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PubMed1987

Chronic treatment with antidepressants decreases the number of [3H]SCH 23390 binding sites in the rat striatum and limbic system.

Binding of [3H]SCH 23390 to dopamine D-1 receptors and of [3H]spiperone to D-2 sites was measured in identical membrane preparations of the striatum and limbic system of rats treated chronically (twice daily, for two weeks) with antidepressants. Chronic administration of imipramine, amitriptyline, mianserin, citalopram, bupropion, iprindole and electroconvulsive shocks, but not benztropine or cyproheptadine (non-antidepressants) decreased the number of [3H]SCH 23390 binding sites, while no change in the parameters of [3H]spiperone binding was observed. The serotonin2 receptor antagonist ketanserin when added to the incubation medium had no effect on [3H]SCH 23390 binding to D-1 sites. The results suggest that D-1 receptor subsensitivity is a component of the therapeutic effect of antidepressants.

Animals↗
PubMedDate not supplied

Persistent activity in limbic system neurons: neurophysiological and modeling perspectives.

Neural activity persisting for one to hundreds of seconds has been postulated to be a substrate of memory. This review article illustrates examples of such activity in limbic system structures including the hippocampus, postsubiculum, and the anterodorsal thalamus. These neuronal responses include better known correlates with the spatial position as well as with head direction of the animal relative to its environment as well as other lesser known examples. Since head direction responses are greater when the animal is actively moving than when passively rotated, it has been proposed that there might be a general mechanism where the behavioral state of the animal can provide modulatory gating of such persistent signals. This would regulate the relative influence of these signals on downstream structures. Neural network attractor models of the head direction cell system are presented to demonstrate how these responses might originate, as well as the dynamics by which they are updated during movements.

Animals↗
PubMed1997

Neuropsychiatric complications after temporal lobe limbic system surgery.

Although control of seizure activity is the main goal of temporal lobectomies for complex partial epilepsy, the results of surgery must be viewed within the larger context of possible ramifications of limbic system disruption. The neuropsychiatric complications may be significant and influence the patient's perceived qualify of life, thus detracting from the benefits of seizure control. It is apparent from the previous studies that the modalities affected are influenced by the laterality of the resection, with left-sided lobectomies more often affecting verbal memory and learning, whereas right-sided resections may cause visual/spatial memory and cognitive declines. Preoperative neuropsychologic testing may help to predict these possible complications. General psychosocial function, memory, and cognition all seem to be less affected when complete seizure control is attained, with nearly 80% experiencing no significant change in neuropsychologic testing and the gain and losses being equal in magnitude. Also, younger patients and those with a shorter history of seizure activity may fare better after surgery because of a greater capacity for neuronal plasticity to subserve these functions. These findings support the contention that early diagnosis and surgical treatment may help to minimize potential neuropsychiatric complications in conjunction with improved postoperative seizure control.

Age Factors↗
PubMed1999

Human memory, cerebral hemispheres, and the limbic system: a new approach.

An integrative approach to human memory is presented in the context of brain asymmetry. The results of psychophysiological investigations suggest that right-hemisphere functioning is closely associated with the limbic system; that association leads to the formation of a polysemantic context. Polysemantic context is determined by multiple interconnections among its elements; each element bears the stamp of the whole context. That context sustains episodic, personal, and emotionally laden memories. Left-hemisphere functioning leads to the formation of a monosemantic context, which is responsible for the maintenance of semantic memories. That distinction--in terms of general organization of material by hemispheres--explains such phenomena as memory disturbances among the very old, the influence of emotions on memory, and confabulations.

Aged↗
PubMed1989

A membrane glycoprotein associated with the limbic system mediates the formation of the septo-hippocampal pathway in vitro.

The ability of a neuronal surface glycoprotein to mediate the formation of neuronal connections was tested in an explant culture system. A monoclonal antibody against the limbic system-associated membrane protein (LAMP) was used in co-cultures containing cholinergic neurons of the septum and their hippocampal target neurons. Antibody treatment had no effect on general axon outgrowth, but significantly diminished the ability of septal cholinergic axons to invade and collateralize in the hippocampus. The results suggest that factors regulating general axon outgrowth may be distinct from those regulating the patterns of outgrowth that define the formation of neural circuits.

Animals↗
PubMed1990

Central dopaminergic transmission is selectively increased in the limbic system of rats chronically exposed to antidepressants.

Repeated electroconvulsive shock (ECS) exposure produced a decrease of [3H]SCH 23390 binding sites and a reduced response of adenylate cyclase activity to dopamine D-1 receptor stimulation in the rat limbic area analogous to that previously observed in rats chronically treated with imipramine. These effects were completely prevented by the repeated administration of a small dose of alpha-methyl-p-tyrosine (alpha-MPT), associated with the tricyclic compound. Increased dopaminergic transmission seems to be involved in the mechanism of antidepressant action. Rats chronically treated with imipramine showed a decrease of dihydroxyphenylacetic acid (DOPAC) concentration restricted to the limbic area. Finally, both imipramine and desipramine blocked the uptake of [3H]dopamine in the limbic system with a 100-fold greater potency than that observed in the basal ganglia.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1993

Clozapine inhibits limbic system kindling: implications for antipsychotic action.

Clozapine and haloperidol were tested for their ability to influence the acquisition of kindled seizures following electrical stimulation of the amygdala and ventral hippocampus. While haloperidol pretreatment did not alter kindling genesis from either limbic region, preexposure to clozapine delayed the rate at which kindling evolved. Analysis of the number of seizure behaviors expressed during epileptogenesis revealed that clozapine produced a relative antagonism of seizure development arresting kindling at the stage-3 level. The kindling inhibition was dependent upon the daily administration of clozapine during the kindling process and was not evident after withdrawal from a chronic schedule of clozapine exposure. A subconvulsive dose of pilocarpine (80.0 mg/kg) produced an overall enhancement of kindling rate, a finding consistent with the excitatory role of acetylcholine (ACh) in kindling. Lower doses of pilocarpine (20.0 and 40.0 mg/kg) that did not alter seizure advancement partially antagonized the clozapine-elicited inhibition of amygdaloid kindling. Pilocarpine, however, did not affect the clozapine-induced increase in the number of stage-3 behaviors exhibited during amygdaloid kindling, suggesting that other neurochemical effects of clozapine, not related to its anticholinergic properties, modulate the kindling suppression. Clozapine's unique actions on limbic system sensitization were discussed in relation to its effectiveness as an antipsychotic agent.

Acetylcholine↗
PubMed2006

MDMA induces caspase-3 activation in the limbic system but not in striatum.

Several studies, carried out in chronic (+/-) 3,4-methylenedioxymethamphetamine (MDMA) abusers, have shown memory loss and cognitive impairment, as well as persistent electroencephalographic changes. This suggests that, at least in humans, forebrain areas, including the limbic system, might be altered by MDMA. Consistently, recent experimental evidences suggest that, in rodents, MDMA, besides effects on the basal ganglia, produces alterations in the hippocampus. Therefore, the aim of the present article was to investigate whether treatment with MDMA produces activation of the caspase-3 enzyme, which is part of an enzymatic pathway involved in cell death, within limbic areas (i.e., hippocampus, amygdala, and piriform cortex) and striatum. A marked induction of caspase-3 activity was demonstrated in the amygdala and hippocampus, although MDMA did not affect caspase-3 activity neither in the striatum nor in the frontal cortex. These data indicate that limbic structures possess a high sensitivity to MDMA with respect to the activation of at least one step in the apoptotic pathway. Potential implications and pitfalls of such an experimental observation are reported.

Animals↗
PubMedDate not supplied

Trimethyltin, a selective limbic system neurotoxicant, impairs radial-arm maze performance.

Rats were trained for fifteen sessions in an automated eight arm radial maze prior to treatment with 6 mg/kg trimethyltin chloride. This compound is a neurotoxicant which primarily damages the limbic system, in particular pyramidal cells in the CA3 region of the hippocampus. Following treatment the animals exhibited a marked and persistent impairment of maze performance characterized by decreased selection accuracy and an altered spatial pattern of responding within the maze. These results offered additional evidence that CA3 pyramidal neurons or their connections play an important, if not essential, role in radial-arm maze performance. It was suggested that trimethyltin might be a useful tool for elucidating the neural substrates of both radial maze performance and learning and memory processes.

Analysis of Variance↗
PubMed1980

A subcortical pathway links sensory and limbic systems of the forebrain.

The subcortical afferents and cortical projections of the lateral dorsal nucleus of the thalamus were investigated using anterograde and retrograde axonal transport of horseradish peroxidase (HRP). The lateral dorsal nucleus receives afferent projections from several nuclei of the pretectal complex, and sends efferent projections to several subdivisions of limbic cortex. These connections constitute a two stage pathway that could convey visual and somatosensory information to the limbic system.

Afferent Pathways↗
PubMed1987

A controlled study of Tourette syndrome. VII. Summary: a common genetic disorder causing disinhibition of the limbic system.

Tourette syndrome (TS) is one of the most common genetic disorders affecting man. Approximately one in 100 individuals manifests one or more of the aspects of the TS gene. This series of papers has emphasized that although motor and vocal tics are the hallmark of TS, the complete range of behavioral problems is much broader. This spectrum of behavior can be explained on the basis of the TS gene causing an imbalance of the mesencephalic-mesolimbic dopamine pathways, resulting in disinhibition of the limbic system.

Animals↗
PubMed1991

Sleep deprivation decreases mu and delta opioid receptor binding in the rat limbic system.

Sleep deprivation induced by the platform technique is considered to be a heavy stressful situation in rats. At the end of the sleep deprivation period (72 h) the rat displayed particular behavior characterized by wakefulness, a high degree of motor and exploratory activity, increased alertness and reactivity to environmental stimuli. Our previous results indicated that this behavior was antagonized by the administration of the opioid receptor antagonist naloxone and increased by opioid agonists. In this paper we show that concomitantly with this behavior, a decreased Bmax of mu and delta opioid receptors is present in the limbic system of these animals. These data suggest an active role of limbic mu and delta receptors in the generation of arousal and insomnia related to sleep deprivation induced stress.

Animals↗
PubMed1992

The limbic system and food-anticipatory circadian rhythms in the rat: ablation and dopamine blocking studies.

Rats behaviorally anticipate a fixed, daily opportunity to feed by entrainment of circadian oscillators that are physically separate from the light-entrainable circadian pacemaker that has been localized to the suprachiasmatic nucleus. Neural substrates mediating food-entrained rhythms are unknown. A variety of anatomical and functional observations suggest possible involvement of the limbic system and its dopaminergic component in the regulation of these rhythms. To test this hypothesis, the activity rhythms of rats bearing large, combined ablations of the hippocampus and amygdala or nucleus accumbens and medical forebrain anterior to the thalamus were examined under ad-lib feeding, 2 h daily feeding, and total food deprivation conditions. Some hippocampal-ablated rats showed alterations of free-running rhythms under ad-lib feeding, but none of the ablations impaired the rats' ability to anticipate daily feeding, or 'remember' the phase of feeding time during subsequent food deprivation. Additional groups of intact rats were treated with the dopamine antagonist haloperidol (0.3 mg/kg or 2.0 mg/kg) 30 min prior to daily feeding, but this also did not prevent the emergence of food-entrained rhythms. The limbic and dopamine systems do not appear to play a necessary role in the generation or entrainment of food-anticipatory circadian rhythms.

Amygdala↗
PubMed2000

Case report: limbic system activation by intravenous lidocaine in a patient with a complex regional pain syndrome and major depression.

Intravenous lidocaine is used to treat various neuropathic pain states. Systemic local anesthetics have been reported to cause behavioral alteration via limbic system activation. This case report describes a dramatic behavioral change in a patient receiving intravenous lidocaine and suggests a possible use of lidocaine to discriminate somatic and affective pain characteristics.

Journal Article↗
PubMed2006

5HTTLPR polymorphism and enlargement of the pulvinar: unlocking the backdoor to the limbic system.

BACKGROUND: The 5HTTLPR genetic variant of the serotonin transporter (SERT), which consists of a long (SERT-l) and short (SERT-s) allele, has emerged as a major factor influencing emotional behavior and brain anatomy. The pulvinar nucleus of the thalamus projects to important limbic nuclei including the amygdala and cingulate cortex, is involved in the processing of stimuli with emotional content, and contains an abundance of SERT. METHODS: Stereological methods were used to measure pulvinar neuron number in postmortem tissue from major depressive disorder (n = 11), bipolar disorder (n = 11), schizophrenia (n = 12), and control (n = 15) specimens from the Stanley Foundation Neuropathology Consortium. The effect of SERT genotype on pulvinar volume and neuron number was investigated by using analysis of covariance. RESULTS: Analysis of covariance with diagnosis, SERT genotype, age, hemisphere, postmortem interval, and time-in-formalin covariates identified a 20% increase in pulvinar neuron number and volume in SERT-ss subjects. CONCLUSIONS: The elevated number of pulvinar neurons in subjects with a SERT-ss genotype may serve to enhance subcortical input of emotionally relevant stimuli to the limbic system, providing a mechanism for the 5HTTLPR genetic variant to affect predisposition to conditions such as major depression.

Alleles↗
PubMedDate not supplied

Hypometabolism in the limbic system of cancer patients observed by positron emission tomography.

Brain images obtained by a positron emission tomography with 18F-fluorodeoxyglucose from 19 pretreatment cancer patients with variable cancers except brain cancers were compared with those from 17 inpatients with benign diseases. Relative reduction in regional cerebral metabolism of glucose was found mainly in the limbic structures including the bilateral orbitofrontal cortex, lateral frontal cortex, cingulate gyrus, thalamus, hippocampus and parahippocampal gyrus, insulae, and basal ganglia. The regional metabolism tended to be low in the patients who had severe pains which required opiates and morphines, and tended to be preserved in the patients who were already disclosed of their malignancy based on previous studies such as biopsy. Our findings would support that psychological deficits in cancer patients are associated with abnormalities in regional brain metabolism in the limbic system.

Aged↗
PubMed2006

Distinct regulation of metabotropic glutamate receptor (mGluR1 alpha) in the developing limbic system following multiple early-life seizures.

The effects of repeated neonatal seizures on metabotropic glutamate receptors (mGluRs) during critical periods of brain development are unknown. Therefore, we characterized the expression of Group I (mGluR1 and mGluR5) and Group II (mGluR2/3) metabotropic glutamate receptor proteins in the developing limbic system in response to a varied neonatal seizure history. Status epilepticus was induced with kainic acid (KA) either once (1x KA) on postnatal (P) day (P13), twice (2x KA) on P6 and P9 or P13, or three times (3x KA) on P6, P9, and P13. In control hippocampus, mGluR1alpha protein expression differed at all stages of development examined, whereas mGluR2/3 and mGluR5 protein expression patterns were mature by P15. After KA-induced status epilepticus, there was a significant elevation in mGluR1alpha protein expression within a select group of inhibitory interneurons of the CA1 stratum oriens-alveus that was enhanced with increasing number of neonatal seizures. mGluR2/3 and mGluR5 subtypes were unchanged. Increases were also observed within neurons of the amygdala and piriform cortex. Selective increases of mGluR1alpha subtypes within limbic structures may contribute to the resistance and tolerance of the immature hippocampus from damage. This may occur by excessive stimulation of excitatory synapses to collectively enhance the inhibitory drive of the immature brain by increasing GABA release. Data suggest that the mGluR1alpha subtype plays an important role in regulating hippocampal network activity after early-life seizures.

Age Factors↗