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PubMed2002

Repeated interactions with females elevate metabolic capacity in the limbic system of male rats.

The effect of heterosexual social experience on brain metabolic capacity was investigated by measuring the activity of cytochrome oxidase, a rate-limiting enzyme in oxidative metabolism. Male Sprague-Dawley rats were kept naïve or allowed to copulate with receptive females three (3 F males) or 16 times (16 F males). Throughout the vomeronasal system and other limbic areas, 16 F males had elevated metabolic capacity relative to naïve and 3 F males, whereas no significant differences in brain metabolism were found between 3 F and naïve males. Behavioral differences were also found between 3 F and 16 F males. In a second experiment, we assessed differences in brain metabolism between sexually active and inactive males given only one opportunity to copulate and found no significant difference in neural metabolism between these males. This suggests that the differences found in the first experiment were primarily driven by differences in repeated experience rather than by sexual performance between 16 F and 3 F males. We speculate that these changes in brain metabolic capacity could be related to immediate early gene expression during copulation and could underlie the long-term behavioral changes accompanying heterosexual social experience.

Animals↗
PubMed1993

Serotonin uptake sites and serotonin receptors are altered in the limbic system of schizophrenics.

Serotonin (5-HT) uptake sites were mapped by autoradiographic means with [3H]cyano-imipramine ([3H]CN-IMI), the 5-HT1A receptor with [3H]8-hydroxy-2-[di-n-propyl-amino]tetralin ([3H]8-OH-DPAT), and the 5-HT2 receptor with both [3H]ketanserin and [125I]lysergic acid diethylamide ([125I]LSD) in eight nonneurologic controls and 10 cases with a diagnosis of schizophrenia. In the striatum, there was a marked heterogeneous patterning of 5-HT uptake sites that corresponded to the striosomal/matrix compartmentalization of the striatum. This organization was not matched with an equally heterogeneous pattern of either 5-HT2 or 5-HT1A receptors. For the isocortex, a general organizational scheme was observed with the 5-HT1A receptor expression high in the external laminae and deep laminae, but 5-HT2 receptor expression was higher in the internal laminae. There was a laminar distribution of 5-HT uptake sites that approximated the combined distributions of the 5-HT1A receptor and the 5-HT2 receptor. In the parahippocampal gyrus and hippocampus, the distribution of 5-HT uptake sites was complementary to the distribution of 5-HT1A and 5-HT2 receptors. In schizophrenic cases, there was a large increase in the number and altered striosomal/matrix organization of 5-HT uptake sites in the striatum. There was also an increase in the numbers of 5-HT2 receptors in the nucleus accumbens and ventral putamen of the schizophrenics. The number of 5-HT1A receptors was not modified. There was a marked reduction in 5-HT uptake sites in the external and middle laminae of the anterior cingulate, frontal cortex, and posterior cingulate, and no changes were observed in the motor cortex, temporal cortex, or hippocampus. Increased numbers of 5-HT1A receptors were found in the posterior cingulate, motor cortex, and hippocampus. Serotonin2 receptors were substantially elevated in the posterior cingulate, temporal cortex, and hippocampus, but not in the frontal, anterior cingulate, or motor cortices. Examination of the temporal lobe and hippocampus of a group of nonschizophrenic suicides (n = 8) indicated the alterations in 5-HT system in the limbic regions of the striatum, the limbic cortex, and hippocampus of the schizophrenic cases may be disease specific.

Adolescent↗
PubMed1980

An iontophoretic survey of opioid peptide actions in the rat limbic system: in search of opiate epileptogenic mechanisms.

Iontophoretic and micropressure drug application and lesion techniques were used to investigate the cellular source of rat limbic system epileptiform responses to opioid peptides [19]. Iontophoretically applied morphine, methionine enkephalin or beta-endorphin inhibited the spontaneous or glutamate-activated firing of the great majority of single neurons in medial and lateral septum, amygdala and cingulate cortex. These inhibitions in firing were antagonized by iontophoresis of naloxone. In contrast to inhibitory effects in other limbic areas, morphine and the opioid peptides predominantly excited CA1 and CA3 pyramidal neurons in a naloxone-sensitive manner, as previously reported [36]. On rare occasions, iontophoretically applied beta-endorphin evoked repetitive waveforms similar to interictal population EPSPs or spikes. Micropressure application of opiates and peptides also excited hippocampal neurons indicating such responses were not current-induced artefacts. The possible role of the excitatory cholinergic septal hippocampal pathway in the facilitatory response of hippocampal units to the opiates was tested with iontophoretically applied atropine and scopolamine, or lesions of septal nuclei. None of these manipulations reduced the opioid-induced excitations; rather, septal lesions enhanced excitatory and epileptiform responses to the opiates. These results support the hypothesis that opiate-evoked epileptiform activity in the limbic system arises from enhanced pyramidal cell activity in the hippocampal formation, probably by a non-cholinergic mechanism.

Action Potentials↗
PubMed1994

Herpes simplex encephalitis in the temporal cortex and limbic system after trigeminal nerve inoculation.

Herpes simplex virus type 1 causes an encephalitis in humans that is primarily restricted to the temporal lobe and limbic system. The distribution of lesions suggests that virus enters the brain from a single site and then spreads transneuronally to infect connected structures. Two obvious sites of potential viral entry are the olfactory and trigeminal nerves. Trigeminal nerve entry is more likely because it innervates the oral cavity, a common site of initial infection, and the trigeminal ganglion is the most common site of viral latency. In previous reports, however, experimental trigeminal nerve infection has never led to the pattern of disease observed in humans. By directly inoculating virus into the murine tooth pulp, the mandibular division of the trigeminal nerve was selectively infected. This division, which innervates the oral cavity, is the one most commonly infected in humans. Intrapulp inoculation led to an encephalitis primarily affecting the temporal cortex and limbic system. Thus, spread via the trigeminal nerve provides an explanation for the distribution of herpes simplex virus observed in the human encephalitis.

Animals↗
PubMed2000

Neuronal degeneration in the limbic system of weanling rats exposed to saline, hyperthermia or d-amphetamine.

Neuronal degeneration was detected in the tenia tecta and other regions of the anterior limbic system of male weanling rats 3 days after four doses of 5 mg/kg d-amphetamine (4 x 5 mg/kg AMPH) when seizures occurred during AMPH exposure. Neurodegeneration in the parietal cortex, loss of tyrosine hydroxylase immunoreactivity in the caudate-putamen (CPu) and decreases in CPu tissue dopamine levels in weanlings was much less than those previously observed in adults. The neurotoxicity seen in the parietal cortex and CPu of the weanlings was much less than previously seen in adults even though severe hyperthermia and the behavior of retrograde propulsion occurred during AMPH exposure. Neurodegeneration was not detected in any of the previously mentioned brain regions in controls and weanlings made hyperthermic by a warm environment. However, signs of spontaneous neurodegeneration were seen in the posterior piriform cortex (Pir), posteriolateral cortical amygdaloid nucleus (PLCo), and the amygdalopiriform transition area (APir) of control weanlings. The doses of AMPH and the degree of hyperthermia necessary to induce seizures were substantially lower in weanlings compared to those previously observed in adult rats. Further studies will be necessary to determine if the susceptibility of weanlings to AMPH-induced seizures is related to or dependent on the same processes involved in producing degeneration in the posterior limbic system of saline controls.

Animals↗
PubMed1980

Distribution of acetylcholinesterase in the limbic system of the brain of the rabbit.

The aim of the study is to present a detailed and thorough description of the acetylcholinesterase enzyme (AChE) content of the limbic structures of the rabbit, now commonly used in our laboratory for investigating the electrographic-behavioral correlations of the cholinergic limbic system. We use 'chemitrodes' for intracerebral mi croinjections of cholinomimetic drugs; a detailed histochemical study (using Koelle's method) of the distributions of AChE enzyme in the limbic system of the rabbit was deemed necessary. Such areas as the septum and the amygdala are particularly poorly described in the rabbit and an attempt was made to clarify the confusion that still exists in the literature on the comparative anatomy and exact localization of these structures. On the whole, it could be inferred from this study that AChE-bearing neurons are generally better developed in phylogenetically older parts of the brain. Practically all the relays in Papez's 'cortical circuits of emotion' have a fairly AChE activity. As noted by us in other phyogenetically lower macrosmatic mammals, the reaction of AChE in the rabbit brain is more intense than in primates.

Acetylcholinesterase↗
PubMed1997

Opiate receptors modulate estrogen-induced cholecystokinin and tachykinin but not enkephalin messenger RNA levels in the limbic system and hypothalamus.

Cholecystokinin, substance P and methionine enkephalin all regulate the display of reproductive behaviour. Their expression is exquisitely regulated by estrogen in the limbic-hypothalamic circuit, a circuit that regulates the display of estrogen-sensitive female reproductive behavior. Relatively little is known, however, about the interaction of endogenous opioid peptides with cholecystokinin and substance P in the limbic-hypothalamic circuit. Opiates antagonize the release of cholecystokinin and substance P in the hypothalamus and periaqueductal gray and stimulate cholecystokinin messenger RNA levels in the amygdala. To determine the effect of endogenous opioid input on estrogen-induced cholecystokinin, enkephalin and substance P expression, in situ hybridization histochemistry was used to examine estrogen-induced messenger RNA levels of these neuropeptides in specific nuclei of the limbic system and hypothalamus in the presence of opiate receptor antagonists. Estrogen treatment of ovariectomized rats significantly elevated cholecystokinin messenger RNA levels in the central portion of the medial preoptic nucleus, the encapsulated portion of the bed nucleus of the stria terminalis and the posterodorsal medial amygdala, as well as increased preproenkephalin and preprotachykinin messenger RNA levels in the ventromedial hypothalamic nucleus and the posterodorsal medial amygdala. The universal opiate receptor antagonist naltrexone and the delta-opiate receptor antagonist naltrindole each potentiated the estrogen-induced increase and elevated cholecystokinin messenger RNA levels an additional 1.9- to 2.8-fold depending on the nucleus examined, but had no effect on the estrogen-induced expression of either preproenkephalin or preprotachykinin messenger RNA. beta-Funaltrexamine, a mu-opiate receptor antagonist, had no effect on the medial preoptic or medial amygdaloid cholecystokinin messenger RNA levels or on the estrogen-induced expression of preproenkephalin messenger RNA but did cause a decrease in estrogen-induced cholecystokinin messenger RNA levels in the bed nucleus of the stria terminalis and a decrease in the preprotachykinin messenger RNA levels in the ventromedial hypothalamic nucleus. These results indicate that endogenous opioids, acting on the delta-opiate receptor within nuclei of the limbic-hypothalamic circuit, restrain the estrogen-induced increase of cholecystokinin messenger RNA expression. Activation of the mu-opiate receptor, however, may facilitate cholecystokinin messenger RNA expression in the bed nucleus of the stria terminalis and preprotachykinin messenger RNA expression in the ventromedial hypothalamic nucleus. Thus, endogenous opioid peptides may act in a site- and receptor-specific manner to modulate estrogen-induced neuropeptide levels in the limbic system and hypothalamus.

Animals↗
PubMed1992

Stress ulcer modulation by limbic system structures.

A number of studies suggest that the telencephalic limbic system modulates stress ulcer development. The amygdala is assumed to connect sensory experiences, including stressful stimuli, with the emotional reactions and gastrointestinal effects normally produce. The hippocampal formation (entorhinal cortex, dentate gyrus, hippocampus) is part of a gating system, modulating the organism's coping ability. Changes in transmission in this temporal brain region are linked to individual differences in stress ulcer severity. Interactions among "classical" transmitters and several neuropeptides mediate these differences.

Animals↗
PubMed2003

Altering behavior with gene transfer in the limbic system.

There is now sufficient knowledge of the workings of the limbic system to allow experimental manipulation of behaviors anchored in limbic function. While such manipulations have traditionally involved lesions, stimulation or pharmacological approaches, it has become plausible to use gene transfer technology to alter patterns of gene expression in the nervous system. In this review, I consider ways in which gene transfer has been used to alter limbic function. These involve altering (a) cognition, (b) the rewarding properties of addictive substances, (c) patterns of social affiliation, and (d) responses to stress.

Animals↗
PubMed1996

Isolation of a monoclonal antibody reactive to brain microsome-associated antigen, lap-1, and its preferential localization in limbic system of rat brain.

The distribution and subcellular localization of AH9 antigen, recognized by a monoclonal antibody AH9, were examined in rat brain. Highest expression was observed in the lamina lucidum of the dentate gyrus of the rat hippocampus. Synaptic subfields of other limbic areas also expressed AH9 antigen at a substantial level. The molecular size of the AH9 antigen is 15 kDa and it was found in the microsomal fraction of brain but not of heart or kidney. These results indicate that AH9 antigen is a novel synaptosomal protein that is relatively specific to the limbic system, at least in the rat brain. We designated AH9 antigen as a limbic system associated protein-1, lap-1.

Animals↗
PubMed1979

Unit activity of limbic system neurons: effects of morphine, diazepam and neuroleptic agents.

The effects of morphine, diazepam and three neuroleptic agents (chloropromazine, perphenazine and haloperiodol) on neuronal firing rats were studied in the limbic system of immobilized cats. Parietal craniotomy was carried out under 1.5--4.0% halothane. Extracellular potentials from single cells in the cingulate gyrus, septum and lateral hypothalamic areas were recorded using glass-coated, platinum-iridium microelectrodes. In general, intravenous adminstration of morphine sulfate augmented the spontaneous firing rates of most of the neurons studied. In contrast, diazepam produced a marked attenuation of both spontaneous and morphine augmented firing rates, whereas the neuroleptic agents had no significant or consistent effects on the morphine augmented firing rates of neurons in these limbic areas. These data indicate that the limbic system may play an important role in the behavioral excitement in cats induced by morphine administration and also the depressant effect of the tranquilizer diazepam. In contrast, the inability of the neuroleptic agents to antagonize the morphine augmented neuronal firing rates suggest these agents may act outside the limbic areas studied here.

Animals↗
PubMed1989

Chronic imipramine reduces [3H]SCH 23390 binding and DA-sensitive adenylate cyclase in the limbic system.

[3H]SCH 23390 binding and dopamine (DA)-stimulated adenylate cyclase activity were measured in brain membrane preparations from rats chronically treated with imipramine (10 mg/kg twice daily for 14 days). [3H]SCH 23390 binding sites were decreased by 27% in the limbic system but only 14% in the striatum. The responsiveness of adenylate cyclase to DA was reduced by 38% in the limbic system but was not modified in the striatum. Concomitant treatment with alpha-methyltyrosine (alpha-MPT) (50 mg/kg daily for 14 days) prevented the imipramine-induced reduction in both [3H]SCH 23390 binding sites and the responsiveness of adenylate cyclase to DA.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1988

Noradrenergic effects in tardive dyskinesia, akathisia and pseudoparkinsonism via the limbic system and basal ganglia.

1. This paper proposes that the neuropsychiatric symptoms of tardive dyskinesia, akathisia and pseudoparkinsonian tremor are modulated by a noradrenergic pathway that projects from the locus coeruleus to the limbic system. 2. The proposed pathway is found to the consistent with neuroanatomical and neurochemical data in the literature. 3. The proposed pathway is found to be clinically consistent with observations by ourselves and others on the efficacy of clonidine and beta-adrenoreceptor blockers like propranolol for treating akathisia and pseudoparkinsonian tremor. It is also consistent with reports by ourselves and others that some patients with tardive dyskinesia benefit from treatment with propranolol or clonidine. 4. Noradrenergic modulation of the limbic system by way of the locus coeruleus accounts for a number of clinical observations, such as the worsening of tardive dyskinesia by stress, the greater risk for tardive dyskinesia in patients with affective disorder, the time-of-onset of tardive dyskinesia, and the coexistence of tardive dyskinesia and pseudoparkinsonism. 5. The functional significance of beta-adrenoreceptors in the basal ganglia is considered from an evolutionary perspective. 6. The model proposed in this article appears to have considerable heuristic value because it may further our understanding of Gilles de la Tourette syndrome and attention deficit disorder (hyperkinesis).

Akathisia, Drug-Induced↗
PubMed2001

Neuropathology of the limbic system and brainstem in West syndrome.

Both West syndrome (WS) and Lennox-Gastaut syndrome (LGS) are associated with various developmental disorders and it has been discussed whether the cerebral cortex or subcortical structures are important in the pathogenesis of both epileptic syndromes. Here we briefly review the literature on the neuropathological findings in WS and LGS, and present our data on immunohistochemical analysis of the brainstem and limbic lesions in autopsy cases of lissencephaly and sequels of hypoxic ischemic encephalopathy (HIE) caused by perinatal asphyxia manifested as both WS and LGS (WS/LGS). Nowadays, the neuroradiological examinations and surgical pathology in WS cases demonstrate dysplastic cerebral lesions more frequently than previously expected. On the other hand, we have delineated the common brainstem lesions such as small size of the tegmentum and spongy state and/or gliosis in the central tegmental tract in a number of WS autopsy cases of various etiologies. Recently, we reported the reduced expression of tyrosine hydroxylase, methionine enkephalin and parvalbumin in the brainstem in autopsy cases of lissencephaly and sequels of HIE manifested as WS/LGS, regardless of the cerebral changes. In the same subjects, we examined the expression of glutamate transporters and calcium-binding proteins in the limbic system by immunohistochemistry. These represent markers of glutamate neurotoxicity and the GABAergic inhibitory neuron system, respectively. The altered expressions of glial glutamate transporters and calcium-binding proteins in the limbic system seemed to reflect temporal lobe sclerosis, irrespective of the past history of WS, and there were no differences in the limbic involvement between the cases manifested as WS/LGS and disease controls of sequels of HIE not manifested as WS/LGS. It is more likely that the brainstem lesions contribute to the pathogenesis of WS and/or LGS more than the heterogeneous limbic lesions in these cases.

Brain Stem↗
PubMedDate not supplied

Progressive supranuclear palsy with limbic system involvement: report of a case with ultrastructural investigation of neurofibrillary tangles in various locations.

An autopsied case of a 65-year-old woman with progressive supranuclear palsy (PSP) characterized by dementia, hallucination and delirium is described. On neuropathologic examination, widespread neurofibrillary tangles (NFTs) associated with neuronal cell loss and gliosis were observed in the basal ganglia, subthalamic nucleus and various brain stem nuclei, corresponding to the well-established pathology of PSP. In addition, a large number of NFTs with neuronal cell loss were shown in the hippocampus, parahippocampal gyrus, amygdaloid nucleus, subcallosal area, anterior perforated substance, cingulate gyrus and anterior olfactory nucleus. Ultrastructurally, NFTs observed in the periaqueductal central grey, locus ceruleus and hippocampus were composed almost exclusively of straight tubules. On the other hand, those in the amygdaloid and anterior olfactory nuclei were composed mainly of twisted tubules of Alzheimer type. NFTs composed of twisted tubules alone were not observed. The present case was considered as a rare peculiar type of PSP which showed massive systemic appearance of NFTs in the so-called limbic system.

Female↗
PubMedDate not supplied

Limbic system abnormalities associated with mesial temporal sclerosis: a model of chronic cerebral changes due to seizures.

In a landmark 1966 study, widespread cerebral abnormalities were discovered at histopathologic examination of autopsied brains from patients with long-standing temporal lobe epilepsy. In the brains diagnosed with mesial temporal sclerosis (MTS), these abnormalities involved not only the hippocampus but also other structures of the limbic system and medial temporal lobe. Many of these changes are evident at magnetic resonance imaging. Because many of these abnormalities are found within limbic structures along a known neuroanatomic pathway (the Papez circuit), they suggest a pattern of cerebral damage related to the physiologic interconnections between the hippocampus and associated limbic structures. It appears that limbic damage associated with MTS more often affects the structures most closely connected to the hippocampus along the Papez circuit. The frequency and widespread distribution of these cerebral abnormalities suggest that MTS is not limited to the medial temporal lobe but instead represents a limbic system disorder.

Amygdala↗
PubMed2000

Gating of information flow within the limbic system and the pathophysiology of schizophrenia.

Although first thought of as a dopaminergic disorder, there is little direct evidence to support a primary pathology in the dopamine system as the etiological factor in schizophrenia. In contrast, evidence is amassing in support of a cortical disturbance in this disorder; one consequence of which is a disruption in the cortical regulation of subcortical dopamine systems. Our studies show that the hippocampus plays a major role in this interaction, in that, along with the dopamine system, it provides a gating influence over information flow from the prefrontal cortex at the level of the nucleus accumbens. Moreover, chemically-induced disruption of the development of the hippocampus and entorhinal cortex were found to lead to pathophysiological changes in these interactions in the limbic system of adult rats. Therefore, schizophrenia is proposed to be a developmentally-related disorder, in which disruption of the hippocampal influence over the limbic system during ontogeny results in a pathological alteration of corticoaccumbens interactions in the adult organism.

Animals↗