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At least 865 records · Page 48Linked to original sources
PubMed1989

Bilateral transection of the lateral olfactory tract but not removal of the vomeronasal organs inhibits short-photoperiod-induced testicular regression in golden hamsters.

It is now known that removal of the olfactory bulbs increases basal gonadotropin secretion and prevents short-photoperiod-induced testicular regression in Syrian hamsters. The experiments described in the present paper were an attempt to determine which neuronal systems associated with the olfactory bulbs are responsible for this influence on the reproductive neuroendocrine axis. In the first experiment, removal of the vomeronasal organ failed to influence gonadotropin secretion or testes weight in hamsters on long or short photoperiod, suggesting that the vomeronasal-accessory olfactory pathway is not individually responsible for the effect of the olfactory bulbs on gonadotropin secretion. In the second experiment, bilateral transection of the lateral olfactory tracts (LOT) did prevent short-photoperiod-induced testicular regression and the associated decrease in gonadotropin secretion. Since the nervus terminalis is confined to the surface of the medical olfactory bulb pathway, the results of LOT transection indicate that the nervus terminalis, which itself contains gonadotropin releasing hormone, does not mediate the influence of the olfactory bulbs on gonadotropin secretion. These results further suggest that the olfactory bulb influence on gonadotropin secretion is due to neural connections to the pyriform cortex, entorhinal cortex or amygdala.

Animals↗
PubMed1982

The telencephalic limbic system and experimental gastric pathology: a review.

The effects of lesions and stimulations of the telencephalic limbic system on experimental gastric ulcers and erosions are reviewed. It is concluded that the centromedial amygdala and the anterior cingulate gyrus are facilitatory structures, whereas the medial prefrontal cortex, posterior cingulate cortex, entorhinal cortex, hippocampus and posterolateral amygdala are inhibitory areas during stressful experiences, e.g., immobilization. Both the centromedial amygdala and the anterior cingulate gyrus may be part of an "ancillary" pain system, mediating the affective components of aversive experiences. The inhibitory structures, on the other hand, are assumed to be part of a "preventive" mechanism which is initiated by the selective nuclear binding of glucocorticoids when under stress.

Amygdala↗
PubMed1983

Intrahippocampal bethanechol in rats: behavioural, electroencephalographic and neuropathological correlates.

Unilateral microinjections of bethanechol chloride into the CA3 subfield of the dorsal hippocampus in unrestrained rats produced a seizure-related type behavioural and disseminated brain damage syndrome. Injection of bethanechol in the dose of 50 micrograms resulted in locomotor activation, mouth movements, teeth chattering, chewing, wet dog shakes and mild limbic seizures. Shortly after intrahippocampal injection the electroencephalogram (EEG) showed an increase in the frequency of the theta rhythm in both hippocampi. Then EEG showed spiking activity of high frequency in the injected hippocampus, with rapid propagation to the lateral septum, amygdala, neocortex and contralateral hippocampus. The periods of spiking activity of high frequency were followed by depression in the background EEG rhythm with some interspersed spike and wave complexes of very low frequency. Histological examination of frontal forebrain sections revealed disseminated, apparently seizure-mediated pattern of brain damage. The patterning of distant damage after intrahippocampal injections of bethanechol involved the piriform cortex, entorhinal cortex, olfactory tubercle, anterior olfactory nucleus, subiculum, amygdaloid complex, temporoparietal cortex and hypothalamic nuclei. Neuropathological alterations were occasionally observed in the lateral septum and thalamus. These results seem to establish a causative relationship between excessive stimulation of cholinergic muscarinic receptors in the hippocampal formation and epileptic brain damage.

Acetylcholine↗
PubMedDate not supplied

Microvascular changes in aged rat forebrain. Effects of chronic nimodipine treatment.

In the present study the effects of long-term treatment with the 1,4-dihydropyridine calcium antagonist nimodipine on ultrastructural alterations of the microvascular morphology were examined in the frontoparietal cortex, entorhinal cortex and CA1 of the hippocampus in the aged rat. Qualitative observations of cerebral microvasculature of aged (30 months) Wistar rats revealed the presence of microvascular fibrosis, membranous inclusions within the basement membrane and basement membrane thickenings. In several cortical regions the percentage of aberrant microvessels was significantly reduced in the nimodipine-treated rats. The observed microvascular anomalies were classified into five distinct categories of which microvascular fibrosis type II, defined as collagen deposits up to 1 micron within the microvascular basement membrane, showed the strongest reduction in the nimodipine-treated cases. The decrement of the percentage of aberrant microvessels and the relative occurrence of several classes of microvascular deviations showed some variation in the various brain regions examined and was most pronounced in frontoparietal cortex layer III. These results may provide a morphological basis for the improved motor and cognitive performance in aged rats after long-term oral nimodipine administration.

Aging↗
PubMed1988

Trimethyltin-induced neuronal damage in the rat brain: comparative studies using silver degeneration stains, immunocytochemistry and immunoassay for neuronotypic and gliotypic proteins.

Trimethyltin is a neurotoxicant which produces a distinct pattern of neuronal cell death following peripheral administration of a single dose (8 mg/kg, i.p.) in rats. The cupric-silver degeneration stain was used to produce an atlas documenting the distribution and time course of trimethyltin-induced neuronal damage in adult, male Long-Evans rats. Animals were examined at survival times of 1, 2, 3, 4, 5, 7, 10 and 18 days after intoxication. The earliest degeneration was observed at day 1 in the intermediate and ventral divisions of the lateral septal nucleus, followed by development of degeneration on days 2-4 in neuron populations including the septohippocampal nucleus, septohypothalamic nucleus, anterior olfactory nucleus, bed nucleus of the stria terminalis, endopiriform nucleus, parafascicular nucleus, superior colliculus, interstitial nucleus of the posterior commissure, inferior colliculus, pontine nuclei, raphe nuclei, pars caudalis of the spinal trigeminal nucleus, the caudal aspect of nucleus tractus solitarius, dorsal vagal motor nucleus, granule cells in the dentate gyrus, pyramidal cells in CA fields of the hippocampus, and of neurons in the subiculum, pyriform cortex, entorhinal cortex and neocortex (mainly layer Vb and VI). This was followed by degenerative changes on days 5-7 in other structures, including the amygdaloid nuclei, the ventral posterolateral and ventral posteromedial thalamic nuclei and the periaqueductal gray. The distribution of terminal degeneration from these neurons indicate that specific pools of cells are affected in each structure, and the time course suggests somatofugal degeneration. The trimethyltin damage was also assessed with immunocytochemical visualization of a neuronotypic protein, protein-O-carboxyl methyltransferase and a radioimmunoassay for glial fibrillary acidic protein. Protein-O-carboxyl methyltransferase immunoreactivity was altered in neuronal populations damaged by trimethyltin, but did not appear to be either as sensitive or selective an assay of neuronal damage as the silver stain, especially at short survival times. Glial fibrillary acidic proteins were dramatically elevated 21 days after trimethyltin intoxication, particularly in areas of extensive damage. These studies revealed advantages and problems encountered in the use of each technique in assessing neurotoxic effects, forming a basis for discussion of the relative merits of using a battery of specific molecular probes for neurotoxicity evaluations.

Animals↗
PubMed1995

Increased messenger RNA expression of the 695 and 751 amino acid isoforms of the beta-amyloid protein precursor in the thalamus of 17-year-old cynomolgus (Macaca fascicularis) monkeys.

The levels of expression of messenger RNAs of the 695 and 751 amino acid isoforms of the beta-amyloid protein precursor in the brains of three-year-old and 17-year-old cynomolgus monkeys (Macaca fascicularis) were visualized and quantified by in situ hybridization histochemistry using 35S-labelled oligonucleotide probes. The analysis was carried out on coronal brain sections taken through the hippocampus and thalamus at the level of the geniculate nuclei. High densities of beta-amyloid protein precursor695 and beta-amyloid protein precursor751 messenger RNAs were found in the medial aspects of the mediodorsal, centromedian and parafascicular nuclei of the 17-year-old monkeys. The messenger RNA levels of the 695 and 751 isoforms were about two- and seven-fold, respectively, those found in the same nuclei of the three-year-old animals. The levels of these messenger RNA transcripts in the 17-year-old monkeys were not significantly different from those in the three-year-old animals in other brain areas e.g. the temporal cortex, entorhinal cortex and hippocampus. No Alzheimer's disease-like neuropathology in terms of diffuse or senile beta-amyloid plaques, dystrophic neurites or neurofibrillary tangles were detectable by specific innumohistochemical procedures in the above thalamic nuclei of the 17-year-old animals. In addition no reactive gliosis was seen in the thalamus of these monkeys.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1995

Effects of the novelty or familiarity of visual stimuli on the expression of the immediate early gene c-fos in rat brain.

To investigate substrates of recognition memory, the cellular expression of Fos protein in rat brain has been studied after groups of rats were either shown sets of novel or highly familiar objects, or were exposed to the same pattern of illumination without objects being shown. Counts of stained nuclei were made in eight brain regions, where information about novel or familiar visual stimuli is likely to be processed or stored. The counts were relatively high in occipital visual association cortex and area TE of temporal cortex, intermediate in perirhinal cortex, entorhinal cortex, anterior cingulate cortex and the diagonal band of Broca, and low in the hippocampal formation and mediodorsal nucleus of the thalamus. The number of Fos-stained cells was significantly higher for the rats shown novel objects than for those shown familiar objects in perirhinal cortex, area TE, occipital cortex and anterior cingulate cortex. Arguments are advanced that these differences in counts indicate areas involved in the processing and/or storage of information about the novelty or familiarity of visual stimuli, information important to recognition memory.

Animals↗
PubMed2006

Synaptosomal glutamate release and uptake in mice lacking the cellular prion protein.

Glutamate plays a central role in the fast excitatory synaptic transmission and is a key neurotransmitter involved in several neurophysiological processes. Glutamate levels on the synaptic cleft are related to neural excitability, neuroplasticity, and neuronal damage associated with excitotoxicity. Mice lacking the cellular prion protein (PrP(c)) gene (Prnp) present a decreased astrocytic glutamate uptake in cultures, higher neuronal excitability in vitro and sensitivity to pro-convulsant drugs in vivo, and age-dependent memory impairment. Here, we investigate if PrP(c) might be involved in neuronal uptake and release of glutamate. For this purpose, we compared synaptosomal preparations from the cerebral cortex, entorhinal cortex, hippocampus, cerebellum, and olfactory bulb of 3- or 9-month-old PrP(c) null mice and with respective wild-type controls. Although we observed differences in synaptosomal glutamate release and uptake regarding the age of mice and the brain structure studied, these differences were similar for PrP(c) null mice and their respective wild-type controls. Therefore, despite a possible correlation between neuronal glutamate transporters, excitability, and neuronal damage, our results suggest that PrP(c) expression is not critical for neuronal glutamate transport.

Animals↗
PubMed2000

Electroconvulsive seizures modulate levels of thyrotropin releasing hormone and related peptides in rat hypothalamus, cingulate and lateral cerebellum.

We have studied the neuroanatomic extent of electroconvulsive (ECS)-responsive prepro-TRH and TRH-related gene expression and its possible interaction with forced swimming. Young adult male Wistar rats were treated in a 2x2 Latin square protocol of swimming, no swimming, three daily ECS or sham ECS. Sixteen different brain regions were dissected and immunoreactivity measured for TRH (pGlu-His-Pro-NH(2)); TRH-Gly, a TRH precursor; Ps4, a prepro-TRH-derived TRH-enhancing decapeptide, and EEP (pGlu-Glu-Pro-NH(2)). ECS, in addition to elevating TRH-immunoreactivity (TRH-IR), TRH-Gly-IR, Ps4-IR and EEP-IR levels in the limbic regions, as we have previously reported, also significantly increased Ps4-IR levels in hypothalamus, posterior cingulate and lateral cerebellum, and increased TRH-Gly-IR levels in hypothalamus. Interestingly, the combination of ECS and swimming significantly reduced the levels of TRH-Gly-IR in the anterior cingulate compared to the sham ECS-no swim group. The combined use of high-pressure liquid chromatography and the EEP radioimmunoassay (RIA) revealed that pGlu-Tyr-Pro-NH(2) and/or pGlu-Phe-Pro-NH(2) occur in amygdala, anterior cingulate, frontal cortex, entorhinal cortex, lateral cerebellum and striatum and make a substantial contribution to the EEP-IR and TRH-IR. We conclude that ECS can alter the expression and secretion of TRH-related peptides in the hypothalamus, cingulate and lateral cerebellum. Such effects have not previously been reported in these limbic and extra-limbic regions which are increasingly implicated in the autonomic, behavioral and volitional changes which accompany severe depression and its treatment.

Animals↗
PubMed2002

Electrophysiological, behavioral and metabolical features of globus pallidus seizures induced by a microinjection of kainic acid in rats.

There has been few studies of the globus pallidus in relation to epilepsy. In this study, kainic acid (KA)-induced globus pallidus seizure was electrophysiologically, electroencephalographically, histopathologically and metabolically investigated in rats. Sixteen Wistar rats weighing 250-350 g were used. Under intraperitoneal pentobarbital anesthesia, a stainless-steel cannula was inserted stereotaxically into the left globus pallidus pars externa (GPe) for KA injection. For recording EEG, a depth electrode was inserted into the left GPe, just posterior to the tip of the injection guide cannula. Electrodes were also inserted into the right globus pallidus and bilateral sensorimotor cortex (SMC). EEG changes after KA injection were classified as follows: Continuous low-voltage spikes were observed in the left GPe on EEG at stage 1. Intermittent multiple spikes and wave complexes began to propagate to the left SMC at stage 2. Continuous spikes and wave complexes began to propagate to the bilateral SMC at stage 3. Secondary generalized seizures were observed at stage 4. Globus pallidus seizures recurred every 7-9 min and lasted for 4-6 h. However, the seizures gradually subsided and became normal within 18 h. No spontaneous seizure was detected for the next 30 days. Histopathological study revealed a small gliotic lesion with neuronal cell loss around the cannula tip. Neither degeneration nor neuronal cell loss in the ipsilateral hippocampus were observed. The autoradiogram using [14C]2-deoxyglucose during seizure status demonstrated a remarkable increase of local cerebral glucose utilization not only in the GPe but also in the GPi. An increase glucose metabolism was also found in the follows: the medial and lateral septal nucleus, substantia nigra, hippocampus, frontal cortex, parietal cortex, piriform cortex, entorhinal cortex, accumbens nucleus, ventral and lateral nucleus of the thalamus, amygdala, and ventral nucleus of hypothalamus. KA injection into the unilateral GPe evoked not only epileptic excitation of the cortex but also transient enhancement of the globus pallidus-substantia nigra circuit.

Action Potentials↗
PubMed1997

Selective reduction of monoamine oxidase A and B in the frontal cortex of subordinate rats.

We have previously shown that subordination causes a reduction in the levels of 5-hydroxytryptamine and dopamine selectively in the frontal cortex [6]. These monoamines are catabolised mainly by the enzyme monoamine oxidase (MAO) which exists in two isoforms; MAO-A and MAO-B. The present study was carried out to determine whether there is any change in the activity of these two iso-enzymes induced by subordination and if any such alteration is confined to the frontal cortex. The animal model of dominance-subordination used was a worker-parasite paradigm in male Wistar rats. The enzyme activities were measured in five brain regions, the frontal cortex, entorhinal cortex, hippocampus, hypothalamus and striatum, using kynuramine as the substrate. Clorgyline and L-deprenyl were used in vitro to block the activities of MAO-A and MAO-B, respectively. There was a significant (P < 0.001) reduction in the activity of MAO-A as well as MAO-B selectively in the frontal cortex of the subordinate animals. This finding may suggest a reduced neurotransmitter turnover in the serotonergic and dopaminergic neurons terminating in the frontal cortex.

Animals↗
PubMed1999

The 5HT(1A) receptor ligand, S15535, antagonises G-protein activation: a [35S]GTPgammaS and [3H]S15535 autoradiography study.

4-(Benzodioxan-5-yl)1-(indan-2-yl)piperazine (S15535) is a highly selective ligand at 5-HT(1A) receptors. The present study compared its autoradiographic labelling of rat brain sections with its functional actions, visualised by guanylyl-5'-[gamma-thio]-triphosphate ([35S]GTPgammaS) autoradiography, which affords a measure of G-protein activation. [3H]S15535 binding was highest in hippocampus, frontal cortex, entorhinal cortex, lateral septum, interpeduncular nucleus and dorsal raphe, consistent with specific labelling of 5-HT(1A) receptors. In functional studies, S15535 (10 microM) did not markedly stimulate G-protein activation in any brain region, but abolished the activation induced by the selective 5-HT(1A) agonist, (+)-8-hydroxy-dipropyl-aminotetralin ((+)-8-OH-DPAT, 1 microM), in structures enriched in [3H]S15535 labelling. S15535 did not block 5-HT-stimulated activation in caudate nucleus or substantia nigra, regions where (+)-8-OH-DPAT was ineffective and [3H]S15535 binding was absent. Interestingly, S15535 attenuated (+)-8-OH-DPAT and 5-HT-stimulated G-protein activation in dorsal raphe, a region in which S15535 is known to exhibit agonist properties in vivo [Lejeune, F., Millan, M.J., 1998. Induction of burst firing in ventral tegmental area dopaminergic neurons by activation of serotonin (5-HT)(1A) receptors: WAY100,635-reversible actions of the highly selective ligands, flesinoxan and S15535. Synapse 30, 172-180.]. The present data show that (i) [3H]S15535 labels pre- and post-synaptic populations of 5-HT(1A) sites in rat brain sections, (ii) S15535 exhibits antagonist properties at post-synaptic 5-HT(1A) receptors in corticolimbic regions, and (iii) S15535 also attenuates agonist-stimulated G-protein activation at raphe-localised 5-HT(1A) receptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2002

Cognitive deficits and CNS damage after a 4-day binge ethanol exposure in rats.

Impairments of learning and memory are common neuropsychological sequelae of chronic alcohol abuse. Alcoholics often have impairments of anterograde memory, including spatial memory dysfunction, and a tendency toward response perseveration. This study was designed to assess the effects of binge ethanol exposure on neurodegeneration and cognitive function. Rats were given ethanol three times daily for 4 days. Silver staining revealed neurodegeneration in the olfactory bulb, piriform cortex, perirhinal cortex, entorhinal cortex, and dentate gyrus. After withdrawal, behavioral testing in the Morris water maze revealed significant differences in reversal learning between treatment groups. Ethanol-treated animals required more trials to learn the reversal task, entered the previously trained quadrant more often, and spent more time there than controls. [3H]PK-11195 binding, an index of CNS damage, was elevated in the piriform cortex of ethanol-treated animals. Thus, binge ethanol exposure resulted in neurodegeneration of a corticolimbic circuit with common excitatory inputs from the olfactory bulb and was associated with perseverative responding on a spatial learning task. These studies suggest that a single binge drinking episode could cause neurodegeneration and cognitive dysfunction in humans. The perseverative nature of the behavioral deficit could be related to both cognitive dysfunction and the behavioral components of the addiction process.

Animals↗
PubMed1997

Distribution of D4 dopamine receptor in rat brain with sequence-specific antibodies.

The distribution of the dopaminergic D4 receptor in rat brain was studied employing site directed polyclonal antibodies. Antisera were raised in rabbits to two oligopeptides corresponding to amino acids 160-172 of the second extracellular loop (P1) and amino acids 260-273 of the third intracellular loop (P2) of the D4 receptor sequence. Affinity-purified antibodies (anti-P1 and anti-P2) specifically recognized two major bands of 42-45 and 95 kDa in Western blots of denatured preparations of various rat brain areas. Immunocyto-chemistry studies showed that D4 receptor is widely distributed in rat central nervous system (CNS) showing higher labelling in the hippocampus (CA1, CA2, CA3 and dentate gyrus) frontal cortex, entorhinal cortex, caudate putamen, nucleus accumbens, olfactory tubercle, cerebellum, supraoptic nucleus and sustancia nigra pars compacta. In addition, anti-P1 decreased the binding of the antagonist [3H]YM-09151-2 selective for D2, D3 and D4 receptors but did not modify the binding of [3H]raclopride an antagonist selective for D2 and D3, in striatal synaptosomes. Anti-P2 did not modify the binding of these ligands. These results confirm the selectivity of the antibodies towards the D4 receptor and suggest that the binding site for the antagonists might be located at or close to the second extracellular loop of the protein sequence. D4 receptor protein is mainly expressed in plasma membranes and in the peripheral cytoplasm of neurons and is more widely distributed than was originally proposed based on mRNA localization, since it is present both in limbic, diencephalic and motor areas of rat brain.

Amino Acid Sequence↗
PubMed1998

Kainic acid induced expression of interleukin-1 receptor antagonist mRNA in the rat brain.

The endogenous interleukin-1 receptor antagonist (IL-1ra), a protein with partial homology with the proinflammatory cytokine interleukin-1beta (IL-1beta), prevents binding of IL-1beta to the signalling receptor. Exogenous IL-1ra has been shown to reduce the neuronal damage occurring after excitotoxic amino acid administration and ischemia. In the present study, in situ hybridization histochemistry was employed to investigate the regulation of endogenous IL-1ra mRNA expression in the rat brain after peripheral administration of kainic acid (10 mg/kg). IL-1ra mRNA expression was markedly induced in the hippocampus, thalamus, amygdala, piriform cortex, perirhinal cortex, entorhinal cortex, and to a lesser extent in the hypothalamus, and parietal and temporal cortex. The expression was first detected at 5 h after the kainic acid administration and it was markedly increased at 24 h. No signal was detected at 4 days after the injection. The majority of the cells expressing IL-1ra mRNA displayed the morphological characteristics of microglia. Expression of IL-1ra mRNA in neurons occurred mainly in the piriform and perirhinal cortex. The distribution pattern of IL-1ra mRNA expressing microglia-like cells was similar to that of cells labelled with ED1, a marker for activated microglia. The induction of IL-1ra mRNA expression may represent an endogenous response to balance IL-1 receptor mediated activity in the brain following kainic acid administration, conceivably to elicit neuroprotective and/or antiinflammatory effects.

Animals↗
PubMed1999

Dimorphic expression of medial basal hypothalamic-preoptic area calbindin-D(28K) mRNA during perinatal development and adult distribution of calbindin-D(28K) mRNA in Sprague-Dawley rats.

The calcium-binding protein, calbindin (CALB) is: (a) distributed throughout the central nervous system (CNS), (b) abundant in neurons and, (c) thought to act as a buffer by binding intracellular calcium, mediating neurogenesis (cell profileration) and neuronal programmed cell death. Using Northern analysis, CALB mRNA distribution was characterized in 12 different adult brain regions. Additionally, CALB mRNA levels were characterized in the medial basal hypothalamus (MBH) and preoptic area (POA) in perinatal male and female rats, in order to compare this mRNA pattern to the dimorphic MBH-POA CALB protein profile our laboratory previously reported. Three CALB mRNA species were detected (at 1.9, 2.8 and 3.2 kilobase pairs) in all CNS regions. The smallest mRNA transcript (at 1.9 kilobase pairs) was the most abundant of the three CALB mRNAs. To quantify these mRNA signals, CALB mRNA levels were normalized to 18s ribosomal RNA bands. Among the various adult brain sites assayed, the cerebellum expressed the highest CALB mRNA signals. High CALB mRNAs were observed in the MBH-POA, olfactory bulb and hippocampal regions. Moderate CALB mRNA levels were seen in the striatum and frontal cortex while moderate to low CALB mRNA levels were observed in the posterior cortex, entorhinal cortex, midbrain, pons, thalamus and medulla. During perinatal development, MBH-POA CALB mRNA levels were lowest at gestation day (GD) 18, increased four-fold in newborns and remained at moderate levels during early postnatal development. Male CALB mRNA levels were notably greater than female values at GD 18 and in newborns. Whereas, at PND 2, the CALB mRNA levels were approximately equivalent in males and females. These findings suggest that in the adult CNS CALB mRNAs vary among different brain regions. The present male vs. female MBH-POA CALB mRNA levels confirm previously reported dimorphic protein patterns of MBH-POA CALB during perinatal development. Thus, the genesis of sexually dimorphic structures may be influenced by the dimorphic CALB expression in the MBH-POA region.

Animals↗
PubMed2001

Role of endogenous opioid system in the regulation of the stress response.

Numerous studies and reviews support an important contribution of endogenous opioid peptide systems in the mediation, modulation, and regulation of stress responses including endocrine (hypothalamopituitary-adrenal, HPA axis), autonomic nervous system (ANS axis), and behavioral responses. Although several discrepancies exist, the most consistent finding among such studies using different species and stressors is that opioids not only diminish stress-induced neuroendocrine and autonomic responses, but also stimulate these effector systems in the non-stressed state. A distinctive feature of the analgesic action of opioids is the blunting of the distressing, affective component of pain without dulling the sensation itself. Therefore, opioid peptides may diminish the impact of stress by attenuating an array of physiologic responses including emotional and affective states. The widespread distribution of enkephalin (ENK) throughout the limbic system (including the extended amygdala, cingulate cortex, entorhinal cortex, septum, hippocampus, and the hypothalamus) is consistent with a direct role in the modulation the stress responses. The predictability of stressful events reduces the impact of a wide range of stressors and ENK appears to play an important role in this process. Therefore, ENK and its receptors could represent a major modulatory system in the adaptation of an organism to stress, balancing the response that the stressor places on the central stress system with the potentially detrimental effects that a sustained stress may produce. Chronic neurogenic stressors will induce changes in specific components of the stress-induced ENKergic system, including ENK, delta- and mu-opioid receptors. This review presents evidences for adaptive cellular mechanisms underlying the response of the central stress system when assaulted by repeated psychogenic stress, and the involvement of ENK in these processes.

Adaptation, Psychological↗
PubMed1996

Abnormal, ubiquitinated cortical neurites in patients with diffuse Lewy body disease.

Although it is known that the severity of dementia in patients with diffuse Lewy body disease is related to cortical Lewy body density, the morphological substrate of dementia in these patients is poorly understood. Vibratome sections processed free-floating for ubiquitin immunohistochemistry in three patients with the common form and one patient with the pure form has shown the presence of large numbers of abnormal, ubiquitinated neurites in the cerebral cortex, mainly cingulate cortex, entorhinal cortex and temporal lobe, and hippocampal complex, regions in which, precisely, Lewy bodies are most abundant. Abnormal neurites are a consistent change which results in abnormal neuronal connectivity. Abnormal cortical neurites, rather than cortical Lewy bodies, may play a significant role in the development and progression of cognitive deficits in patients with diffuse Lewy body disease.

Adult↗