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PubMed2006

Dendritic pruning of the medial amygdala during pubertal development of the male Syrian hamster.

The medial amygdala (Me), a brain region essential for mating behavior, changes in size during puberty. In pre-, mid-, and late pubertal (21, 35, and 49 days of age) male Syrian hamsters, we examined neuronal structure in Me and protein levels of spinophilin and synaptophysin in the amygdaloid complex for evidence of synaptic plasticity coincident with behavioral and physiological development. Body weight, testes weight, and testosterone levels increased during puberty. Mounting behavior, including ectopic, nonintromittive, and intromittive mounts, also increased. Neuronal structure in the posterodorsal medial amygdala (MePD) was assessed in Golgi-impregnated neurons. Pruning occurred during puberty in the number of dendrites emanating from the cell body and in terminal dendritic spine densities. Approximately half of all MePD neurons analyzed had an axon emanating from a dendrite rather than the cell body. However, prepubertal males were more likely to have the axon emanating from a higher order dendritic segment (secondary or tertiary) than were mid- and late pubertal males. Finally, protein levels in the amygdaloid complex varied with pubertal age. Spinophilin decreased, while synaptophysin and GAPDH protein levels increased. These results suggest that puberty is a period of dramatic synaptic plasticity in Me. Specifically, pruning of dendrites and spines, in combination with axonal changes, is likely to modify the afferent influences and electrophysiological properties of Me neurons. Because the Me is an integral component of a social behavior neural network, these changes may be related not only to sexual behavior, but also to other behaviors that mature during puberty, including aggressive, risk-taking, fear-related, and parental behaviors.

Aging↗
PubMed1996

Opposite changes in the expression of enkephalin in the amygdala and hypothalamus after lesions of the bed nucleus of the stria terminalis in the rat.

The expression of enkephalin in neurons of the rat forebrain was studied by in situ hybridization and immunohistochemistry after unilateral injections of ibotenic acid into the bed nucleus of the stria terminalis. Initially, we observed that the destruction of nerve cell bodies in this nucleus resulted in a prominent bilateral increase in the number of neuronal perikarya immunoreactive for [Met]enkephalin in the lateral/basolateral amygdaloid complex-especially in the anterior division of the latter nucleus-as compared with NaCl-injected rats. In a separate set of experiments, this effect was associated with a significant (two times) enhancement of the number of nerve cell bodies containing preproenkephalin A messenger RNAs in the same amygdaloid nucleus ipsilateral to the injection, as compared with controls. In the hypothalamus of both experimental and control rats, the nerve cell bodies immunoreactive for [Met]enkephalin were few since the animals were not pretreated with colchicine, and the effects of the lesion were difficult to appreciate. However, using in situ hybridization, numerous nerve cell bodies containing preproenkephalin A messenger RNAs were detected bilaterally in the perifornical area, the paraventricular (parvocellular division) and the ventromedial nuclei of the hypothalamus. In the latter nucleus, the lesion of the bed nucleus of the stria terminalis resulted in a strong decrease (about two times) in the number of labelled cell bodies as compared with the controls, whereas no significant changes were found bilaterally in the paraventricular nucleus. In agreement with some data of the literature, our results indicate that the bed nucleus of the stria terminalis plays an important role in the regulation of neuropeptide genes expression in certain regions of the limbic system. Such a role is often exerted by nerve fibres afferents to the nerve cell bodies considered. However, from numerous neuroanatomical data of the literature, it appears more probable that the induction or inhibition of the expression of enkephalin in presynaptic neurons is due to the disappearance of their postsynaptic target in the bed nucleus of the stria terminalis.

Amygdala↗
PubMed1989

Neurons of origin and fiber trajectory of amygdalofugal projections to the medial preoptic area in Syrian hamsters.

The amygdaloid neurons of origin and the trajectory of amygdaloid fibers to the medial preoptic area of the adult male Syrian hamster were identified by using horseradish peroxidase (HRP) histochemistry. After iontophoresis of HRP into the medial preoptic area, retrogradely labeled amygdaloid neurons were located in the dorsal and caudal parts of the medial amygdaloid nucleus and throughout the amygdalohippocampal area. No amygdaloid neurons were labeled after HRP applications confined to the most rostral portion of the medial preoptic area (anterior to the body of the anterior commissure). Following more caudal medial preoptic area injections (body of the anterior commissure to the suprachiasmatic nucleus) the distribution of retrogradely labeled cells in the medial amygdaloid nucleus and the amygdalohippocampal area revealed no topographic organization of the amygdalopreoptic connections. When amygdaloid neurons were labeled, the amygdalohippocampal area contained two to five times as many HRP-filled cells as the medial amygdaloid nucleus. Retrogradely transported HRP could be followed from the medial preoptic area to the amygdala through fibers in the dorsomedial quadrant of the stria terminalis. In addition, electrolytic lesions of the stria terminalis prior to iontophoresis of HRP into the medial preoptic area prevented retrograde transport to neurons in both the dorsocaudal medial amygdaloid nucleus and the amygdalohippocampal area. These results confirm earlier observations describing the location of autoradiographically labeled efferents from the medial amygdaloid nucleus to the medial preoptic area and provide new information about the restricted region within the medial amygdaloid nucleus from which these projections arise. They also suggest that, unlike the projections from the medial amygdaloid nucleus to the bed nucleus of the stria terminalis, the efferents to the medial preoptic area travel entirely in the stria terminalis.

Amygdala↗
PubMed2002

Intracerebral microinjections of delta 9-tetrahydrocannabinol: search for the impairment of spatial memory in the eight-arm radial maze in rats.

The purpose of this study was to identify brain sites that contribute to the delta(9)-tetrahydrocannabinol (delta(9)-THC)-induced impairment of spatial memory in rats. Rats were tested in the eight-arm radial maze after microinjections of delta(9)-THC into one of 14 different brain regions. The bilateral microinjection of delta(9)-THC (20 microg/side) impaired spatial memory when injected into the dorsal hippocampus (DH), ventral hippocampus (VH) or dorsomedial thalamus nucleus (DMT). However, rats treated with delta(9)-THC into DMT produced preseverative behavior which has not been observed by systemic administration of delta(9)-THC. On the other hand, spatial memory was unaffected by microinjections of delta(9)-THC into the other 11 areas examined: frontal (FC) and frontoparietal (FPC) cortex, central (ACE) and basolateral (ABL) amygdaloid nucleus, medial caudate putamen (CPM), lateral hypothalamus (LH), mammillary body (MB), basal forebrain (BF), medial septal nucleus (SEP) and dorsal (DR) and median (MR) raphe nucleus. These results suggest that DH and VH may be important brain sites for the delta(9)-THC-induced impairment of spatial memory.

Animals↗
PubMed2000

Immunohistochemical localisation of the 5-HT2C receptor protein in the rat CNS.

5-HT2C receptor mRNA has a widespread distribution in the human and rat CNS but the absence of a specific high affinity ligand has made autoradiographic localisation of the receptor difficult. By raising polyclonal antibodies against the rat 5-HT2C receptor protein this study reports the immunohistochemical distribution of this receptor in the rat CNS. A sephadex purified 5-HT2C antiserum visualised a single immunopositive band (54 kDa) in Western blots of membranes prepared from several rat brain regions and caused intense membrane immunofluorescence in HEK 293 cells transfected with h5-HT2C cDNA, which were both attenuated by incubation with the antigenic peptide sequence (200-300 microM). 5-HT2C-like immunoreactivity was located on neurones throughout the CNS. The most abundant 5-HT2C-like immunoreactive cell bodies were in the anterior olfactory nucleus, medial and intercalated amygdaloid nuclei, hippocampus layers CA1 to CA3, laterodorsal and lateral geniculate thalamic nuclei, caudate-putamen and several areas of the cortex (including piriform and frontal), consistent with this receptor being located postsynaptic to serotonergic neurones. Immunopositive neurones were also found in the dorsal raphé, suggesting that 5-HT2C receptors may be on some serotonergic neurones. The overall distribution of 5-HT2C-like immunoreactivity complements previous findings with conventional radioligands and agrees well with reported levels of 5-HT2C receptor mRNA.

Amino Acid Sequence↗
PubMed1998

Gamma-aminobutyric acid-immunoreactive neurons in the amygdala of the rat - sex differences and effect of early postnatal castration.

The distribution of GABA-immunoreactive neurons in the rat amygdala was determined by immunohistochemical methods. Sex differences in the number of GABA-immunoreactive cell bodies were observed in the medial, central, cortical and basolateral amygdaloid nuclei. Females had more numerous GABA-expressing neurons than males (P < 0.01). Castration of neonatal males had controversial effects on this sex difference in the different parts of the amygdaloid complex. In the cortical and basolateral amygdala castrated males showed a female pattern of GABA-expression. In the central amygdala no effect of castration on the number of GABA-immunoreactive cells was found. In the medial amygdaloid nucleus numbers of GABAergic neurons in castrated males differed both from intact males and females. The results of the present study suggest that the expression of GABA in the neurons of the amygdala is under complicated gonadal hormone regulation.

Amygdala↗
PubMed1982

Neuroimmunomodulation: neural anatomical basis for impairment and facilitation.

Rats with bilateral electrolytic lesions of specific limbic nuclei show alterations in lymphoid cell number and in lymphocyte activation induced in vitro by concanavalin A (Con A). The number of splenocytes decreases after lesioning in the anterior hypothalamus (p less than 0.001), ventromedial hypothalamus (p less than .0.2), and mamillary bodies (p less than. 0.001). The number of thymocytes decreases after lesioning of the anterior hypothalamus (p less than 0.001) and increases after hippocampal lesioning (p less than 0.001). Spleen cell responsiveness to con A decreases subsequent to lesioning of the anterior hypothalamus, whereas reactivity was enhanced after lesion placement in the mamillary bodies (p less than 0.002), hippocampus (p less than 0.001), and amygdaloid complex (p less than 0.001). Thymocyte mitogen reactivity is increased by lesions of the hippocampus (p less than 0.001) and amygdaloid complex (p less than 0.001). These effects manifest themselves maximally 4 days after lesioning, with a return to normal by day 14. These preliminary data indicated that quantitative and qualitative lymphocyte functions are altered by ablation of selected brain nuclei, thereby suggesting the presence of neural modulation of immune function.

Amygdala↗
PubMed1990

[Neuroexcitotoxic action of db-cAMP: lesioning of neuronal cell bodies while sparing fibers of passage].

In our previous study, we have demonstrated that intra-amygdaloid injection of dibutyryl-cAMP causes neuronal damage in the injected AM and the CA 1-3 subfields of the ipsilateral hippocampus in addition to epileptic seizures. This result suggested that db-cAMP is a new neuroexcitotoxin. In this study, we examined comparative morphological effect on acetylcholinesterase (AChE) following intra-amygdaloid injection of db-cAMP or, kainate. In Expt. 1, twenty rats received 100 micrograms db-cAMP (N = 10), 0.5 micrograms kainate (N = 4), or saline as a vehicle (N = 6), through the implanted cannula under non-anesthesia. Either kainate or db-cAMP produced epileptic seizures, while saline induced no electroclinical ictal response. Following db-cAMP or kainate injection, neuronal loss was observed in the injected AM, but AChE positive fibers were intact. In the hippocampus ipsilateral to the injected AM, the loss of pyramidal cells was also noted in accordance with the severity of seizure intensity. In the piriform cortex ipsilateral to the injected AM, the loss of AChE-positive fibers were seen, but sparing neuronal cell bodies. In Expt. 2, nineteen rats were injected with 100 micrograms db-cAMP (N = 7), 0.5 micrograms kainate (N = 7), or saline as a vehicle (N = 5) under pentobarbital anesthesia. Kainate or db-cAMP produced few sporadic spikes.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholinesterase↗
PubMedDate not supplied

Topography of Pick body distribution in Pick's disease: a contribution to understanding the relationship between Pick's and Alzheimer's diseases.

A case of Pick's disease with the onset at 51 years old and a 15-year clinical course was studied. The brain, weighing 740 g, showed striking atrophy limited to the frontal and temporal lobes and inferior parietal lobules of both sides. The topographic distribution of Pick bodies (PBs) was investigated; PBs were present most densely in the amygdaloid, hippocampus, innominate substance, posterior cingulate and insula, inferior parietal lobule, posterior inferior temporal gyrus, and fusiform and lingular gyri. They were present less densely in the anterior frontal and temporal gyri, occipital gyri, caudate, hypothalamus, claustrum, putamen, pallidum, and olfactory bulbs and tubercles. Their presence was sparse in the pre- and post central gyri and superior parietal lobule. The calcarine and cerebellum were spared. The tectum and central grey of the midbrain, red nuclei, substantia nigra, locus ceruleus, superior central nuclei, tegmental reticular nuclei, pontine nuclei, dorsal vagal nuclei, and arcuate nuclei, were also severely affected. This distribution pattern of PBs was very similar to that of Alzheimer's neurofibrillary tangles in Alzheimer's disease, except for the pontine and arcuate nuclei. Electron microscopy of PBs disclosed two component fibrils: smooth-surfaced straight tubular filaments with a diameter of 15nm +/- 3 and no periodic constrictions, and long-period (160nm) constricted fibrils. The morphology of these two fibrils of PBs, respectively resembled the straight filaments and paired helical filaments in Alzheimer's neurofibrillary tangles.

Aged↗
PubMed1988

Distribution and characterization of neuropeptide Y-like immunoreactivity in the brain of the crested newt.

The newt brain represents a simplified model for the increasingly complex vertebrate neuronal organization. The localization of neuropeptide Y-like (NPY-like) containing neurons in the brain of Triturus cristatus was studied by means of indirect immunofluorescence, peroxidase-antiperoxidase, and avidin-biotin techniques using a highly specific antiserum. NPY-like positive cell bodies were observed in several areas, most notably in the telencephalon (primordium hippocampi and amygdaloid complex), the preoptic and suprachiasmatic areas, the hypothalamus, the dorsal thalamus, the tegmentum, and the rhombencephalon (laterolateral grey column and raphe area). Nerve fibres were particularly abundant in the pallium, striatum, septum, amygdaloid, preoptic neuropils, and pars intercalaris diencephali. Bundles of NPY-immunoreactive fibres also were visualized in the dorsal thalamus and in the posterior hypothalamus. The pars intermedia lacked any NPY-like positive fibres. Neuronal processes also were found in the tectum mesencephali and in the body of the cerebellum. A prominent NPY-like fibre network was observed in the octavolateralis. Concentrations of NPY measured by means of a specific radioimmunoassay were threefold higher in the hypothalamus (15.2 +/- 1.3 ng/mg proteins) than in the rhombencephalon (4.9 +/- 0.3) and the mesencephalon (4.3 +/- 0.2). The concentration found in the telencephalon was 2.1 +/- 0.3 ng/mg proteins. Sephadex G-50 gel chromatography of whole brain extracts indicated the presence of high molecular weight forms of NPY-like material in addition to the authentic peptide. Both amphibian and mammalian NPY peptides had an apparent molecular weight of 4,000 daltons, as evidenced by immunoblotting analysis. High-performance liquid chromatography demonstrated, however, that the newt peptide was slightly less hydrophobic than porcine NPY. The present findings indicate that NPY-immunoreactive neurons are widely distributed in the brain of urodeles. Our data indicate that the NPY molecule has been relatively well preserved during evolution.

Animals↗
PubMed1985

Local cerebral glucose utilization in the free moving mouse: a comparison during two stages of the activity-rest cycle.

The 2-deoxy-D[1-14C]glucose ([14C]DG) technique has been applied to the free moving mouse for the quantitative determination of local cerebral glucose utilization (LCGU). Reproducible values for LCGU were obtained indicating that the [14C]DG method had a sufficient resolution power to allow visualization and quantification of very small structures provided that glucose and [14C]DG plasma concentrations were measured on microsamples, autoradiographs prepared from proper tissue sections and suitable techniques used for analysis of the maps thus obtained. LCGU was measured in free moving mice during two stages of the light-dark cycle, one corresponding to a period of rest and the other to a period of high motor activity. In the two groups of animals LCGU was heterogeneous in the grey matter, the highest values being found in the auditory regions, the cerebellar and vestibular nuclei. LCGU was found to be lower in drowsy animals during the day than in active animals during the night and the difference was significant in the 8 following structures: the sensorimotor cortex, the septal nuclei, the nucleus of the olfactory tract, the basal amygdaloid nucleus, the ventral nucleus of the thalamus, the lateral geniculate body, the medial geniculate body and the auditory cortex. On the contrary, the suprachiasmatic nucleus was very active during the day and relatively inactive during the night as previously reported in the rat.

Animals↗
PubMed1996

Amygdaloid input to transiently tyrosine hydroxylase immunoreactive neurons in the bed nucleus of the stria terminalis of the rat.

Several studies have reported transient expression of tyrosine hydroxylase in a subpopulation of neurons in the bed nucleus of stria terminalis of preadolescent rats. The tyrosine hydroxylase immunoreactive (TH) neurons, which are of small to medium size and often display a typical bipolar configuration, are confined to the intermediate part of the lateral bed nucleus. By the use of a combination of experimental tracer techniques and immunocytochemical methods, we have demonstrated that these neurons receive a significant number of amygdaloid afferents, which establish mostly symmetric synaptic contacts on the cell bodies and sparsely spined dendritic shafts of the TH neurons. TH neurons also receive a small number of tyrosine hydroxylase-positive terminals of unspecified origin.

Amygdala↗
PubMed1992

Bilateral destruction of neocortical and perirhinal projection targets of the acoustic thalamus does not disrupt auditory fear conditioning.

The present study examined whether complete bilateral destruction of auditory cortex would interfere with auditory fear conditioning in rats. Complete destruction of auditory cortex required lesions of temporal neocortical and perirhinal periallocortical areas. Fear conditioning was assessed by measuring freezing and arterial pressure responses elicited by an acoustic stimulus after pairing with footshock. Animals with complete bilateral lesions of auditory cortex showed conditioned arterial pressure and freezing responses comparable to those of unoperated controls. In contrast, bilateral destruction of the acoustic thalamus interfered with the conditioning of both responses. These results demonstrate that the auditory cortex is not required for the conditioning of fear responses to simple acoustic stimuli and add to the growing body of evidence that fear conditioning can be mediated by subcortical (amygdaloid) projections of the acoustic thalamus.

Acoustic Stimulation↗
PubMed1987

Evidence that locus coeruleus is the site where clonidine and drugs acting at alpha 1- and alpha 2-adrenoceptors affect sleep and arousal mechanisms.

The behavioural and electrocortical (ECoG) effects of clonidine were studied after microinjection into the third cerebral ventricle, or microinfusion into some specific areas of the rat brain rich in noradrenaline-containing cell bodies (locus coeruleus) or into areas receiving noradrenergic terminals (dorsal hippocampus, amygdaloid complex, thalamus, frontal and sensimotor cortex). The ECoG effects were continuously analysed and quantified by means of a Berg-Fourier analyser as total power and as power in preselected bands of frequency. Clonidine (9.4 to 75 nmol) given into the third cerebral ventricle produced behavioural sedation and sleep and a dose-dependent increase in ECoG total voltage power as well as in the lower frequency bands. Much lower doses were required to produce similar behavioural and ECoG spectrum power effects after either unilateral or bilateral microinfusion of clonidine into the locus coeruleus. Doses of clonidine equimolar to those given into the third cerebral ventricle, were almost ineffective in inducing behavioural and ECoG sleep after their microinfusion into the dorsal hippocampus. In addition, a dose (0.56 nmol) of clonidine which, given into the locus coeruleus, produced marked behavioural sleep and ECoG synchronization, lacked effects when given into the ventral or anterior thalamus, into the amygdaloid complex or onto the frontal and sensimotor cortex. The behavioural and ECoG spectrum power effects of clonidine given into the third cerebral ventricle or into the locus coeruleus were prevented by antagonists of alpha 2-adrenoceptors but not by alpha 1-adrenoceptor antagonists. Intraventricular microinjection, or microinfusion into the locus coeruleus, of yohimbine, a selective alpha 2-adrenoceptor antagonist, produced behavioural arousal, increase in locomotor and exploratory activity, tachypnoea and ECoG desynchronization with a significant reduction in total voltage power. Similar stimulatory effects were also observed after microinjection of phentolamine into the same sites. No significant effects on behaviour and ECoG activity were evoked after intraventricular injection or microinfusion into the locus coeruleus of prazosin or methoxamine.

Adrenergic alpha-Antagonists↗
PubMed1988

[Amnesic syndrome caused by infarction in the area of the left anterior choroidal artery].

A case of infarction in the left anterior choroidal artery territory presenting as a regressive amnestic syndrome, associated with the usual syndrome, is reported. This amnesia had the same characteristics as that found in the left posterior cerebral artery territory infarction. The anterior choroidal artery supplies the medial part of the temporal lobe, the amygdaloid nucleus, part of the hippocampus, uncal gyrus, and the mamillary body. Therefore, an amnestic syndrome can occur together with an infarction in the AChA territory. To our knowledge this is the first report of that occurrence.

Aged↗
PubMed1987

Thalamocortical and thalamo-amygdaloid projections from the parvicellular division of the posteromedial ventral nucleus in the cat.

Projections from the parvicellular division of the posteromedial ventral thalamic nucleus (VPMpc) of the cat were examined. After injection of horseradish peroxidase conjugated with wheat germ agglutinin (WGA-HRP) into the VPMpc, both anterogradely labeled axon terminals and retrogradely labeled neuronal cell bodies were found ipsilaterally in three discrete regions of the cerebral cortex, i.e., in the orbital cortex, caudoventral part of the infralimbic cortex, and medial part of the fundus of the posterior rhinal sulcus (perirhinal area); in the subcortical regions, anterogradely labeled axon terminals were seen ipsilaterally in the rostrodorsal part of the lateral amygdaloid nucleus. Neuronal connections between these VPMpc-recipient regions were further verified by injecting WGA-HRP into each of the three cortical and the lateral amygdaloid regions. After injection of WGA-HRP into each of the three cortical regions, labeled neuronal cell bodies and axon terminals were seen ipsilaterally in the VPMpc, especially in its medial part, and in the other two of the three VPMpc-recipient cortical regions. In the rostrodorsal part of the lateral amygdaloid nucleus, both axon terminals and neuronal cell bodies were labeled after WGA-HRP injection into the perirhinal area, and only axon terminals were labeled after WGA-HRP injection into the orbital cortex, but no labeling was observed after WGA-HRP injection into the infralimbic cortex. After injection of WGA-HRP into the rostrodorsal portion of the lateral amygdaloid nucleus, both axon terminals and neuronal cell bodies were labeled ipsilaterally in the perirhinal area and the ectorhinal area, and only neuronal cell bodies were labeled ipsilaterally in the VPMpc (especially in its medial part) and orbital cortical region; no labeling was observed in the infralimbic cortex. The present results indicate that the VPMpc of the cat is connected reciprocally with the orbital, infralimbic, and perirhinal cortical regions on the ipsilateral side, that the three VPMpc-recipient cortical regions are reciprocally connected with each other, that the VPMpc sends fibers ipsilaterally to the rostrodorsal part of the lateral amygdaloid nucleus, which may relay information from the VPMpc to the perirhinal cortical area, and that the VPMpc-recipient area in the lateral amygdaloid nucleus receives cortical fibers from the orbital and perirhinal cortical regions.

Amygdala↗