential cleavage of the synthetic peptide substrate glutaryl-ala-ala-phe-4-methoxy-2-naphthylamide by enkephalinase and exogenous aminopeptidase M. Enzyme distribution was examined in segments from cervical, thoracic, lumbar, and sacral cord. At all spinal cord levels, enkephalinase was localized to discrete regions of the gray matter. The substantia gelatinosa displayed rich enkephalinase staining which overlapped the inner and outer zones of lamina II. A staining pattern similar to that observed in lamina II was observed in the spinal trigeminal nucleus in the medulla. In lamina III the enzyme was associated with small and medium-sized cells. Lamina IV showed staining associated with medium-sized and large cell bodies. The medial boundary of the dorsal gray of laminae IV and V had medium-sized fusiform cells which stained for enkephalinase. In the lateral reticulated areas of lamina V, enkephalinase reaction product was localized to scattered medium-sized and large cells compressed against the white matter of axon bundles. Staining in lamina VI was similar in appearance to lamina V. Enkephalinase reaction product was widely distributed in the ventral horn. Numerous ventral horn motor neurons of varied size and morphology in laminae VIII and XI stained richly for the enzyme. The enzyme was also localized to medium-sized and large cells in lamina X and to cells of the central cervical nucleus. The size and morphology of the cell types associated with the enzyme supported a neuronal association for enkephalinase. The regional distribution of the enzyme overlapped that of enkephalin- and substance-P rich regions of the spinal cord. These findings support a role for enkephalinase in the metabolic regulation of centrally acting neuropeptides.

Differential response of neutral endopeptidase 24.11 ("enkephalinase"), and cholinergic and opioidergic markers to hypoglossal axotomy.

Neutral endopeptidase 24.11 (NEP; "enkephalinase") may inactivate a number of centrally active neuropeptides including the enkephalins and substance P. In most areas of the central nervous system, the cell types which express NEP activity are not known. The hypoglossal nucleus (N.XII) was selected as a model system to characterize the cytochemical localization of NEP. The effect of hypoglossal nerve axotomy upon the distribution of NEP activity in the hypoglossal nucleus was compared to the effect upon cholinergic markers, the mu opiate receptor, and the enkephalins. By use of a fluorescence histochemical method, NEP was localized at all levels of N.XII to the soma and proximal processes of the majority of the apparent motor neurons in the nucleus. Fluorescent double-labeling studies revealed the presence of numerous enkephalinergic varicosities which localized to the neuropil surrounding NEP-stained motor neurons. To determine whether NEP was synthesized by these motor neurons, 18 rats received a unilateral transection of the hypoglossal nerve. A pronounced decrease in NEP staining in N.XII was observed on the operated side as early as 3 days following axotomy. This decrease persisted at all levels of the nucleus for about 5 weeks. By 7 weeks, the staining between the control and operated sides was indistinguishable. By contrast, there was no apparent change in the density or distribution of enkephalin-immunoreactive varicosities in five animals examined 6 to 32 days following axotomy. Radioligand binding of [3H]DAMGO to the mu-opiate receptor in N.XII was studied in 20 animals by quantitative autoradiography at 2, 6, and 11 days after axotomy. No significant changes in the level of radioligand binding to the mu-receptor were detected in response to axotomy. In contrast to the opiate system, the cholinergic enzymes choline acetyltransferase, acetylcholinesterase, and pseudocholinesterase showed a coordinate decrease in motor neuron-associated staining on the operated side of N.XII at 3, 6, and 11 days following axotomy which paralleled the decrease in NEP staining. By contrast, the lysosomal enzyme marker, acid phosphatase, showed a pronounced increase in staining on the operated side. The results of this study are consistent with the synthesis of NEP by cholinergic N.XII motor neurons and indicates that the enkephalins and NEP in N.XII are closely associated, but derive from separate neuronal populations. The widespread overlap in the distribution of NEP-stained motor neurons and enkephalinergic varicosities in N.XII provides additional anatomical support for a potential role for NEP in the inactivation of centrally active enkephalins.(ABSTRACT TRUNCATED AT 400 WORDS)

Redistribution of lipofuscin in aged neurons induced by colchicine.

The effect of a single, 40 micrograms, intracerebroventricular injection of colchicine on the distribution of neuronal lysosomes and lipofuscin granules in aged mice was studied. At the light microscope level we observed that colchicine induced a redistribution of dipeptidyl aminopeptidase II (Dpp II), a lysosomal and lipofuscin granule marker enzyme, from the cell bodies of neurons to the dendrites; cell bodies became depleted of Dpp II while dendrites became enriched with this enzyme. Quantitation of this phenomenon at the electron microscope level demonstrated that colchicine induced a rapid and significant decrease in the density of lysosomes and lipofuscin granules from the somata of neurons whereas in dendrites we observed a significant increase in the density of these organelles.

Dissociation of the acute effects of alcohol on implicit and explicit memory processes.

The effects of alcohol (0, 0.3 and 0.6 g/kg) on learning and memory were assessed in independent groups of male student volunteers. Subjects were shown a list of words and asked to form an image of a scene involving each word 1 hr after drinking an alcohol-containing beverage. Alcohol consumption impaired the ability of subjects to explicitly remember the words in a test of free recall. However, no impairment was observed if memory for the same material was assessed implicitly using a backwards-reading or word-completion task. That is, both alcohol-and placebo-treated subjects showed similar degrees of priming. The data indicate that alcohol's effects on memory are selective.

Residual and acute effects of flurazepam and triazolam in normal subjects.

Residual and acute effects of flurazepam and triazolam were studied in two double-blind, crossover, placebo controlled, single-dose experiments. Psychological and physiological effects were determined 10 h after night administration (flurazepam 30 mg and triazolam 0.5 mg), and for 6 h after morning ingestion (flurazepam 15 mg and triazolam 0.25 mg). Both drugs produced similar "hangover" effects, impairing motor performance and increasing sleepiness on the following morning. After morning administration pronounced sedative effects were found with triazolam, while flurazepam effects were mild and hard to distinguish from placebo. The clinical relevance of these findings is discussed, suggesting that these drugs may be conceived as belonging to two different types of hypnotic agents.

Tranylcypromine isomers: single-dose effects in normal human subjects.

Moderately high single doses of (+)- and (-)tranylcypromine were given to normal subjects, in the morning and evening, in two double-blind placebo-controlled experiments. Effects were determined up to 24h later by psychological and physiological measures. No significant differences were found on most measures, but the subjects consistently reported stronger effects after the (+)isomer. Both active drugs induced sedative effects when given in the morning. Following the evening administration, delayed sleep onset was reported after the (-)isomer, while the (+)isomer was associated with more awakenings during the night. The mechanisms responsible for these effects are discussed.

Acute reversal of flunitrazepam effects by Ro 15-1788 and Ro 15-3505: inverse agonism, tolerance, and rebound.

A phase 1 double blind crossover comparison of a new benzodiazepine antagonist (Ro 15-3505) with Ro 15-1788 and placebo, in the reversal of sedative and psychophysiological effects of single IV doses of flunitrazepam (2 mg), was carried out in 12 normal volunteers. The antagonists were equally effective, leading to full reversal of all effects with a potency ratio of approximately 2.5 mg Ro 15-1788 for 1 mg Ro 15-3505. Inverse agonism, in the form of unpleasant feelings and symptoms, was reported by all subjects following Ro 15-3505 but none after Ro 15-1788. Adaptational phenomena such as acute tolerance and rebound of sedative effects of flunitrazepam were also detected and their potential implications are discussed.

Colchicine causes intrasomatic neurofilament bundles in the mesencephalic trigeminal nucleus and intradendritic bundles in other brain regions.

The effect of a single intracerebroventricular injection of colchicine on the distribution of organelles in neurons of the mesencephalic nucleus of the trigeminal nerve, the inferior colliculus and the deep cerebellar nuclei was studied. In the mesencephalic nucleus of the trigeminal nerve colchicine produced a dramatic accumulation of neurofilament bundles in the soma of these neurons and did not produce a reduction in the number of lysosomes. In other neuronal populations studied, colchicine produced neurofilament bundles in the dendrites and a reduction of lysosomes from the soma of neurons.

Fate of lysosomes transported to the dendrites by a colchicine-induced mechanism.

Lysosomes in hypoglossal motoneurons were retrogradely labeled with fluorescent latex microspheres and their distribution as well as that of acid phosphatase was examined after a single 50 microgram intracerebroventricular (i.c.v.) injection of colchicine. In saline injected controls the fluorescent label was distributed mainly in cell bodies. Twenty-four hours after the colchicine injection we observed a re-distribution of fluorescent label from the cell body of neurons to the dendrites. Seventy-two hours after the colchicine injection the fluorescent label had returned from the dendrites to the cell body. A similar pattern was obtained by following the effect of colchicine on the distribution of acid phosphatase reaction product. We conclude that the reappearance of fluorescent label in cell bodies following colchicine treatment is the result of the retrograde transport of dendritic lysosomes.

The localization of GABAA receptors in mice with mutations affecting the structure and connectivity of the cerebellum.

The distribution of cerebellar [3H]muscimol binding sites was studied autoradiographically in normal C57BL/6J mice and in the weaver, reeler, Purkinje cell degeneration and staggerer mutant mice. In the normal 79-day-old mouse cerebellum, the highest concentration of [3H]muscimol binding sites was observed in the granule cell layer. A much lower grain density was present over the Purkinje cell and molecular layers and negligible numbers of binding sites were seen over the deep cerebellar nuclei and white matter. A significant decrease in [3H]muscimol labeling was observed over the cerebellar cortex of the 81-86-day-old weaver mutant; this was most pronounced in the vermis where granule cell loss was the greatest. Over the hemispheres, where fewer granule cells degenerate, a higher density of binding sites remained. In the 27-29-old reeler cerebellum, where Purkinje cells are malpositioned, no labeling was seen over the deep Purkinje cell masses. In the quasi-normal superficial cortex, labeling density over the surviving granule cell layer was only slightly decreased. In the 54-57-day-old Purkinje cell degeneration mutant, where essentially all Purkinje cells have disappeared by day 45, a 29% decrease in grain density over the granule cell layer was observed, while labeling was still present in the molecular layer. Virtually no [3H]muscimol labeling was detected over any part of the cerebellar cortex of the 25-27-day-old staggerer mutant (which lacks parallel fiber-Purkinje cell synapses), although clusters of surviving granule cells were present in significant numbers in the lateral aspects of the cortex. Our autoradiographic data indicate that GABAA receptors are associated with granule cells in both the molecular and granule cell layers. Furthermore, our results raise the possibility that the maintenance of receptor levels may be dependent upon synaptic contacts between the granule cell and its main postsynaptic target, the Purkinje cell.

'Non-specific' cholinesterase-containing neurons of the dorsal thalamus project to medial limbic cortex.

Thalamocortical neurons that contain 'non-specific' cholinesterase (ChE) were studied with cholinesterase histochemistry and experimental axonal tracing techniques in adult rats. In addition to the presence of ChE that is ubiquitous in capillary endothelium, neurons that contain ChE are found in 3 distinct regions of the dorsal thalamus, the thalamic reuniens nucleus (Re), the anterior dorsal nucleus (AD) and a region that includes the lateral part of the central lateral nucleus (CL) and the ventral portion of the lateral dorsal nucleus (LD). ChE activity appears light in cerebral cortex in general but histochemical staining is slightly greater in neuropil of the cingulate gyrus. Anterograde transport techniques with autoradiography demonstrated that neurons in the LD-CL region project to anterior cingulate cortex and the dorsal retrosplenial area. Anterograde degeneration techniques demonstrated that AD projects primarily to ventral retrosplenial cortex. Injections of horseradish peroxidase (HRP) in the anterior cingulate cortex resulted in double labeled cells (cells containing both ChE and HRP reaction products) primarily in LD and CL. HRP injections into ventral retrosplenial cortex resulted in double labeled cells in AD and Re. HRP injections in the subiculum resulted in double labeled cells in Re. Lesions placed in the region of thalamocortical projections resulted in a loss of ChE in the ipsilateral cingulate gyrus, as measured both histochemically and enzymatically. The finding that neurons containing ChE project to medial limbic cortex suggests that the ChE may be involved in the function of the thalamocortical component of the limbic system.

The effect of antimitotic agents on the intraneuronal distribution of lysosomes.

We previously showed that a single injection of colchicine into the lateral cerebral ventricle of the rat causes a redistribution of lysosomes from their normal localization in neuronal cell bodies into dendrites. In the present report we have examined the time course and specificity of this effect using a variety of microtubule poisons. Dipeptidylaminopeptidase II (Dpp II), a lysosomal marker enzyme, histochemistry was used to visualize lysosomes at the light microscopic level. Acid phosphatase, another lysosomal enzyme, histochemistry was used to confirm the Dpp II localization of lysosomes. Two h after an intracerebroventricular (i.c.v.) injection of colchicine, the distribution of neuronal lysosomes was drastically altered. Lysosomes in a number of neuronal populations were observed to move from the soma to the dendrites. This effect was maximal between 12 and 24 h and was partially reversed by 96 h. Injections of colcemid or podophyllotoxin, drugs that bind to tubulin rapidly, and much less tightly than colchicine, produced a much less pronounced alteration in the intraneuronal distribution of lysosomes. Injections of vinblastine or vincristine, whose binding kinetics range between that of colchicine and that of colcemid and podophyllotoxin, resulted in a redistribution of lysosomes which was less pronounced than the effects of colchicine but more pronounced than that caused by colcemid and podophyllotoxin. Likewise, treatment with other related compounds, 2-methoxy-5-(2',3',4'-trimethoxyphenyl)tropone (A-C compound) and lumicolchicine, whose binding to tubulin is extremely rapid and reversible or non-existent, produced little or no alteration in the intraneuronal distribution of lysosomes. The results suggest that lysosome redistribution may be dependent upon a relatively slow dissociation rate constant of these drugs from tubulin, and this transport may occur when normal microtubule function is compromised.

Neuronal localization of pseudocholinesterase in the rat cerebellum: sagittal bands of Purkinje cells in the nodulus and uvula.

The histochemical distribution of pseudocholinesterase was studied in the rat cerebellum using Koelle's copper-thiocholine method. Throughout the cerebellum, pseudocholinesterase is uniformly localized in the endothelial cells of blood vessels and in the cell bodies and processes of the Bergmann glia. In addition, we demonstrate that exclusively in the ventral uvula and in the nodulus (lobules IXc and X of Larsell) pseudocholinesterase is localized in a small subpopulation of Purkinje cells. The cell bodies and dendrites of these labeled Purkinje cells form at least 4 distinct parallel bands extending along the sagittal plane of each of the lobules. Two broad bands on either side of the midline, approximately 800-900 microns wide and composed of 15-20 Purkinje cells have been designated as A bands. Two narrower bands, approximately 160-300 microns wide and composed of 5-7 Purkinje cells, on the lateral aspects of the lobules have been designated as B bands. The unique distribution of pseudocholinesterase in a small and anatomically restricted population of neurons suggests that in the cerebellum this enzyme may play a role in the metabolism of neuroactive substances.

Distribution of 'non-specific' cholinesterase-containing neurons in the dorsal thalamus of the rat.

This report describes the distribution of histochemically identified 'non-specific' cholinesterase (ChE)-containing neurons in the dorsal thalamus of the rat. Juvenile or young adult Long-Evans or Sprague-Dawley rats were sacrificed by formalin perfusion. Some animals received systemic injections of 1.5-2.0 mg/kg DFP 4-24 h prior to sacrifice. Separate series of 50 micron frozen sections were processed for cholinesterase histochemistry using acetylthiocholine, butyrylthiocholine, or propionylthiocholine as substrates. Adjacent sections processed with each of the 3 substrates allowed comparison of the distributions of neurons containing the histochemical reaction products. Neurons containing moderate to high concentrations of ChE reaction product were found in 3 distinct regions of the dorsal thalamus. First, neurons staining intensely for ChE were found in a cluster that corresponds to the thalamic reuniens nucleus. Second, a cluster of neurons staining intensely for ChE was found in a region that included the lateral part of the central lateral nucleus and extended laterally into the ventral-lateral part of the lateral dorsal nucleus. Third, moderate ChE staining was observed in the neurons of the anterior dorsal nucleus. Of these regions, only the anterior dorsal nucleus shows moderate to high levels of acetylcholinesterase. The function of ChE in normal brain function is unknown. It is particularly interesting, however, that the thalamic nuclei containing ChE-positive neurons send thalamocortical projections to the medial limbic cortex, including cingulate, retrosplenial and subicular cortices.

Redistribution of neuronal lysosomes induced by colchicine: an electron microscopic quantitative study.

We have previously demonstrated that a single injection of the microtubule poison colchicine, into the lateral cerebral ventricle of the rat, induced a rapid redistribution of the lysosomal marker enzymes, dipeptidylaminopeptidase II (Dpp II) and acid phosphatase, from their normal location in neuronal cell bodies out into the dendrites. In the present study, we have quantitatively analyzed this phenomenon at the electron microscopic level by identifying and counting the number of lysosomes and mitochondria in neuronal cell bodies and dendrites of control and colchicine-treated rats. Areas examined included the anterior dorsal (AD) thalamus, pontine nucleus, and facial nucleus. The results show that the cytoplasm of these neurons contains significantly fewer large lysosomes after treatment with colchicine while the dendrites become abnormally enriched with large and small lysosomes after treatment. Lysosomes were rarely seen in the axons of either control or colchicine-treated animals. A significant increase in the density and the shape of mitochondria was also observed in the dendrites following colchicine treatment. The data presented support the hypothesis that neurons contain a transport system which selectively translocates lysosomes, and possibly other organelles, into dendrites. The size, shape, and number of these organelles may change as a result of this transport.