Amygdala

Cross references:   Amygdaloid Hippocampal Convergence  
Hippocampus     Nucleus Accumbens Septi    Ventral Tegmental Area   
Bed Nucleus of the Stria Terminalis     Figure Labels     Dictionary     
Fear     Stress    Pain    


Kolb and Whishaw discuss the amygdala on numerous pages, somet
imes with pictures: [K&W: 58, 424-435 & 502-510]. 



Amygdala (Wiki) 
    "The amygdalae, singular: amygdala; are almond-shaped groups of nuclei located deep within the medial temporal lobes of the brain in complex vertebrates, including humans.[2] Shown in research to perform a primary role in the processing and memory of emotional reactions, the amygdalae are considered part of the limbic system.[3]"  

Amyg.png Location of the amygdala in the human brain  

The figure shows the underside (ventral view) of a semi-transparent human brain, with the front of the brain at the top. The red blobs show the approximate location of the en:amygdala in the en:temporal lobes of the human brain. Note: the amygdala is covered by the ventral temporal cortex (i.e., it is inside the transparent brain).
 



http://upload.wikimedia.org/wikipedia/commons/b/bc/Constudoverbrain.png

    "
The regions described as amygdala nuclei encompass several structures with distinct functional traits. Among these nuclei are the basolateral complex, the cortical nucleus, the medial nucleus, and the central nucleus. The basolateral complex can be further subdivided into the lateral, the basal, and the accessory basal nuclei.[3][4][5]
    Anatomically, the amygdala[6] and more particularly, its central and medial nuclei,[7] have sometimes been classified as a part of the basal ganglia.
"  
    "
The amygdala sends impulses to the hypothalamus for activation of the sympathetic nervous system, to the thalamic reticular nucleus for increased reflexes, to the nuclei of the trigeminal nerve and the facial nerve, and to the ventral tegmental area, locus coeruleus, and laterodorsal tegmental nucleus for activation of dopamine, norepinephrine and epinephrine.[4]
"  
My comment
    No mention of any connection to the
Dorsal Raphe Nucleus .          



THE CIRCUITS OF THE BODY'S ALARM SYSTEM (BTB) 
intermediate - cellular 
       

 

The amygdala is a complex structure of the brain and has about twelve sub-regions. Though not all of the regions are involved in fear reactions, many of them maintain connections that participate in such reactions actively.

    From experiments with lesions and tracing of neural pathways, we now recognize the lateral nucleus as the gateway into the amygdala. It is through the lateral nucleus that the amygdala receives information from the outside world. For example, in experiments with fear conditioned by sounds, the stimulus that exits the auditory thalamus enters the amygdala via the lateral nucleus.

    The structure through which information exits the amygdala has also been clearly identified. It is the central nucleus, which controls the bodily reactions associated with fear.

    Within the amygdala, a number of internal pathways have been identified by which information is routed from the lateral nucleus to the central nucleus. There is one pathway that goes directly from the lateral nucleus to the central nucleus.

    The neurons of the lateral nucleus also project their axons to several other, intermediate nuclei: the basal nucleus (with its parvicellular and magnocellular divisions), the accessory basal nucleus, and the medial nucleus. These structures then relay the information to the central nucleus.

     Each of these nuclei can be modulated by brain structures that can influence the emotions, such as the hippocampus, the frontal cortex, and the hypothalamus.  See also:  Hippocampus  and  Hypothalamus  .  Most of them can also be subdivided into sub-regions whose connectivity also appears to be very specific.


THE AMYGDALA AND ITS ALLIES (BTB) 
advanced - neurological   
http://thebrain.mcgill.ca/flash/a/a_04/a_04_cr/a_04_cr_peu/a_04_cr_peu.html       
THE TWO PATHWAYS OF FEAR

    The amygdala is a structure located deep in the anterior inferior temporal lobe of the brain. The amygdala receives projections mostly from the sensory regions of the thalamus and the cortex, but also from several other structures such as the hippocampus and the prefrontal cortex.

    As with the  Hippocampus , most of the neural pathways that enter the amygdala are paired with other pathways that exit it. One of these output pathways is the ventral amygdalofugal pathway, which plays an important role in associative learning–of a conditioned fear, for example. The gratifying or aversive nature of a stimulus is associated by connections of this pathway to the nucleus accumbens  (See also:  Nucleus Accumbens Septi  ), which plays a recognized role in the brain’s pleasure circuits. The other main destinations of this pathway are the ventral striatum, the septum, the Hypothalamus, the nuclei of the Brainstem, and certain parts of the cortex (orbitofrontal, piriform, cingulate, etc.).

 

    Another important pathway emerging from the amygdala is the  Stria Terminalis  , which is to the amygdala as the fornix is to the hippocampus. Like the fornix, the   Stria Terminalis  projects only to sub-cortical structures such as the Hypothalamus and the septum. The Hypothalamus and the septum also receive projections from the amygdala by another route–the ventral amygdalofugal pathway–as well as from the Hippocampus. Moreover, the Hippocampus and the amygdala are located beside and have many connections with each other.  

    The basal ganglia, a group of sub-cortical nuclei, are another area of the brain that seems to be closely involved in voluntary emotional activity. The basal ganglia are known to be involved in controlling movement, and their interaction with the amygdala supports this active, voluntary component of the behavioural expression of emotion.

    Meanwhile, the automatic bodily responses involved in emotions such as fear are controlled mainly by the outputs of the amygdala to the nuclei of the Sympathetic Nervous System in the Brainstem and to the Hypothalamus, which itself controls the Hormonal secretions of the Pituitary Gland.

The outputs of the amygdala provide a good idea of what is necessary for the experience of an emotion such as fear. The connections from the amygdala to the cortex can influence attention to and perception and memory of dangerous situations. The amygdala can also influence the cortex indirectly, through its connections to the attention system in the  Brainstem . Other parts of the  Brainstem trigger the cascade of physiological reactions associated with fear that send feedback to the brain. When this feedback is combined in working memory with the other “ingredients” just described, it produces the feeling of experiencing an emotion.    See:  Stress 




1990   

The effects of separate or combined infusions of corticotrophin-releasing factor and vasopressin either intraventricularly or into the amygdala on aggressive and investigative behaviour in the rat.  
Only abstract available online.   
Also reported in:  
Criminal CRH & Vassopressin     
    "
These experiments show that combined infusions of
Corticotropin-releasing hormone (CRH) (CRF) and Arginine Vasopressin (AVP) into either the lateral Ventricule or the amygdalae have synergistic effects on aggressive, investigative and other behaviours occurring during social interaction between male rats. They suggest, therefore, that the two peptides interact at intracerebral sites to control behaviour much as they do on the Anterior Pituitary to regulate ACTH release. "  
    "
There was a U-shaped effect on aggressive behaviour after intra-amygdala infusions of
Corticotropin-releasing hormone (CRH) CRF, lower doses increasing Agonistic Behavior, higher ones decreasing it. This was not seen after Ventricular System infusions. AVP had no effect by either route; however, given together with CRF it potentiated the latter's effect on aggressive behaviour.  Combined infusions of both peptides given either  intracerebroventricularly (icv = into the Ventricular System ) or into the amygdala decreased investigative behaviour."    
    "
These experiments show that the behavioural effects of CRF and AVP on social interaction have different profiles, and that the effects of each peptide differ when it is given 
intracerebroventricularly (icv = into the Ventricular System ) or directly into the amygdala. There is also clear evidence for synergistic effects of the two peptides on behavior after infusion by either route."  


1991    440<518 
Distribution of amygdala input to the nucleus accumbens septi: an electrophysiological investigation.   

    See:  Amygdaloid Hippocampal Convergence 


1992   
Corticotropin-releasing factor antagonist reduces emotionality in socially defeated rats via direct neurotropic action.
 
Only abstract available online.       
    "
A
Corticotropin-releasing hormone (CRH) CRF antagonist, alpha-hel CRF9-41, administered  intracerebroventricularly (icv = into the Ventricular System ) (5 and 25 micrograms i.c.v.) immediately post- Stress and 5 min prior to maze testing reversed the heightened emotionality produced by the resident exposure  Stressor."  
    "
Intra-amygdaloid administration of lower doses of the CRF antagonist (125, 250 and 500 ng i.c.) also reversed, dose-dependently, the effect of exposure to an aggressive resident without altering the behavior of unstressed control animals.  
    Further, the enhanced release of
ACTH and corticosterone (See:  Cortisol) following social conflict was not modified over the short term by the intra-amygdaloid dose of CRF antagonist (250 ng i.c.) which was effective in reversing  Stress-induced hyper-emotionality.  
    These results suggest that
Limbic System    Corticotropin-releasing hormone (CRH) CRF substrates exert an anxiogenic effect on the exploratory behavior of socially defeated rats via a Pituitary-Adrenal-independent mechanism."    


1992   
Convergence of projections from the rat hippocampal formation, medial geniculate and basal forebrain onto single amygdaloid neurons: an in vivo ext...  
http://www.ncbi.nlm.nih.gov/pubmed/1525648   



1994    395<518 
Input from the amygdala to the rat nucleus accumbens: its relationship with tyrosine hydroxylase immunoreactivity and identified neurons. 
    "
Both tyrosine hydroxylase-positive fibres from the mesolimbic dopamine system and amygdala projection fibres from the basolateral nucleus are known to terminate heavily in the nucleus accumbens. Caudal amygdala fibres travelling dorsally via the stria terminalis project densely to the nucleus accumbens shell, especially in the dopamine rich septal hook.  
    The amygdala has been associated with the recognition of emotionally relevant stimuli while the mesolimbic dopamine system is implicated with reward mechanisms. There is behavioural and electrophysiological evidence that the amygdala input to the nucleus accumbens is modulated by the mesolimbic dopamine input, but it is not known how these pathways interact anatomically within the nucleus accumbens. 
     Using a variety of neuroanatomical techniques including anterograde and retrograde tracing, immunocytochemistry and intracellular filling, we have demonstrated convergence of these inputs on to medium-sized spiny neurons. The terminals of the basolateral amygdala projection make asymmetrical synapses predominantly on the heads of spines which also receive on their necks or adjacent dendrites, symmetrical synaptic input from the mesolimbic dopamine system. Some of these neurons have also been identified as projection neurons, possibly to the ventral pallidum. We have shown a synaptic level how dopamine is positioned to modulate excitatory limbic input in the nucleus accumbens."  


2004        
The Role of the Central Nucleus of the Amygdala in Mediating Fear and Anxiety in the Primate    
Full length PDF available online.  Must download to copy-and-paste. 
from the PDF   
    "These findings demonstrate involvement of the primate central nucleus of the amygdala (CeA) region in mediating threat-related anxiety and acute fear-related behavioral and 
Hormonal responses. In addition to reducing snake fear and PituitaryAdrenal activity, the CeA lesions resulted in decreased expression of threat-induced freezing and reduced  Cerebrospinal Fluid (CSF)  Corticotropin-releasing hormone (CRH) (CRF) concentrations."  
   "... we found that bilateral CeA lesions decreased snake
fear."  
    "The data also revealed that the lesions affected the 
PituitaryAdrenal system. Although group effects were not observed for Cortisol, there were significant negative correlations between CeA lesion size and basal and  Stress-induced Cortisol concentrations. 
   
ACTH concentrations were significantly decreased in both the bilaterally and the asymmetrically lesioned animals. Because ACTH concentrations were reduced across both baseline and stress conditions, it is likely that the lesions resulted in an overall reduction in PituitaryAdrenal activity. Studies in rodents also demonstrate that CeA lesions blunt  Stress-induced ACTH secretion"   
    "In summary, the present study demonstrates a role for the primate CeA in mediating anxiety-related defensive responses, acute fear responses,
PituitaryAdrenal activity, and brain Corticotropin-releasing hormone (CRH) (CRF) systems."  
my comment   
    I searched PubMed for 'amygdala crh'.  There were 216 hits, but none described amydalar input to the CRHergic neurons in the
Paraventricular nucleus (PVN).  On the other hand, there were several references describing the amygdala as both a source and a recipient of CRH. 
    When I searched PubMed for 'hippocampus chr', I got only 23 hits, and none were useful. 



2004   
A CRH1 antagonist into the amygdala of mice prevents defeat-induced defensive behavior.
  (PubMed)  - 2004   
Only abstract available online.       
    "
Corticotropin-releasing hormone (CRH) is believed to play an important role in the regulation of behavioral responses to  Stress. CRH(1) receptor (See:  CRH Receptors  ) antagonists may reduce stress responsivity.
    Stress increases CRH in the amygdala, important in memory consolidation." 
    "We infused the CRH(1) antagonist antalarmin (0.25 microg/125 nl) bilaterally into the amygdala of mice immediately after defeat and measured their response to a nonaggressive intruder stimulus mouse placed within their home cage 24 h after defeat. ... Defeated mice that received antalarmin into the amygdala exhibited significantly less defensive posture than did vehicle-treated defeated mice."  
    "These findings support a role for CRH in the amygdala to promote consolidation of emotional memory and indicate that antagonism of CRH(1) receptors in the amygdala may prevent the development of exaggerated fear responses in stressed mice.
"    


2004   
Involvement of central amygdalar and bed nucleus of the stria terminalis corticotropin-releasing factor in behavioral responses to social defeat.      Repeated in:   Bed Nucleus Stria Terminalis  .   
Only abstract available online. 
    "
The authors investigated whether
Corticotropin-releasing hormone (CRH) (CRF) within the central nucleus of the amygdala (CeA) and  Bed Nucleus Stria Terminalis (BNST) is a critical component of the neural circuitry mediating conditioned defeat.  
    In this model, hamsters that have experienced social defeat subsequently display only submissive-defensive
Agonistic Behavior instead of territorial aggression.  
    Conditioned defeat was significantly reduced following infusion of the CRF receptor antagonist D-Phe CRF((12-41)) into the BNST but not into the CeA.  
    In another experiment, hamsters given unilateral lesions of the CeA and infusions of D-Phe CRF((12-41)) into the contralateral BNST displayed significantly less submissive behavior than did controls. These data suggest that CRF acts within a neural circuit that includes the amygdala and the BNST to modulate agonistic behavior following social defeat.
"   



2008   
155<519  
Basolateral amygdala neurons facilitate reward-seeking behavior by exciting nucleus accumbens neurons.
  
    Abstract: 
    "Both the nucleus accumbens (NAc) and basolateral amygdala (BLA) contribute to learned behavioral choice. Neurons in both structures that encode reward-predictive cues may underlie the decision to respond to such cues, but the neural circuits by which the BLA influences reward-seeking behavior have not been established. Here, we test the hypothesis that the BLA drives NAc neuronal responses to reward-predictive cues. First, using a disconnection experiment, we show that the BLA and dopamine projections to the NAc interact to promote the reward-seeking behavioral response. Next, we demonstrate that BLA neuronal responses to cues precede those of NAc neurons and that cue-evoked excitation of NAc neurons depends on BLA input. These results indicate that BLA input is required for dopamine to enhance the cue-evoked firing of NAc neurons and that this enhanced firing promotes reward-seeking behavior."      
   
Free PMC Article   


2009    137<519     
Activity-dependent depression of medial prefrontal cortex inputs to accumbens neurons by the basolateral amygdala. 
Abstract: 
    "
The encoding of reward-predictive stimuli by neurons in the nucleus accumbens (NAcc) depends on integrated synaptic activity from the basolateral amygdala (BLA) and medial prefrontal cortex (mPFC) afferent inputs. In a previous study, we found that single electrical stimulation pulses applied to the BLA facilitate mPFC-evoked spiking in NAcc neurons in a timing-dependent manner, presumably by a fast glutamatergic mechanism. In the present study, the ability of repetitive BLA activation to modulate synaptic inputs to NAcc neurons through dopamine- or N-methyl-D-aspartate (NMDA)-dependent mechanisms is characterized. NAcc neurons receiving excitatory input from both mPFC and BLA were recorded in urethane-anesthetized rats. Train stimulation of the BLA depressed mPFC-evoked spiking in these neurons. This was not attributable to mechanisms involving NMDA or dopamine D1, D2, D3 or D5 receptors, since blockade of these receptors did not affect the BLA-mediated depression. BLA-mediated depression was only evident when the BLA stimulation evoked spikes in the recorded neuron; thus, depolarization of the recorded neuron may be critical for this effect. The ability of the BLA to suppress mPFC-to-NAcc signaling may be a mechanism by which normal or pathologically heightened emotional states disrupt goal-directed behavior in favor of emotionally-driven responses."  
   
Free PMC Article 


2011   

Excitatory transmission from the amygdala to nucleus accumbens facilitates reward seeking.   
Abstract: 
    "
The basolateral amygdala (BLA) has a crucial role in emotional learning irrespective of valence. The BLA projection to the nucleus accumbens (NAc) is thought to modulate cue-triggered motivated behaviours, but our understanding of the interaction between these two brain regions has been limited by the inability to manipulate neural-circuit elements of this pathway selectively during behaviour. To circumvent this limitation, we used in vivo optogenetic stimulation or inhibition of glutamatergic fibres from the BLA to the NAc, coupled with intracranial pharmacology and ex vivo electrophysiology. Here we show that optical stimulation of the pathway from the BLA to the NAc in mice reinforces behavioural responding to earn additional optical stimulation of these synaptic inputs. Optical stimulation of these glutamatergic fibres required intra-NAc dopamine D1-type receptor signalling, but not D2-type receptor signalling. Brief optical inhibition of fibres from the BLA to the NAc reduced cue-evoked intake of sucrose, demonstrating an important role of this specific pathway in controlling naturally occurring reward-related behaviour. Moreover, although optical stimulation of glutamatergic fibres from the medial prefrontal cortex to the NAc also elicited reliable excitatory synaptic responses, optical self-stimulation behaviour was not observed by activation of this pathway. These data indicate that whereas the BLA is important for processing both positive and negative affect, the glutamatergic pathway from the BLA to the NAc, in conjunction with dopamine signalling in the NAc, promotes motivated behavioural responding. Thus, optogenetic manipulation of anatomically distinct synaptic inputs to the NAc reveals functionally distinct properties of these inputs in controlling reward-seeking behaviours."    
   
Free PMC Article






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