Biomedical subjects

J E Ledoux

Publications and source records attributed to J E Ledoux.

At least 19 recordsLinked to original sources

PubMed2005

Fear learning transiently impairs hippocampal cell proliferation.

We sought to determine whether contextual fear conditioning, a hippocampal-dependent task, would affect neurogenesis in the dentate gyrus of the hippocampus, and if so, to identify which aspect of the training experience accounts for the change. The immediate shock deficit paradigm was used, together with bromodeoxyuridine immunohistochemistry, to isolate the contribution of different aspects of contextual fear conditioning to neurogenesis. Contextual fear learning caused a 33% decrease in the number of proliferating cells that was anatomically restricted to the dentate gyrus with no change in cell survival or differentiation. This attenuation was not related to exposure to the conditioned stimulus alone, the footshock unconditioned stimulus alone, or the expression of fear to the context after training. Instead, the effect of context conditioning on cell proliferation appears to be specifically due to the formation of an association between the context and shock during training, an amygdala dependent function.

Animals↗

PubMed2005

The lateral amygdala processes the value of conditioned and unconditioned aversive stimuli.

The amygdala is critical for acquiring and expressing conditioned fear responses elicited by sensory stimuli that predict future punishment, but there is conflicting evidence about whether the amygdala is necessary for perceiving the aversive qualities of painful or noxious stimuli that inflict primary punishment. To investigate this question, rats were fear conditioned by pairing a sequence of auditory pips (the conditioned stimulus, or CS) with a brief train of shocks to one eyelid (the unconditioned stimulus, or US). Conditioned responding to the CS was assessed by measuring freezing responses during a test session conducted 24 h after training, and unconditioned responding to the US was assessed by measuring head movements evoked by the eyelid shocks during training. We found that pre-training electrolytic lesions of the amygdala's lateral (LA) nucleus blocked acquisition of conditioned freezing to the CS, and also significantly attenuated unconditioned head movements evoked by the US. Similarly, bilateral inactivation of the amygdala with the GABA-A agonist muscimol impaired acquisition of CS-evoked freezing, and also attenuated US-evoked responses during training. However, when amygdala synaptic plasticity was blocked by infusion of the NR2B receptor antagonist ifenprodil, acquisition of conditioned freezing was impaired but shock reactivity was unaffected. These findings indicate that neural activity within the amygdala is important for both predicting and perceiving the aversive qualities of noxious stimuli, and that synaptic plasticity within LA is the mechanism by which the CS becomes associated with the US during fear conditioning.

Acoustic Stimulation↗

PubMed2004

Unconditioned stimulus pathways to the amygdala: effects of posterior thalamic and cortical lesions on fear conditioning.

Plasticity in the lateral nucleus of the amygdala is thought to be critical for the acquisition of Pavlovian fear conditioning. The pathways that transmit auditory conditioned stimulus information originate in auditory processing regions of the thalamus and cortex, but the pathways mediating transmission of unconditioned stimuli to the amygdala are poorly understood. Recent studies suggest that somatosensory (footshock) unconditioned stimulus information is also relayed in parallel to the lateral nucleus of the amygdala from the thalamus (the posterior intralaminar thalamic complex, PIT) and the cortex (parietal insular cortex). In the present study we reexamined this issue. Our results showed that bilateral electrolytic lesions of the PIT alone blocked fear conditioning, whereas bilateral excitotoxic PIT lesions had no effect. These electrolytic PIT lesions did not affect fear conditioning using a loud noise as unconditioned stimulus, defining the effects of PIT lesions as a disruption of somatosensory as opposed to auditory processing. Finally, we performed combined bilateral excitotoxic lesions of the PIT nuclei and electrolytic lesions of the parietal insular cortex. These, like excitotoxic lesions of PIT alone, had no effect on the acquisition of fear conditioning. Thus, somatosensory regions of the thalamus and cortex may well be important routes of unconditioned stimulus transmission to the amygdala in fear conditioning, but information about the unconditioned somatosensory stimulus is also transmitted from other sources that send fibers through, but do not form essential synapses in, the thalamus en route to the amygdala.

Amygdala↗

PubMed2004

Lesions in the bed nucleus of the stria terminalis disrupt corticosterone and freezing responses elicited by a contextual but not by a specific cue-conditioned fear stimulus.

The bed nucleus of the stria terminalis (BNST) is believed to be a critical relay between the central nucleus of the amygdala (CE) and the paraventricular nucleus of the hypothalamus in the control of hypothalamic-pituitary-adrenal (HPA) responses elicited by conditioned fear stimuli. If correct, lesions of CE or BNST should block expression of HPA responses elicited by either a specific conditioned fear cue or a conditioned context. To test this, rats were subjected to cued (tone) or contextual classical fear conditioning. Two days later, electrolytic or sham lesions were placed in CE or BNST. After 5 days, the rats were tested for both behavioral (freezing) and neuroendocrine (corticosterone) responses to tone or contextual cues. CE lesions attenuated conditioned freezing and corticosterone responses to both tone and context. In contrast, BNST lesions attenuated these responses to contextual but not tone stimuli. These results suggest CE is indeed an essential output of the amygdala for the expression of conditioned fear responses, including HPA responses, regardless of the nature of the conditioned stimulus. However, because lesions of BNST only affected behavioral and endocrine responses to contextual stimuli, the results do not support the notion that BNST is critical for HPA responses elicited by conditioned fear stimuli in general. Instead, the BNST may be essential specifically for contextual conditioned fear responses, including both behavioral and HPA responses, by virtue of its connections with the hippocampus, a structure essential to contextual conditioning. The results are also not consistent with the hypothesis that BNST is only involved in unconditioned aspects of fear and anxiety.

Animals↗

PubMed2004

Disruption of reconsolidation but not consolidation of auditory fear conditioning by noradrenergic blockade in the amygdala.

Consolidation is a process through which labile memories are made persistent [Science 287 (2000) 248]; [Annu Rev Psychol 55 (2004) 51]. When retrieved, a consolidated memory is rendered labile again and undergoes reconsolidation [Learn Mem 7 (2000) 73]; [Trends Neurosci 26 (2003) 65]). Reconsolidation thus offers the opportunity to manipulate memory after it is formed, and may therefore provide a means of treating intrusive memories associated with post-traumatic stress disorder (PTSD). Reconsolidation is most usually studied using protein synthesis inhibitors, which is not practical in humans. However, the beta adrenergic receptor antagonist propranolol impairs consolidation of declarative memory in humans [Science 287 (2000) 248]; [Nature 371 (1994) 702] and consolidation and reconsolidation of inhibitory avoidance learning in rats [Brain Res 368 (1986) 125]; [J Neurosci 19 (1999) 6623]. Here, we show that systemic or intra-amygdala infused propranolol blocks reconsolidation but not consolidation. If the effects on reconsolidation are verified in humans, the results would suggest the possibility that propranolol after memory retrieval might be an effective way of treatment of intrusive memories in PTSD. That the systemic effects of propranolol on reconsolidation are achieved via an action in the amygdala is especially important in light of the fact that PTSD involves alterations in the amygdala [Arch Gen Psychiatry 53 (1996) 380].

Acoustic Stimulation↗

PubMed2001

The brain decade in debate: III. Neurobiology of emotion.

This article is a transcription of an electronic symposium in which active researchers were invited by the Brazilian Society of Neuroscience and Behavior (SBNeC) to discuss the advances of the last decade in the neurobiology of emotion. Four basic questions were debated: 1) What are the most critical issues/questions in the neurobiology of emotion? 2) What do we know for certain about brain processes involved in emotion and what is controversial? 3) What kinds of research are needed to resolve these controversial issues? 4) What is the relationship between learning, memory and emotion? The focus was on the existence of different neural systems for different emotions and the nature of the neural coding for the emotional states. Is emotion the result of the interaction of different brain regions such as the amygdala, the nucleus accumbens, or the periaqueductal gray matter or is it an emergent property of the whole brain neural network? The relationship between unlearned and learned emotions was also discussed. Are the circuits of the former the underpinnings of the latter? It was pointed out that much of what we know about emotions refers to aversively motivated behaviors, like fear and anxiety. Appetitive emotions should attract much interest in the future. The learning and memory relationship with emotions was also discussed in terms of conditioned and unconditioned stimuli, innate and learned fear, contextual cues inducing emotional states, implicit memory and the property of using this term for animal memories. In a general way it could be said that learning modifies the neural circuits through which emotional responses are expressed.

Amygdala↗

PubMed2000

Cells in the posterior thalamus project to both amygdala and temporal cortex: a quantitative retrograde double-labeling study in the rat.

Auditory information from the posterior thalamus reaches the lateral nucleus of the amygdala (LA) by way of two pathways: a direct thalamo-amygdala projection and a polysynaptic thalamo-cortico-amygdala projection. However, the quantitative extent of thalamic neurons that project to the LA or to the auditory association cortex (AAC) is not known. Furthermore, the extent and topographical distribution of bifurcating cells that project to both LA and AAC are also unknown. Therefore, separate tracers were injected into LA and either into all of AAC or within discrete regions of AAC, such as temporal areas TE3 or perirhinal cortex (PRh), and quantitative analyses were performed on labeling within the subregions of the auditory thalamus in rats. Following LA injections, retrogradely labeled cells were most numerous in the posterior intralaminar nucleus (PIN; 48.0% of all labeled thalamic cells), whereas labeled cells following injections of the entire AAC were most numerous in the dorsal division of the medial geniculate nucleus (MGd; 32.9% of all labeled thalamic cells). Following AAC injections localized to only TE3, the MGd again had the majority of labeled cells (35.9%), whereas following AAC injections localized to PRh, the PIN had the most labeled cells (32.8%). Double-labeled cells were found in all the thalamic regions studied and were most commonly observed in the PIN (43.7% of all double-labeled cells following injections into LA and throughout the AAC). The percentage of double-labeled cells as a proportion of either LA-projecting or AAC-projecting cells varied among the thalamic nuclei studied, ranging from 2.9% up to 42.4%. The topographic distribution of double-labeled cells in the thalamic nuclei resembled that of single-labeled cells following LA injections more than single-labeled cells following AAC injection. These findings suggest that double-labeled cells contribute substantially to many of the direct thalamo-amygdala and indirect thalamo-AAC-amygdala projections. Among other functions, these bifurcating cells may help regulate the processing of input to the LA arriving from these two pathways to allow for certain types of plasticity in the LA during fear conditioning.

Amygdala↗

PubMed2000

Afferents from the auditory thalamus synapse on inhibitory interneurons in the lateral nucleus of the amygdala.

Physiological studies suggest that afferents to the lateral nucleus of the amygdala (LA) from the auditory thalamus initiate feedforward inhibition [Li et al. (1996b)]. This model of neural processing requires that thalamic afferents synapse directly onto inhibitory interneurons. To determine whether such synaptic contacts occur, we combined anterograde tract tracing with interneuron immunocytochemistry. The anterograde tracer biotinylated dextran amine (BDA) was injected into the auditory thalamus. Inhibitory interneurons in the LA were identified using antibodies directed against gamma aminobutyric acid (GABA) or one of the calcium binding proteins (CBPs), parvalbumin (PARV), calbindin (CALB), or calretinin (CALR), since CBPs identify distinct populations of GABAergic cells within the amygdala. The distribution of GABAergic and CBP interneurons in each subregion of the LA was examined by light microscopy and the relationships between thalamo-amygdala terminals and interneurons were examined by confocal and electron microscopy. Immunoreactive cells were distributed in all three subdivisions of LA, except for CALR-ir neurons, which were sparse in the dorsal subregion and were found mainly in the ventromedial and ventrolateral subregions. Confocal microscopy revealed some thalamo-amygdala terminals in close proximity to LA interneurons, while electron microscopy showed that thalamo-amygdala terminals made direct synaptic contacts onto distal dendritic processes of inhibitory neurons. These data provide morphological evidence that thalamic afferents synapse directly onto inhibitory interneurons in LA, and are consistent with the possibility that inputs from the auditory thalamus initiate feedforward inhibition in LA. This architecture could play an important role in the suppression of background neural noise, thereby enhancing the response of LA cells to incoming auditory stimuli.

Afferent Pathways↗

PubMed1999

Organization of projections to the lateral amygdala from auditory and visual areas of the thalamus in the rat.

Projections to the amygdala from the auditory thalamus have been implicated in the associative conditioning of fear responses to acoustic stimuli. Thalamo-amygdala auditory projections enter the amygdala via the lateral nucleus (LA). It is well documented that these projections originate in the medial division (MGm) of the medial geniculate nucleus (MGN), the posterior intralaminar nucleus (PIN), and the suprageniculate nucleus (Sg). It is not known, however, whether these thalamic projections terminate in a topographic fashion within the LA. We therefore used several retrograde tract tracing techniques to determine whether the terminations of thalamo-amygdala fibers have a topographic organization within the LA. These tracers were injected into various locations within the LA, and the distribution of the retrogradely labeled cells throughout the thalamus was analyzed. In general, rostral to caudal distinctions in the thalamus are maintained in the LA, such that projections from throughout the MGN terminate in the anterior part of the LA, whereas the caudal part of the MGN projects to the caudal part of the LA. Furthermore, the density of cells that give rise to thalamo-amygdala projections varies within each thalamic nucleus along the rostro-caudal axis. The patterns of thalamo-amygdala connectivity observed support previous parcellation schemes that segregate the LA into dorsal, medial, and lateral areas, and suggest that the LA should be further divided into anterior and posterior parts. In addition to the well-known projections to the LA originating from PIN, MGN, and Sg, we also found substantial projections from the dorsal portion of the MGN (MGd) and the lateral posterior thalamic nucleus (LP). These findings suggest that some of the functional segregation in the thalamus may be preserved in the LA, and that the role of the MGd and LP in thalamo-amygdala transmission should be reconsidered.

Amygdala↗

PubMed1999

Afferents from rat temporal cortex synapse on lateral amygdala neurons that express NMDA and AMPA receptors.

The lateral nucleus of the amygdala (LA) is a critical component of the circuitry through which environmental stimuli are endowed with emotional meaning through association with painful or threatening events. Individual cells in LA receive convergent input from auditory processing areas in the thalamus and cortex, and the excitatory amino-acid L-glutamate (Glu) participates in synaptic transmission in both pathways. Previously, we characterized the ultrastructure of pre- and postsynaptic processes in the thalamo-amygdala pathway, and showed the relation of presynaptic inputs to N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydoxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor subunits. In the present study, we examined the nature of cortico-amygdala synaptic interactions with Glu receptors in LA and determined whether they are similar or different from those in the thalamo-amygdala pathway. Cortical afferents to the LA were identified by anterograde transport of biotinylated-dextran amine (BDA) and postsynaptic sites were labeled immunocytochemically using antisera directed against the R1 subunit the NMDA receptor, and the R1 and R2/3 subunits of the AMPA receptor. Electron microscopy revealed that the vast majority of cortical afferents (99%) synapse onto distal dendritic processes and most of these processes (62%) contained at least one glutamate receptor subtype. Cortical afferents synapsed on approximately the same proportion of immunoreactive targets for each glutamate receptor subtype examined. These data provide morphological evidence that cortical afferents form direct synaptic contacts with LA neurons that express both NMDA and AMPA receptors and are consistent with recent physiological studies demonstrating the participation of NMDA and AMPA receptors in cortico-amygdala-transmission. These results are nearly identical to those obtained in the studies of the thalamo-amygdala pathway.

Afferent Pathways↗

PubMed1997

Emotional memory and psychopathology.

A leading model for studying how the brain forms memories about unpleasant experiences is fear conditioning. A cumulative body of work has identified major components of the neural system mediating this form of learning. The pathways involve transmission of sensory information from processing areas in the thalamus and cortex to the amygdala. The amygdala's lateral nucleus receives and integrates the sensory inputs from the thalamic and cortical areas, and the central nucleus provides the interface with motor systems controlling specific fear responses in various modalities (behavioural, autonomic, endocrine). Internal connections within the amygdala allow the lateral and central nuclei to communicate. Recent studies have begun to identify some sites of plasticity in the circuitry and the cellular mechanisms involved in fear conditioning. Through studies of fear conditioning, our understanding of emotional memory is being taken to the level of cells and synapses in the brain. Advances in understanding emotional memory hold out the possibility that emotional disorders may be better defined and treatment improved.

Animals↗

PubMed1997

Interamygdaloid projections of the basal and accessory basal nuclei of the rat amygdaloid complex.

Previous studies suggest that the left and right amygdalae are interconnected in rodents. The origin and topography of these connections have, however, remained obscure. In the present study, we investigated the interamygdaloid projections originating in the different divisions of the basal and accessory basal nuclei of the rat amygdala by using the Phaseolus vulgaris leucoagglutinin anterograde tract-tracing technique. The basal nucleus gave rise to substantial interamygdaloid projections. However, the density of the projections depended on the location of Phaseolus vulgaris leucoagglutinin injection in the basal nucleus. The magnocellular and intermediate divisions projected heavily to the homonymous regions on the contralateral side, as well as to the nucleus of the lateral olfactory tract. The parvicellular division projected lightly to the homonymous region on the contralateral side, to the contralateral anterior amygdaloid area and to the medial division of the central nucleus. The contralateral projections originating in the accessory basal nucleus were light compared to those of the basal nucleus. These data indicate that interamygdaloid connections in the rat brain are extensive and topographically organized. Via these connections, one amygdala may rapidly activate the contralateral side. This may explain, for example, why the epileptic seizures in one amygdala spread contralaterally and cause the development of independent seizure activity in kindling model of temporal lobe epilepsy.

Amygdala↗

PubMed1997

Lateral nucleus of the rat amygdala is reciprocally connected with basal and accessory basal nuclei: a light and electron microscopic study.

Information flow within the intra-amygdaloid circuitry has been generally believed to be unidirectional rather than reciprocal, in which case sensory inputs entering the amygdala via the lateral nucleus would not be modulated by inputs from other amygdaloid regions. In the present study we extend our earlier findings which indicated that the lateral nucleus of the rat amygdala is reciprocally connected with the basal and accessory basal nuclei. The type of synaptic contacts made by these connections is also characterized at the ultrastructural level. An anterograde tracer, Phaseolus vulgaris leucoagglutinin, was injected into the basal (n=22) or accessory basal nuclei (n=12) of the rat amygdala. The results demonstrate that the ventrolateral division of the lateral nucleus receives projections from the basal nucleus, while the medial division receives projections from the accessory basal nucleus. Electron microscopic analyses revealed that axons projecting from the basal nucleus formed both asymmetric and symmetric contacts within the ventrolateral division of the lateral nucleus, whereas axons projecting from the accessory basal nucleus to the medial division of the lateral nucleus formed only asymmetric synapses with their targets. These findings suggest that the lateral nucleus receives both inhibitory and excitatory intra-amygdaloid projections and indicate that information flow within the amygdala is not unidirectional as previously thought. The results of this study provide evidence that the early phase of sensory processing within the amygdala is already modified by inputs from other amygdaloid nuclei.

Amygdala↗

PubMed1996

Intrinsic connections of the rat amygdaloid complex: projections originating in the accessory basal nucleus.

The amygdaloid complex plays an important role in the detection of emotional stimuli, the generation of emotional responses, the formation of emotional memories, and perhaps other complex associational processes. These functions depend upon the flow of information through intricate and poorly understood circuitries within the amygdala. As part of an ongoing project aimed at further elucidating these circuits, we examined the intra-amygdaloid connections of the accessory basal nucleus in the rat. In addition, we examined connections of the anterior cortical nucleus and amygdalahippocampal area to determine whether portions of these nuclei should be included in the accessory basal nucleus (as some earlier studies suggest). Phaseolus vulgaris leucogglutinin was injected into different rostrocaudal levels of the accessory basal nucleus (n = 12) or into the anterior cortical nucleus (n = 3) or amygdalahippocampal area (n = 2). The major intra-amygdaloid projections from the accessory basal nucleus were directed to the medial and capsular divisions of the central nucleus, the medial division of the amygdalohippocampal area, the medial division of the lateral nucleus, the central division of the medial nucleus, and the posterior cortical nucleus. The projections originating in the anterior cortical nucleus and the lateral division of the amygdalohippocampal area differed from those originating in the accessory basal nucleus, which suggests that these areas are not part of the accessory basal nucleus. The present findings and our previous data suggest that each of the deep amygdaloid nuclei have different intra-amygdaloid connections. The pattern of these various connections suggests that information entering the amygdala from different sources can be integrated only in certain amygdaloid regions.

Amygdala↗

PubMed1996

Hippocampal-dependent learning and experience-dependent activation of the hippocampus are preferentially disrupted by ethanol.

A classical fear conditioning paradigm was used to examine the effect of acute ethanol on the acquisition of context conditioning, a hippocampal-dependent associative task, and tone conditioning, a hippocampal-independent task. Administration of ethanol before the presentation of seven tone-shock pairings severely disrupted the acquisition of context conditioning, but had only a slight effect on tone conditioning, when conditioned fear was measured 48 h later. This effect was dose dependent: a dose of 0.5 g/kg had no effect on either context or tone conditioning, while doses of 1.0 and 1.5 g/kg disrupted context conditioning by 78-86%, and tone conditioning by 9-17%. Subsequent experiments indicated that ethanol's preferential effect on context conditioning could not be attributed to the fact that context conditioning is weaker than tone conditioning, ethanol-induced changes in motivational state or state-dependent learning. The effect of ethanol on stimulus-induced increases in hippocampal and neocortical expression of c-fos mRNA, a marker for changes in metabolic neuronal activity, was also examined. Ethanol completely blocked the induction of hippocampal c-fos mRNA by exposure to the conditioning context alone or seven tone-shock pairings, but only attenuated neocortical responses to these stimuli. Together, these results suggest that ethanol disrupts hippocampal-dependent learning by preferentially impairing stimulus processing at the level of the hippocampus.

Animals↗

PubMed1995

Differential localization of NMDA and AMPA receptor subunits in the lateral and basal nuclei of the amygdala: a light and electron microscopic study.

Anatomical and physiological studies indicate that the amino acid L-glutamate is the excitatory transmitter in sensory afferent pathways to the amygdala and in intraamygdala circuits involving the lateral and basal nuclei. The regional, cellular, and subcellular immunocytochemical localizations of N-methyl-D-aspartate (NMDA) and L-alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA), two major classes of glutamate receptors, were examined in these areas of the amygdala. A monoclonal antibody and a polyclonal antiserum directed against the R1 subunit of the NMDA receptor were used. Each immunoreagent produced distinct distributions of perikaryal and neuropilar staining. Dendritic immunoreactivity was localized primarily to asymmetric (excitatory) synaptic junctions, mostly on spines, consistent with the conventional view of the organization and function of NMDA receptors. Whereas the anti-NMDAR1 antiserum produced sparse presynaptic axon terminal labeling and extensive glial labeling, the anti-NMDAR1 antibody labeled considerably fewer glia and many more presynaptic axon terminals. Labeled presynaptic terminals formed asymmetric and symmetric synapses, suggesting presynaptic regulation of both excitatory and inhibitory transmission. Immunoreactivity for different subunits of the AMPA receptor (GluR1, GluR2/3, and GluR4) was uniquely distributed across neuronal populations, and some receptor subunits were specific to certain cell types. Immunoreactivity for GluR1 and Glu2/3 was predominantely localized to dendritic shafts and was more extensive than that of GluR4 due to heavy labeling of proximal portions of dendrites. The distribution of GluR4 immunoreactivity was similar to NMDAR1: GluR4 was seen in presynaptic terminals, glia, and dendrites and was primarily localized to spines. The presynaptic localization of GluR4 in the absence of GluR2 suggests glutamate-mediated modulation of presynaptic Ca++ concentrations. These data add to our understanding of the morphological basis of pre- and postsynaptic transmission mechanisms and synaptic plasticity in the amygdala.

Amygdala↗

PubMed1987

Topographic organization of convergent projections to the thalamus from the inferior colliculus and spinal cord in the rat.

The purpose of this study was to identify thalamic areas receiving convergent sensory inputs from acoustic and spinal projection systems in the rat. The topographic distribution of afferents to the thalamus from the inferior colliculus and spinal cord was examined by using WGA-HRP as an anterograde axonal tracer. Following injections in the inferior colliculus, terminal labeling was present in ventral, medial, and dorsal divisions of the medial genicuate body (MGB) and in adjacent areas of the posterior thalamus, including the posterior limitans nucleus, the posterior intralaminar nucleus, the marginal zone, the peripeduncular region, the lateral or parvicellular part of the subparafascicular nucleus, and a region intercalated between the posterior limitans nucleus and the suprageniculate nucleus. In the caudal thalamus spinal projections remained in the reticular formation medial to the collicular terminal field. At intermediate levels of the MG, however, the spinal projection began to overlap the collicular field, terminating in the medial division of the MG and in the posterior intralaminar nucleus, the marginal zone, the lateral subparafascicular nucleus, and the area between the suprageniculate and posterior limitans nuclei. More rostrally, the convergent field expanded to include aspects of the dorsal MG division. The extent to which afferent projections to the thalamus from the inferior colliculus and spinal cord converge is thus graded in the caudorostral plane, with the greatest overlap occurring at the level of the rostral third of the MGB. These observations identify potential areas of acoustic and somesthetic integration and may account for observations of neuronal plasticity in the thalamus in response to the pairing of acoustic and somesthetic inputs.

Afferent Pathways↗

PubMed1987

Some central neural mechanisms governing resting and behaviorally coupled control of blood pressure.

Systems in the brain control blood pressure by maintaining life-sustaining, resting (tonic) levels and adjusting blood pressure in association with changes in regional blood flow appropriately coupled to behavior or environmental stimulation. Tonic levels of blood pressure are mediated by neurons in the medulla oblongata. The critical neurons appear to correspond to the epinephrine-containing cells of the so-called C1 group located in the rostral ventral lateral medulla. These also mediate baroreceptor reflex responses. Behaviorally coupled changes in blood pressure are often highly stereotyped and vary depending on the behavior being performed in both animals and humans. These reactive circulatory adjustments are largely mediated by forebrain regions working in concert with the medullary centers. Some of the largest increases in blood pressure occur in response to aversive emotional arousal. In hypertensive animals and humans, such changes, which are normally buffered by reflex mechanisms in the brainstem, are exaggerated. In the rat, the neural pathway mediating the coupling, through aversive emotional conditioning, of blood pressure responses to acoustic stimuli involves the transmission of sensory signals through the primary auditory projection system to the medial geniculate body, where the input is then relayed subcortically to the amygdala. The amygdala, presumably by way of connections with the hypothalamus, and from there to the brainstem or spinal cord, controls the learned emotional response. These findings, which implicate a largely unrecognized sensory relay to the amygdala in emotional learning, represent the first demonstration of a direct link between primary sensory system and autonomic control regions in the mammalian brain.

Animals↗