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PubMed1995

Anatomy of the medial temporal lobe.

The medial temporal lobe concept is an example of neurojargon rich in clinical and behavioral meaning, but sparse in neuroanatomical meaning except for topography. Like the concept of anterior speech area, many know roughly where it is located and what its functional correlates are, but not a lot else. At least three anatomical entities qualify as components of the medial temporal lobe. These include the amygdaloid body, the hippocampal formation, and the parahippocampal cortices that cover them superficially and are visible on the external surface of the hemisphere. For the greater part of this century, topographical observations, dissection, and descriptive data from passive staining methods have formed the principal source of information about the anatomy of the medial temporal lobe. However, in the past two decades much new information has emerged from experimental neuroanatomical studies in nonhuman primates and from neuropathological studies in humans. With magnetic resonance imaging (MRI), previous neuroanatomical detail, which earlier may have seemed like descriptive minutia, has now come alive and assumed substantial relevance in neurological and psychiatric diagnosis. Some of the emerging concepts as they relate to the neuroanatomy of the primate brain are highlighted and summarized here.

Amygdala↗

PubMed1996

Bilateral medial temporal lobe damage without amnesic syndrome: a case report.

After the case report H.M. [42], unilateral neurosurgical interventions in the mediotemporal area have no longer been performed, if damage to the contralateral mediotemporal region was present, because of running the risk of provoking a postoperative amnesic syndrome. We present a patient with bilateral mediotemporal cysts and medically refractory complex partial seizures originating in the left mediotemporal region. Although our patient had additional right mediotemporal damage and poor non-verbal learning and memory, the left amygdaloid body and the left hippocampal formation were resected because the patient passed a selective anterior temporal lobe Amobarbital test. Postoperatively, our patient's non-verbal memory recovered to normal, but his verbal memory declined. Nevertheless, he was non-amnesic and seizure-free.

Age of Onset↗

PubMed2007

Neurons expressing serotonin-1B receptor in the basolateral nuclear group of the amygdala in normally behaving and aggressive dogs.

The present study aimed to quantify neurons expressing the serotonin-1B receptor and evaluate numerical differences in normally behaving and pathologically aggressive dogs in order to assess whether the serotonin-1B receptor is involved in pathological canine aggression. Because previous studies have reported structural alterations in the basolateral nuclear group (BNG) of the amygdaloid body of aggressive dogs, this structure was selected as region of interest in the present study. Indirect immunohistochemistry was applied to visualise the serotonin-1B-receptor-positive neurons. Immunoreactivity was located predominantly within the neuronal cell bodies and adjacent neuronal processes. In the aggressive dogs the BNGs contained a significantly higher number of serotonin-1B-receptor-positive neurons compared to the normally behaving dogs. This number was strongly correlated with the total number of neurons per BNG, which was also significantly increased in aggressive dogs compared to normal dogs. The percentage of neurons expressing the serotonin-1B receptor did not differ significantly between both groups. No significant asymmetries were observed for the number and percentage of serotonin-1B-receptor-positive neurons. Potential relationships between the present findings and the etiology of aggressive behaviour, the neuroprotective role of the serotonin-1B receptor and receptor dysfunction are discussed.

Aggression↗

PubMed2006

Neuromedin C microinjected into the amygdala inhibits feeding.

Bombesin-like peptides including gastrin releasing peptide and neuromedin C are known to inhibit feeding. Bombesin receptors have been found in moderate to high densities in the amygdaloid body, which is essentially involved in the regulation of feeding and body weight. In the present experiments neuromedin C (15, 30, and 60 ng), a carboxyterminal decapeptid fragment of gastrin releasing peptide, was bilaterally microinjected into the central part of the amygdala in ad libitum fed male CFY rats. Food intake was measured every 5 min for 30 min and also 6 min following neuromedin C or vehicle microinjections. Fifteen nanograms neuromedin C significantly suppressed liquid food consumption for 5 min and 30 ng for 25 min. However, 60 ng was not effective. Neuromedin C effects were blocked by prior application of the bombesin receptor antagonist [Leu(13)-psi(CH(2)NH)-Leu(14)]-bombesin. Neuromedin C treatment increased latency to feeding, decreased food intake, decreased the time spent feeding and their ratio, the number and the duration of feeding episodes during the first 5 min, without modifying body temperature or stereotype activity. Results indicate that neuromedin C may decrease the efficiency of feeding and that activation of bombesin receptors in the central amygdala may reduce appetite.

Amygdala↗

PubMed2004

Phosphohippolin expression in the rat central nervous system.

The FXYD family is a small single-span membrane protein family; recently, we have identified a novel member of this family from the cDNA library of the rat hippocampus and named phosphohippolin (Php) (Mol. Br. Res. vol. 86, 2001). The deduced amino acid sequence of this novel Php comprises 93 residues with a core motif of FXYD and a single transmembrane domain. This indicates that Php belongs to FXYD6 subfamily of the seven FXYD subfamilies (FXYD1-7). Php shows a 48.1% homology with rat phospholemman (FXYD1), a transmembrane family protein. In this study, polyclonal antibodies against the carboxyl-terminal sequence of rat Php were raised and purified. The spatial expression of the Php protein was in the neuronal fibers of the medial part of lateral habenula nucleus, thalamus, hypothalamus, stria terminalis, zona incerta, amygdaloid body and cingulum, olfactory bulb, hippocampus, cerebral cortex and cerebellum. A unique Php distribution was identified in the cerebellum, with a predominant expression pattern in the granule layer of lobules VI-IX of the posterior lobe. Developmental studies demonstrated that the highest level of Php expression was seen in the postnatal (PN) 3-week-old rat brain, and a significant amount of Php still existed in the adult brain. These findings suggest that Php may play an important role in the excitability of neurons in the central nervous system during postnatal development, as well as those in the adult brain.

Aging↗

PubMed2002

Gastrin-releasing peptide microinjected into the amygdala inhibits feeding.

Bombesin (BN)-like peptides including gastrin-releasing peptide (GRP) are known to inhibit feeding. In the amygdaloid body BN receptors have been found in moderate to high densities. The central part of the amygdala (ACE) is essentially involved in the regulation of feeding and body weight. In the present experiments GRP was injected into the ACE and liquid food intake, general behavioural activity, as well as core temperature, were examined in male CFY rats. Food intake was measured every 5 min for 30 min and at the 40th and the 60th min following GRP or vehicle microinjections. Bilateral application of 50, 100 or 150 ng GRP resulted in transient inhibition of food intake while bilateral injection of 25 or 300 ng GRP did not modify feeding. Effect of GRP was eliminated by prior application of BN receptor antagonist [Leu(13)-psi(CH(2)NH)-Leu(14)]BN. After GRP or vehicle treatments animals were video-monitored and food intake, the first meal latency (FML), intermeal intervals (IMI), the time spent feeding (FT), grooming, resting and exploration were analysed at 5-min intervals for 30 min. However, FML did not change after GRP, the first IMI increased and intake, FT and intake/FT significantly decreased during the first 5 min. Duration of resting gradually increased after GRP and animals spent less time with exploration after GRP treatment than after vehicle injection. These differences were significant during the 25-30-min period. In body temperature, no significant changes were observed. Our results show that GRP in the ACE inhibits feeding and that GRP may decrease the efficiency of eating and may act as a satiety signal.

Amygdala↗

PubMed1997

Distribution and subcellular localization of motilin binding sites in the rabbit brain.

We previously reported the existence of motilin receptors in the cerebellum of the rabbit. We now explored the existence of motilin receptors in other brain regions and determined their association with neurons by subcellular fractionation studies. Autoradiographic studies with [(125)I]nle13-porcine motilin on rabbit coronal brain sections revealed specific binding sites in the hippocampus, thalamus, hypothalamus and amygdaloid body. Receptor binding studies allowed the identification of two binding sites. In all regions the density of the high-affinity binding site was lower than in the cerebellum, but its affinity was the same, except for the hypothalamus. No differences were found for affinity or density of the low-affinity receptor site. Homogenates of rabbit cerebellum were subjected to differential centrifugation. The highest motilin binding (10-times more than in the postnuclear supernatant) was found in the fraction which also showed maximal enrichment of [11-3H]saxitoxin binding (selective marker for voltage-sensitive Na+ channels), 6.9-fold, and cytochrome c oxidase activity (mitochondrial marker), 2.4-fold. In discontinuous sucrose density gradient centrifugation the motilin and saxitoxin binding both peaked in the 0.85-1 M layer, while cytochrome c oxidase was maximal in the 1.2 M layer. In conclusion, motilin receptors exist in several regions of the rabbit brain and are probably associated with synaptosomes. These findings further support a neurotransmitter role for motilin in the brain.

5'-Nucleotidase↗

PubMed2005

[Cerebral vasculitis secondary to Varicella-Zoster virus infection].

INTRODUCTION: Central nervous system infection by the varicella-zoster virus (VZV) can be responsible for myelitis, meningitis, ventriculitis and large and small-vessels encephalitis. CASE REPORT: We report the case of a 57-year-old-man hospitalized for deteriorating general health. Physical examination revealed likely encephalitis associated with headache without meningeal syndrome. Successive cerebral MRIs showed bilateral necrosis of the amygdaloid bodies and multiple deep and sub-cortical infarcts suggestive of vasculitis. Cerebral arteriography was normal. Three cerebral fluid examinations disclosed mononuclear pleiocytosis with few red blood cells. PCR analysis for VZV was only positive at the third time. DISCUSSION: The diagnosis of VZV encephalitis is difficult without the rash typical of zoster and because of the low sensitivity of PCR VZV in comparison with PCR HSV. CONCLUSION: In active viral disease, where the prognosis depends on early treatment, we highlight the usefulness of repeated PCR analysis and the search for antibodies in blood and cerebrospinal fluid.

Amygdala↗

PubMed2001

Sequential changes in AMPA and NMDA protein levels during Fe(3+)-induced epileptogenesis.

Seizure susceptibility is related to enhanced glutamatergic excitatory synaptic transmission with alterations in the expressions of ionotropic glutamate receptors. We wondered if levels of AMPA and NMDA receptor subunits changed following epileptogenesis induced by amygdalar FeCl(3) injection. We used Western blots to measure levels of subunits in the ipsilateral and contralateral hippocampus at various times after FeCl(3) injection into the amygdaloid body. With acute seizures, at +5 days after the injection, levels of GluR1, NMDAR1, and NMDAR2 were markedly increased in both hippocampi, with quantities at least 2-4 times baseline. By +15 and +30 days after injection, when chronic spontaneous seizures were occurring, the levels of GluR2 were increased, while GluR1 and NMDAR1&2A/B were decreased. Increased NMDAR1&2A/B levels at +5 days are consistent with the occurrence of upregulation of NMDA receptor production in the early stages of epileptogenesis. Since GluR2 suppresses glutamate receptor-mediated Ca(2+)-influx, increased expression of GluR2 with development of chronic, recurrent seizures may be a compensatory effect during epileptogenesis from neural responses to propagated seizures.

Amygdala↗

PubMed2000

Sequential changes in glutamate transporter mRNA levels during Fe(3+)-induced epileptogenesis.

Severe head injury in humans can cause recurrent seizures; this form of epilepsy appears to correlate with the occurrence of parenchymal hemorrhage. The injection of ferric cations, one component of hemoglobin, into rat amygdala, causes lipid peroxidation, and recurrent spontaneous seizures. We wondered whether the regulation of glutamate might be perturbed as a result of severe head injury, which might then act as a mechanism of chronic epileptogenesis. Levels of glutamate transporter glutamate-aspartate transporter (GLAST), glutamate transporter-1 (GLT-1), and excitatory amino-acid carrier (EAAC-1) mRNA were measured in ipsilateral and contralateral hippocampi and cerebral cortex removed from rats at 60 min, 24 h, and 5, 15 and 30 days after FeCl(3) injection into the amygdaloid body. While the neuronal transporter EAAC-1 mRNA was elevated bilaterally for up to 30 days following the microinjection that initiated seizures, GLT-1 mRNA, derived from glial cells, returned to basal levels. At 15 and 30 days after injection, however, when the experimental animals were experiencing spontaneous limbic behavioral seizures, GLAST mRNA was down-regulated. Epileptogenesis may correlate with the impairment of glial glutamate transport, leading to an excitation and imbalance of transmitter influences within the hippocampi and cerebral cortex.

ATP-Binding Cassette Transporters↗

PubMed1997

Neuroimmunomodulation via limbic structures--the neuroanatomy of psychoimmunology.

During the last 20 years, mutual communications between the immune, the endocrine and the nervous systems have been defined on the basis of physiological, cellular, and molecular data. Nevertheless, a major problem in the new discipline "Psychoneuroimmunology" is that controversial data and differences in the interpretation of the results make it difficult to obtain a comprehensive overview of the implications of immunoneuroendocrine interactions in the maintenance of physiological homeostasis, as well as in the initiation and the course of pathological conditions within these systems. In this article, we will first discuss the afferent pathways by which immune cells may affect CNS functions and, conversely, how neural tissues can influence the peripheral immune response. We will then review recent data, which emphasize the (patho)physiological roles of hippocampal-amygdala structures and the nucleus accumbens in neuroimmunomodulation. Neuronal activity within the hippocampal formation, the amygdaloid body, and the ventral parts of the basal ganglia has been examined most thoroughly in studies on neuroendocrine, autonomic and cognitive functions, or at the level of emotional and psychomotor behaviors. The interplay of these limbic structures with components of the immune system and vice versa, however, is still less defined. We will attempt to review and discuss this area of research taking into account recent evidences for neuroendocrine immunoregulation via limbic neuronal systems, as well as the influence of cytokines on synaptic transmission, neuronal growth and survival in these brain regions. Finally, the role of limbic structures in stress responses and conditioning of immune reactivity will be commented. Based on these data, we propose new directions of future research.

Humans↗

PubMed2000

Expression of the purported sigma(1) (sigma(1)) receptor in the mammalian brain and its possible relevance in deficits induced by antagonism of the NMDA receptor complex as revealed using an antisense strategy.

Sigma (sigma) receptors have generated a great deal of interest on the basis of their possible role in psychosis, neuroprotection and various other behaviors including learning processes. The existence of at least two classes of sigma receptor binding sites (sigma(1) and sigma(2)) is now well established. The recent cloning of the mouse, guinea pig and human sigma(1) receptors has allowed the study of the discrete distribution of the sigma(1) receptor mRNA in rodent and human brain tissues using in situ hybridization. Overall, the sites of expression of specific sigma(1) receptor mRNA signals were in accordance to the anatomical distribution of sigma(1) receptor protein first established by quantitative receptor autoradiography. Specific sigma(1) receptor hybridization signals were found to be widely, but discretely distributed, in mouse and guinea pig brain tissues. The highest levels of transcripts were seen in various cranial nerve nuclei. Lower, but still high hybridization signals were observed in mesencephalic structures such as the red nucleus, periaqueductal gray matter and substantia nigra, as well as in some diencephalic structures including such as the habenula and the arcuate, paraventricular and ventromedial hypothalamic nuclei. Superficial (I-II) and deeper (IV-VI) cortical laminae were moderately labeled in the mouse brain. Moderate levels of sigma(1) receptor mRNA were also found in the pyramidal cell layer and the dentate gyrus of the hippocampal formation. Other structures such as the thalamus and amygdaloid body also expressed the sigma(1) receptor mRNA although to a lesser extent. In murine peripheral tissues, strong hybridization signals were observed in the liver, white pulp of the spleen and the adrenal gland. In the postmortem human brain, moderate levels of sigma(1) receptor mRNA, distributed in a laminar fashion, were detected in the temporal cortex with the deeper laminae (IV-VI) being particularly enriched. In the hippocampal formation, the strongest hybridization signals were observed in the dentate gyrus while all other subfields of the human hippocampal formation expressed lower levels of the sigma(1) receptor mRNA. Antisense oligodeoxynucleotides against the purported sigma(1) receptor were used next to investigate the possible role of this receptor in dizocilpine (MK-801)/NMDA receptor blockade-induced amnesia. Following a continuous intracerebroventricular infusion of a specific sigma(1) receptor antisense into the third ventricle (0.4 nmol/h for 5 days), sigma(1)/[3H](+)pentazocine binding was significantly reduced in mouse brain membrane homogenates while a scrambled antisense control was without effect. Moreover, the sigma(1) receptor antisense treatments (5 nmol/injection, every 12 hx3 or 0.4 nmol/h for 5 days) attenuated (+)MK-801/NMDA receptor blockade-induced cognitive deficits in the treated mice while a scrambled antisense control had no effect. Taken together, these results demonstrate the widespread, but discrete, distribution of the sigma(1) receptor mRNA in the mammalian central nervous system. Moreover, antisense treatments against the purported sigma(1) receptor gene reduced specific sigma(1)/[3H](+)pentazocine binding and modulated cognitive behaviors associated with NMDA receptor blockade providing further evidence for the functional relevance of the cloned gene.

Amnesia↗

PubMed2006

A remote and highly conserved enhancer supports amygdala specific expression of the gene encoding the anxiogenic neuropeptide substance-P.

The neuropeptide substance P (SP), encoded by the preprotachykinin-A (PPTA) gene, is expressed in the central and medial amygdaloid nucleus, where it plays a critical role in modulating fear and anxiety related behaviour. Determining the regulatory systems that support PPTA expression in the amygdala may provide important insights into the causes of depression and anxiety related disorders and will provide avenues for the development of novel therapies. In order to identify the tissue specific regulatory element responsible for supporting expression of the PPTA gene in the amygdala, we used long-range comparative genomics in combination with transgenic analysis and immunohistochemistry. By comparing human and chicken genomes, it was possible to detect and characterise a highly conserved long-range enhancer that supported tissue specific expression in SP expressing cells of the medial and central amygdaloid bodies (ECR1; 158.5 kb 5' of human PPTA ORF). Further bioinformatic analysis using the TRANSFAC database indicated that the ECR1 element contained multiple and highly conserved consensus binding sequences of transcription factors (TFs) such as MEIS1. The results of immunohistochemical analysis of transgenic lines were consistent with the hypothesis that the MEIS1 TF interacts with and maintains ECR1 activity in the central amygdala in vivo. The discovery of ECR1 and the in vivo functional relationship with MEIS1 inferred by our studies suggests a mechanism to the regulatory systems that control PPTA expression in the amygdala. Uncovering these mechanisms may play an important role in the future development of tissue specific therapies for the treatment of anxiety and depression.

Amygdala↗

PubMed1985

The insular lobe in primates including humans.

The insular lobe reaches its greatest extent and morphologic differentiation in primates culminating in humans. It consists of four to six gyri that appear like a fan covered by the frontal, parietal, and temporal opercula. The human insula has three cytoarchitectonic subdivisions that are similar to those described for the rhesus macaque. Recent studies have addressed the myelo- and chemoarchitectonics of the primate insula. With the aid of a variety of methods investigators have demonstrated that the insular lobe has connections with: (1) portions of the frontal, parietal, and temporal lobes as well as of the cingulate gyrus, (2) the basal nuclei especially the tail of the caudate, putamen, and claustrum, (3) the amygdaloid body and other limbic constitutents, and (4) the dorsal thalamus. Experimental studies coupled with observations in humans provide the basis for a number of suggestions regarding the functional aspects of the insular lobe. The insula may play a role as a: (1) visceral sensory area, (2) visceral motor area, (3) supplementary motor area, (4) vestibular area, and (5) an area related to certain aspects of speech and/or language. While the broad concept of the insula has been outlined, the elucidation of its connections and functions remains to be completed by future researchers.

Amygdala↗

PubMed2006

Increased number of neurons expressing androgen receptor in the basolateral amygdala of pathologically aggressive dogs.

The present study aimed to determine the extent to which the androgen receptor (AR) is directly involved in the hormonal modulation of pathological canine aggressive behaviour in the basolateral nuclear group (BNG) of the amygdaloid body. A stereological quantification of AR-positive neurons was performed in the BNGs of normally behaving and aggressive male dogs. The BNG was selected because it is involved in sexual and behavioural activities that are influenced by androgens. In the aggressive dogs the BNG contained a significantly higher number of AR-positive neurons compared with normally behaving dogs suggesting differences in androgen activity within the BNGs of both the groups. However, additional mechanisms are likely to be involved because the AR-negative fraction of BNG neurons was also increased in the aggressive dogs. It was concluded that most of the AR was unliganded because a cytoplasmic staining pattern of AR positivity was observed in the canine BNG neurons. This indicates that genomic androgen actions, which are mediated through the AR are of minor importance in the testosterone modulation of canine aggression within the BNG. Other non-genomic mechanisms through which androgens may exert their action in the BNG are discussed. The aromatase pathway is suggested to be the main mechanism through which testosterone exerts its action within the BNG.

Aggression↗

PubMed1998

Complex functional attributes of amygdaloid gustatory neurons in the rhesus monkey.

To reveal specific functions of glucose-sensitive (GS) and glucose-insensitive (GIS) cells in chemical information processing, single neuron activity was recorded in the amygdaloid body (AMY) of macaques during: 1) gustatory stimulations and 2) micro-electrophoretic administration of chemicals. Of the 629 neurons tested, 56 (8.9%) responded to, usually two or more, taste qualities. Hedonically distinct tastants usually elicited opposite firing rate changes of the gustatory cells. Seventy percent of the gustatory responses were recorded from GS neurons (17% of all AMY cells). Catecholamines (CAs) induced discharge rate changes in a majority of taste-responsive neurons: The GS gustatory cells were suppressed by norepinephrine (in the form of noradrenaline HCl, NA), whereas the GIS taste-responsive neurons were facilitated by dopamine (DA). Furthermore, NA- and/or DA-antagonists were able to attenuate or suppress taste-elicited responses of several of these cells. These and previous data indicate a specific functional organization of AMY gustatory cells: The GS and GIS taste neurons appear to be involved in differential integration of feeding-associated humoral-metabolic, motivational and exogenous chemical information.

Amygdala↗

PubMed1994

MRI volumetry of medial temporal lobe structures in amnesia following herpes simplex encephalitis.

Using a magnetic resonance imaging-based volumetry, we quantified the volumes of the hippocampal formation (HF), parahippocampal gyrus (PHG), amygdaloid body (AMB), and anterior temporal neocortex (ATN) in 5 post-herpes simplex encephalitic (post-HSE) patients with temporal lobe damage and memory impairment at 12-52 months after the onset, and in 10 age-matched control subjects. In the post-HSE patients, the HF (p < 0.001) and PHG (p < 0.005) were significantly atrophic, while the AMB (p = 0.155) and ATN (p = 0.102) were smaller but not significantly. Performances on the verbal learning memory tests correlated highly with the HF volume, and length of dense retrograde amnesia with the PHG atrophy. Two patients with severe lasting amnesia had a marked atrophy of the HF and PHG, while 3 patients with good recovery from initial amnesia had temporal lobe structures larger than 50% of the control mean volumes. These results suggest that anterograde and retrograde memory functions involve different neural structures; the former is related to the HF and the latter to the PHG. For producing lasting amnesia, either severe HF damage or a combined damage of the HF and PHG might be necessary.

Acyclovir↗

PubMed1999

The scientific basis for the reputed activity of Valerian.

The underground organs of members of the genus Valeriana (Valerianaceae), as well as related genera such as Nardostachys, are used in the traditional medicine of many cultures as mild sedatives and tranquillizers and to aid the induction of sleep. V. officinalis is the species most commonly used in northern Europe and still retains its official pharmacopoeial status although it is most commonly encountered as an ingredient of herbal medicines. This plant is still the subject of considerable research aimed at establishing the chemical and pharmacological basis of the activity which has been clearly shown in a number of animal and clinical studies. The constituents of the volatile oil are very variable due to population differences in genetics and to environmental factors. The major constituents include the monoterpene bornyl acetate and the sesquiterpene valerenic acid, which is characteristic of the species, in addition to other types of sesquiterpene. Some of these have been shown to have a direct action on the amygdaloid body of the brain and valerenic acid has been shown to inhibit enzyme-induced breakdown of GABA in the brain resulting in sedation. The non-volatile monoterpenes known as valepotriates were first isolated in 1966 and contribute to the overall activity by possessing sedative activity based on the CNS although the mode of action is not clearly known. The valepotriates themselves act as prodrugs which are transformed into homobaldrinal which has been shown to reduce the spontaneous motility of mice. More recent studies have shown that aqueous extracts of the roots contain appreciable amounts of GABA which could directly cause sedation but there is some controversy surrounding the bioavailability of this compound. Another recent finding is the presence of a lignan, hydroxypinoresinol, and its ability to bind to benzodiazepine receptors. Valerian is a good example of both the negative and positive aspects of herbal drugs. The considerable variation in its composition and content as well as the instability of some of its constituents pose serious problems for standardization but the range of components which contribute to its overall activity suggest that it may correct a variety of underlying causes of conditions which necessitate a general sedative or tranquilizing effect.

Alkaloids↗