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PubMed1991

Inhibition of jaw-opening reflex by stimulation of the central amygdaloid nucleus in the cat.

The effect of stimulation of the amygdaloid complex on the jaw-opening reflex (JOR) was studied in the cat anesthetized with pentobarbital sodium. The conditioning stimulation of the central amygdaloid nucleus (ACE), but not the other amygdaloid nuclei, markedly inhibited the JOR induced by the tooth pulp stimulation. Ipsilateral ACE conditioning stimulation with 300 microA produced inhibition which lasted approximately 500 ms from the cessation of the stimulation. Additionally, the microinjection of monosodium glutamate into ACE elicited inhibition of the JOR that lasted about 10 min. These findings suggest that the excitation of the cell bodies in ACE exerts inhibitory action on the trigeminal nociceptive reflex.

Amygdala↗

PubMed1985

[Cerebral lymphoma associated with lesions of multiple sclerosis].

A 24 year-old man experienced a left retrobulbar neuritis which improved completely after 2 months of non-steroid antiinflammatory therapy. One month after the end of the treatment he developed a Korsakoff-like amnestic syndrome. Three months later he complained of horizontal diplopia. A CT Scan showed a diffuse enhancement of the periventricular areas, corpus callosum and fornix. Diplopia and CT scan abnormalities disappeared after the administration of tetracosactide. Subsequently a progressive worsening of the neurological condition developed, including a 1 1/2 syndrome of Fisher. In C.S.F. proteins ranged from 35 to 66 mg/dl, gammaglobulins from 4 to 5 per cent, cells from 2.2 to 6.8 per mm3 without abnormal cells. Rounded areas of enhancement were observed on CT scan in pons and right occipital lobe. Usual biological tests, abdominal echography and lymphography were normal. Death occurred 15 months after the onset of symptoms. Neuropathological examination showed: 1) a cerebral lymphoma of probable B origin with distinct masses in right occipital lobe and pontine tegmentum and a more diffuse perivascular infiltration on the left side in the amygdaloid nucleus, fourth temporal gyrus, sublenticular area, hypothalamus and in the right internal capsule; 2) multiple small clear-cut foci of demyelination with myelin-axonal dissociation bilaterally in the optic pathways, periventricular regions, corona radiata, cerebral and cerebellar white matter, sublenticular areas, temporal lobes, splenium of the corpus callosum and fornices with secondary atrophy of the mamillary bodies. Both recent and old plaques were observed. Inflammatory perivascular cuffing, when present, consisted of small nontumoral lymphocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1995

Developmental and regional changes in brain norepinephrine levels in diabetic C57BL/KsJ mice: effects of estradiol and progesterone.

Developmental and diabetes-associated changes in regional brain norepinephrine (NE) concentrations, and the influence of estradiol (E) and progesterone (P) on NE levels, were correlated with changes in blood glucose levels and body weight (obesity) in developing 4-16-week-old C57BL/KsJ (db/db) mice relative to corresponding age-matched control (+/?) parameters. Regional brain (i.e. amygdala, hypothalamus and medulla) NE levels were determined by high performance liquid chromatography. The (db/db) mice exhibited overt hyperglycemia and obesity relative to controls between 4 and 16 weeks of age. Hypothalamic NE levels in diabetics were chronically elevated as compared to those of age-matched controls by 8 weeks of age, and remained elevated through 16 weeks of age. Regional amygdaloid and medullary NE concentrations were comparable in (+/?) and (db/db) groups by 16 weeks. E-treatments normalized (db/db) hypothalamic NE concentrations to control levels between 8 and 16 weeks of age, but had no effect on amygdaloid or medullary values. In contrast, in 16 week old (db/db) mice, P-treatments elevated hypothalamic and medullary NE levels compared to controls and expected diabetic levels. These data demonstrate that a marked modification in regional brain NE concentrations occurs in association with the overt expression of the diabetes mutation during development in this species. Observed changes in adrenergic influences in specific CNS loci may be therapeutically modulated by ovarian steroid hormones, especially in the hypothalamic locus which is recognized to possess steroid-concentrating neurons. The observed normalization of regional brain NE concentrations by E-therapy may be causally related to the ovarian steroid-modulation of overt hyperglycemia and diabetes-associated neuronal degeneration in (db/db) mice.

Aging↗

PubMed2001

Fasting, leptin treatment, and glucose administration differentially regulate Y(1) receptor gene expression in the hypothalamus of transgenic mice.

NPY is a potent orexigenic signal and represents a key component of targets through which leptin exerts a regulatory restraint on body adiposity. Part of the orexigenic effects of NPY are mediated by hypothalamic NPY-Y(1) receptors. Here we studied the effect of fasting, leptin, and glucose administration on Y(1) receptor gene expression using a transgenic mouse model carrying a mouse Y(1) receptor/LacZ fusion gene. Transgene expression was determined by quantitative analysis of beta-galactosidase histochemical staining in the paraventricular, arcuate, ventromedial, and dorsomedial hypothalamic nuclei and in the medial amygdala, as a control region. Food deprivation for 72 h decreased transgene expression in the paraventricular nucleus but not in the arcuate nucleus. Leptin treatment, that was per se ineffective, counteracted the decrease of transgene expression induced in the paraventricular nucleus by 72 h fasting. Supplementing the drinking water with 10% glucose increased beta-galactosidase expression both in the paraventricular nucleus and arcuate nucleus of control mice. Finally, none of the treatments altered transgene expression in the dorsomedial hyphothalamic, ventromedial, and amygdaloid nuclei. Results suggest that changes in energetic balance affect Y(1) receptor expression in the paraventricular and arcuate nuclei and that leptin regulates the NPY-Y(1) system in the paraventricular nucleus. Different regulatory signals might modulate the NPY-Y(1) transmission in the dorsomedial hyphothalamic and ventromedial hyphothalamic nuclei.

Animals↗

PubMed2006

Investigation of Lewy pathology in the visual pathway of brains of dementia with Lewy bodies.

We examined 19 autopsied cases of dementia with Lewy bodies (DLB) using pathological and alpha-synuclein-immunohistochemical methods, and investigated Lewy pathology in the primary visual pathway (lateral geniculate body and Brodmann's area 17), secondary visual pathway (pulvinar, Brodmann's areas 18 and 19, and inferior temporal cortex), amygdala and substantia nigra, to clarify the relationship between visual misidentification and Lewy pathology in the visual pathway. Consequently, the secondary visual pathway revealed significantly severer Lewy pathology than the primary visual pathway, suggesting that the degeneration of the secondary visual pathway induces dysfunction in the recognition of objects shape and color. In addition, the amygdala revealed significantly severer Lewy pathology and neuronal loss than the primary and secondary visual pathways, suggesting that the degeneration of the amygdala, which receives the afferent connections from the substantia nigra, fails to modulate the visual processing according to cognition and emotion. These findings suggest that Lewy pathologies in the secondary visual pathway and amygdala may cause the dysfunction of the visuo-amygdaloid pathway and participate in visual misidentification in DLB patients. In addition, we compared Lewy pathology between cases with and without visual hallucinations, and showed no significant differences between the two groups.

Aged↗

PubMed1978

Effects of amygdaloid lesions on reproductive function of grouped caged mice.

Amygdalotomized, sham-operated and intact wild-derived house mice of both sexes were group-caged (8-10) or singly caged for 3 weeks. The weights of ovaries (p is less than 0.05) and uteri (p is less than 0.01) were less in intact and sham-operated grouped females compared to singly caged intact and amygdalotomized females. The weight of the reproductive organs in amygdalotomized grouped female mice was not different from singly caged controls. Body weights among amygdalotomized grouped females were heavier (p is less than 0.05) than singly caged controls. Seminal vesicle weights of intact and sham-operated grouped males were less (p is less than 0.05) than that of singly caged controls and grouped amygdalotomized males. Plasma LH values from the various groups coincided with the morphological data. These results support the hypothesis that increased population density impairs reproductive function in mammals. Perhaps the effects of decreased pituitary-gonadal function associated with overcrowding are mediated via amygdalar nuclei.

Adrenal Glands↗

PubMed1990

Comparative analysis of vasotocin-like immunoreactivity in the brain of the turtle Pseudemys scripta elegans and the snake Python regius.

The distribution of vasotocin in the brains of the turtle Pseudemys scripta elegans and the snake Python regius was studied with immunohistochemical methods. In both species, vasotocin-immunoreactive (VTi) cells were found in the supraoptic nucleus, the paraventricular nucleus and the bed nucleus of the stria terminalis. No VTi cell bodies were seen in the brainstem. Vasotocinergic fibers were found in all major brain divisions. Intrahypothalamic VTi fibers were observed between the supraoptic and the paraventricular nuclei and in the median eminence. An extensive network of extrahypothalamic VTi fibers extends from the olfactory bulb to the spinal cord. Limbic structures, such as the nucleus accumbens, the septal area and the ventral amygdaloid nucleus, contain a moderate to dense VTi plexus. Other areas with a substantial number of VTi fibers are the lateral habenular nucleus, the ventral tegmental area, the substantia nigra, the locus coeruleus and the nucleus of the solitary tract. Sex-related differences in the density of the VTi fibers were observed in the lateral septal nucleus, the mid-brain periaqueductal gray and, to a lesser extent, in the ventral amygdaloid nucleus, the lateral habenular nucleus, the ventral tegmental area and the substantia nigra. In these areas, the density of VTi fibers is higher in males than in females. The distribution of vasotocin-like immunoreactivity in the brains of Pseudemys and Python resembles the pattern previously observed in the lizard Gekko gecko. However, among the three species several differences exist, the most remarkable one being the variation in number of liquor-contacting VTi cells in the paraventricular nucleus.

Animals↗

PubMed1978

The neuroanatomy of amnesia. A critique of the hippocampal memory hypothesis.

The discovery that medial temporal lobe lesions produce amnesia in humans if the lesion extends sufficiently far posteriorly to include the hippocampus forms the keystone of the hippocampal memory hypothesis. Strong supporting evidence comes from the occurrence of mammillary body disease in Korsakoff's psychosis. Disease of the posterior cerebral artery confirmed the observations on the medial temporal lobectomies by showing that pathology in the ventromedial quadrant of the temporal lobe produces amnesia. The occasional piece of contradictory evidence was sufficiently ambiguous to be dismissed or re-interpreted. Although the contradictory evidence that emerged from animal research created severe difficulties, opinion had crystallized on the matter to the degree that the data were unable to force rejection of the hippocampal memory hypothesis. This necessarily led to the conclusion that the animal model is a poor one: either the human hippocampus is unique with respect to memory or the tests which are used in animals do not tap the same mnemonic processes that are impaired by the human lesions. Both these arguments are nearly impossible to refute. The brain of every species is different and there is no way in which monkeys and humans can be tested under identical conditions. There has never been much enthusiasm for the suggestion that the human hippocampus is so different from other animals that this uniqueness could account for the apparent differences between the behavioural effects of human and animal hippocampal lesions. However, many experimenters have devised clever tests of the possibility that the problem is in the animal behavioural measures. Given sufficient circularity of reasoning, the project must necessarily eventually be successful. The argument is that if the usual tests of learning and memory that are used with animals are not disrupted by hippocampal lesions, then these are not tests of the kinds of learning and memory defects displayed by human amnestics. One has only to search for tasks that are disrupted by hippocampal lesions in animals, and these then must tap the same memory processes that are disrupted by the human lesions. The possibility has rarely been seriously considered that it might be damage to some structure in the ventromedial quadrant of the temporal lobe other than the hippocampus that is responsible for the amnesia. The amygdala and entorhinal area have been ruled out by both the human and animal data. However, the temporal stem is a likely possibility. Its position makes it vulnerable to the surgical approach which was used in human medial temporal lobectomies, and its damage in animals produces deficits in learning and retention. When medial temporal lesions were made in monkeys in the same way that they were made in humans, inadvertent damage to the temporal stem occurred along with the intended amygdaloid and hippocampal injury. Symptoms characteristic of damage to the temporal cortex resulted from these lesions and they were probably caused by the damage to the stem...

Alcohol Amnestic Disorder↗

PubMed1985

Acute and chronic effects of dextropropoxyphene on behaviour and central inhibitory neurotransmission in the rat.

There was no overt evidence of the development of physical dependence, as shown by a decrease in the body weight of rats following the abrupt withdrawal of dextropropoxyphene after two weeks administration. The ambulation and rearing scores in the 'open field' apparatus were increased after chronic, but not acute drug administration and returned to control values two days following drug withdrawal. GABA turnover, determined from the rise in GABA concentrations following GABA-transaminase inhibition, was reduced in the frontal and amygdaloid cortex after acute and chronic drug administration; a compensatory rise in GABA turnover in the amygdaloid cortex occurred two days after drug withdrawal. Na+, K+, ATP'ase activity, determined in a synaptosomal fraction from the mid-brain and hippocampus, was decreased in the latter region only during drug administration; a compensatory increase in the activity of this enzyme was found two days after drug withdrawal. These results support the view that chronically administered dextropropoxyphene may cause changes in inhibitory transmission and central neurotransmitter transport.

Animals↗

PubMed1997

Collateral projections of single neurons in the posterior thalamic region to both the temporal cortex and the amygdala: a fluorescent retrograde double-labeling study in the rat.

It has been reported that the acoustic thalamus of the rat sends projection fibers to both the temporal cortical areas and the lateral amygdaloid nucleus to mediate conditioned emotional responses to an acoustic stimulus. In the present study, fluorescent retrograde double labeling with Fast Blue and Diamidino Yellow has been used in the rat to examine whether single neurons in the posterior thalamic region send axon collaterals to both the temporal cortical areas and lateral amygdaloid nucleus. One of the tracers was injected into the lateral amygdaloid nucleus and the other into the temporal cortical areas close to the rhinal sulcus. Neurons double-labeled with both tracers were found mainly in the posterior intralaminar nucleus and suprageniculate nucleus, and to a lesser extent in the subparafascicular nucleus and medial division of the medial geniculate nucleus. No double-labeled neurons were seen in either the dorsal or ventral division of the medial geniculate nucleus. When one of the tracers was injected into the lateral amygdaloid nucleus and the other into either the dorsal portion of the temporal cortex, the dorsal portion of the entorhinal cortex, or the posterior agranular insular cortex, no double-labeled neurons were found in the posterior thalamic region. The present results indicate that a substantial number of single neurons in the acoustic thalamus project to both the limbic cortical areas and lateral amygdaloid nucleus by way of axon collaterals. These neurons may be implicated in affective and autonomic components of responses to multi-sensory stimuli, including acoustic ones.

Amygdala↗

PubMedDate not supplied

Aggregation of alpha-synuclein/NACP in the neuronal and glial cells in diffuse Lewy body disease: a survey of six patients.

BACKGROUND: alpha-Synuclein is now known to be a major component of Lewy bodies (LBs) in Parkinson's disease (PD) and diffuse Lewy body disease (DLBD). Recently, cytoplasmic aggregation of alpha-synuclein has also been reported to occur in glial cells in these diseases. METHODS: We have conducted an immunohistochemical survey to clarify in detail the distribution of alpha-synuclein aggregates in the central nervous system of patients with DLBD. The cerebrum, brainstem, cerebellum and spinal cord of six patients with DLBD were examined immunohistochemically using anti-alpha-synuclein antibodies. RESULTS: In all patients, alpha-synuclein-immunoreactive cytoplasmic inclusions, including those with profiles of typical LBs, were visualized in neurons of the cerebral neocortex, hippocampus, amygdaloid nucleus, hypothalamus, brainstem pigmented nuclei and reticular formation. In some of these patients, similar spherical cytoplasmic inclusions were also detected in neurons of the olfactory bulb, basal ganglia, thalamus, the subthalamic, pontine, inferior olivary and cerebellar dentate nuclei, and in the spinal gray matter. Moreover, alpha-synuclein-immunoreactive cytoplasmic inclusions, which appeared circular or coil-like in shape, were found in glial cells. In four patients with longstanding DLBD, these cytoplasmic inclusions were distributed widely in brain areas, including brainstem, basal ganglia, and cerebral and cerebellar white matter. CONCLUSION: The widespread occurrence of alpha-synuclein aggregates in both neuronal and glial cells is a pathological feature in patients suffering from DLBD.

Aged↗

PubMedDate not supplied

Reversible colchicine-induced disruption of amygdaloid function in sodium appetite.

Bilateral injections of the antimitotic drug colchicine into the medial amygdaloid nuclei resulted in a dissociation of the normally concurrent sodium appetite and water thirst in rats following formalin-induced hypovolemia and hyponatremia. While control rats drank the normally aversive sodium solution as well as water after formalin injection, colchicine-treated animals failed to ingest the sodium solution but did consume the expected amount of water in order to compensate for hypovolemia. Sodium consumption, but not water consumption, remained significantly depressed in the colchicine-treated rats when they were challenged again with formalin 11 days but not 20 days after amygdaloid injections. The latter result suggested complete recovery from the colchicine-induced amygdaloid dysfunction. This study indicates that colchicine may serve as a potentially useful technique for producing reversible lesions of known duration for the assessment of brain-behavior relationships.

Afferent Pathways↗

PubMed2004

Stabilization of thalamo-cortical long-term potentiation by the amygdala: cholinergic and transcription-dependent mechanisms.

Synaptic potentiation allows neurons to enhance excitability and store information for extended time periods. We examined the role of the amygdaloid complex, known to facilitate long-term memory encoding, to influence synaptic strength at thalamo-cortical synapses. In urethane-anaesthetized rats, theta-burst stimulation of the dorsal lateral geniculate nucleus of the thalamus induced early phase (1-2 h) long-term potentiation (LTP) of the field postsynaptic potential (fPSP) recorded in the ipsilateral primary visual cortex. Electrical stimulation (100 Hz) of the amygdala 5 min after thalamic stimulation converted early phase LTP to stable late-phase (> 4 h) LTP. This effect was not correlated with the degree of electrocorticographic activation of V1 induced by amygdala stimulation. Amygdala stimulation without thalamic theta-burst stimulation did not change thalamo-cortical fPSPs. The centrally acting cholinergic-muscarinic receptor antagonist scopolamine (1 mg/kg, i.p.), but not peripherally acting methyl-scopolamine, completely blocked the amygdala-induced conversion of early to late-phase thalamo-cortical LTP. Further, ventricular application of the transcription inhibitor anisomycin (250 micro g) reduced amygdala-induced late-phase LTP induction. These results demonstrate that the amygdaloid complex transforms time-limited synaptic enhancement of thalamo-cortical transmission into long lasting increases in synaptic strength. These processes are mediated, at least in part, by cholinergic and transcription-dependent mechanisms. These amygdaloid-induced effects provide a potential mechanism underlying long-term enhancement of sensory transmission and information encoding in thalamo-cortical networks.

Amygdala↗

PubMed2006

The distribution of dopamine D1 receptor and mu-opioid receptor 1 receptor immunoreactivities in the amygdala and interstitial nucleus of the posterior limb of the anterior commissure: relationships to tyrosine hydroxylase and opioid peptide terminal systems.

Mismatches between dopamine innervation and dopamine D1 receptor (D1) distribution have previously been demonstrated in the intercalated cell masses of the rat amygdala. Here the distribution of enkephalin and beta-endorphin immunoreactive (IR) nerve terminals with respect to their mu-opioid receptors is examined in the intercalated cell masses, along with a further immunohistochemical analysis of the dopamine/D1 mismatches. A similar analysis is also made within the extended amygdala. A spatial mismatch in distribution patterns was found between the mu-opioid receptor-1 immunoreactivity and enkephalin IR in the main intercalated island of the amygdala. Discrete cell patches of dopamine D1 receptor and mu-opioid receptor-1 IR were also identified in a distinct region of the extended amygdala, the interstitial nucleus of the posterior limb of the anterior commissure, medial division (IPACM), which displayed sparse tyrosine hydroxylase or enkephalin/beta-endorphin IR nerve terminals. Furthermore, distinct regions of the main intercalated island that showed dopamine/D1 receptor matches (the rostral and rostrolateral parts) were associated with strong dopamine and cyclic AMP regulated phosphoprotein, 32 kDa-IR in several D1 IR neuronal cell bodies and dendrites, whereas this was not the case for the dopamine/D1 mismatch areas (the rostromedial and caudal parts) of the main intercalated island. The lack of correlation between the terminal/receptor distribution patterns suggests a role for volume transmission for mu-opioid receptor- and dopamine D1 receptor-mediated transmission in distinct regions of the amygdala and extended amygdala. This may have implications for amygdaloid function, where slow long lasting responses may develop as a result of volume transmission operating in opioid peptide and dopaminergic communication.

Amygdala↗

PubMed1998

Medial temporal and whole-brain atrophy in dementia with Lewy bodies: a volumetric MRI study.

OBJECTIVE: Dementia with Lewy bodies (DLB) is emerging as a common cause of degenerative dementia. A recent pathologic study has indicated that the medial temporal lobe in patients with DLB was less atrophic than that in patients with AD. The purpose of this study was to examine whether medial temporal MRI volumetry was useful to differentiate DLB from AD clinically. METHODS: We compared the volumes of the hippocampal formation, amygdaloid complex, and whole brain in 27 patients with probable DLB (based on the criteria of the Consortium on DLB International Workshop), 27 patients with probable AD (based on criteria of the National Institute of Neurological Disease and Stroke/Alzheimer's Disease and Related Disorders Association), and 27 normal elderly subjects using an MRI-based volumetric technique. The three groups were matched for age and sex. Severity of cognitive disturbances represented by their Mini-Mental State Examination score was comparable between the DLB and AD groups. RESULTS: Hippocampal volume (normalized to intracranial volume) in the DLB group was significantly larger than that in the AD group, but significantly smaller than that in the normal control group. There were no significant differences in the amygdala and whole-brain volume between the DLB group and the AD group, but the atrophies of the amygdala and whole brain were more severe in the DLB group than those in the control group. CONCLUSIONS: These findings indicate the usefulness of MRI hippocampal volumetry in clinically discriminating patients with DLB from patients with AD.

Aged↗

PubMed2001

Central representation of the sympathetic nervous system in the cerebral cortex.

The sympathetic-related regions of the cerebral cortex were identified in rats after pseudorabies virus injections were made in functionally different targets: adrenal gland, stellate ganglion which regulates the heart, or celiac ganglion which innervates the gastrointestinal tract. Extensive transneuronal labeling was found in limbic system areas: (1) extended amygdaloid complex, (2) lateral septum, and (3) infralimbic, insular, and ventromedial temporal cortical regions (viz., ectorhinal cortex=Brodmann's area 36, perirhinal cortex=area 35, lateral entorhinal=area 28, and ventral temporal association cortex=Te3 region). Deep temporal lobe structures were prominently labeled, including the amygdalopiriform and amygdalohippocampal transition areas, ventral hippocampus and ventral subiculum. The cortical circuits mediating emotional-autonomic changes (i.e., mind-body control) are discussed.

Amygdala↗

PubMed2002

Obesity-inducing amygdala lesions: examination of anterograde degeneration and retrograde transport.

Small lesions centered in the posterodorsal region of the medial amygdala resulted in excessive weight gains in female rats. Unilateral lesions were nearly as effective as bilateral lesions in the first 48 h after surgery (+21 to +32 g). Assessment of lesion damage was done by both qualitative evaluation and by a quantitative grid-point counting method. The critical sites for weight gain were the intra-amygdaloid bed nucleus of the stria terminalis and the posterodorsal medial amygdaloid nucleus. Incidental damage to the overlying globus pallidus was negatively related to weight gain. The cupric silver method for demonstrating axonal degeneration was applied to brains with obesity-inducing lesions. A dense pattern of degenerating terminals was found in the lateral septum, amygdala, ventral striatum, and ventromedial hypothalamus. Degeneration in the paraventricular nucleus of the hypothalamus was scarce or absent. Small retrograde tracer injections made in either the intra-amygdaloid bed nucleus of the stria terminalis or in the posterodorsal medial amygdaloid nucleus labeled cells in the amygdala, lateral septum, and hypothalamus, reciprocating the anterograde projections from the amygdala to these areas. The data suggest that subdivisions of the posterodorsal amygdala participate in the regulation of feeding in a manner that is similar to the better-known role of this part of the brain in mediating reproductive behavior. Although topographical differences may exist within the amygdaloid and hypothalamic subdivisions regulating these two sexually dimorphic behaviors, the relays engaged by feeding-related connections and those related to reproduction are remarkably parallel.

Amygdala↗

PubMed2005

The bed nucleus of the stria terminalis in the Syrian hamster: subnuclei and connections of the posterior division.

The bed nucleus of the stria terminalis is a key part of a ring of cells extending between the centromedial amygdala and bed nucleus of the stria terminalis referred to as the extended amygdala. The present study describes the architecture of the bed nucleus of the stria terminalis and the connections of subnuclei in posterior bed nucleus of the stria terminalis. The hamster bed nucleus of the stria terminalis is readily allotted to anterior and posterior divisions separated by the fibers of the body of the anterior commissure. The anterior division has four subnuclei: anteromedial, anterointermediate, anterolateral, and anteroventral. Within the posterior division, there are three distinct regions: posteromedial, posterointermediate, and posterolateral. In hamsters, the posterior bed nucleus of the stria terminalis contributes to male sexual behavior, particularly chemoinvestigation. Moreover, the posterior bed nucleus of the stria terminalis is part of a neural circuit essential for mating, including the medial amygdaloid nucleus and medial preoptic area. The connections of bed nucleus of the stria terminalis, posteromedial part, bed nucleus of the stria terminalis, posterointermediate part and bed nucleus of the stria terminalis, posterolateral part were visualized by co-injection of anterograde (Phaseolus vulgaris leucoagglutinin) and retrograde (cholera toxin B) tract tracers. The bed nucleus of the stria terminalis, posterointermediate part and bed nucleus of the stria terminalis, posteromedial part have dense bidirectional connections with medial amygdaloid nucleus and cortical amygdala via the stria terminalis and ventral amygdalofugal pathway. These subnuclei also maintain bidirectional connections with steroid-concentrating areas including lateral septum, medial preoptic area, hypothalamus, and periaqueductal gray. The bed nucleus of the stria terminalis, posterointermediate part and bed nucleus of the stria terminalis, posteromedial part receive projections from the subiculum and send projections to deep mesencephalic nuclei. By contrast, the bed nucleus of the stria terminalis, posterolateral part is connected with the central amygdala, lateral hypothalamus, subthalamic nucleus, nucleus accumbens, substantia innominata, substantia nigra and thalamus. Thus, the bed nucleus of the stria terminalis, posterointermediate part and bed nucleus of the stria terminalis, posteromedial part have similar connections with areas involved in social behaviors. The bed nucleus of the stria terminalis, posterolateral part maintains connections with areas involved in motivational circuits. This supports the concept of distinct circuits within the extended amygdala which differentially link the centromedial amygdala and bed nucleus of the stria terminalis.

Animals↗