Amygdala input to medial prefrontal cortex (mPFC) in the rat: A light and electron microscope study

Bacon, Sarah J.; Headlam, Anthony J.N.; Gabbott, P.L.A.; Smith, A.D.

doi:10.1016/0006-8993(96)00155-2

Cited by 164 publications

(105 citation statements)

References 18 publications

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“…In support of this interpretation, we note that one of the most important afferent connections to medial prefrontal cortex in rodents is from the basolateral nucleus of the amygdala (Bacon et al, 1996). There is additional evidence that this ascending amygdalofrontal pathway provides not only direct excitatory ascending inputs to pyramidal neurons but also to local inhibitory interneurons in the medial prefrontal cortex (Gabbott et al, 2006).…”

Section: Positive and Negative Functional Coupling Of The Amygdalasupporting

confidence: 57%

Functional Coupling of the Amygdala in Depressed Patients Treated with Antidepressant Medication

Chen

Suckling

Ooi

et al. 2007

Neuropsychopharmacol

202

150

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The amygdala plays a central role in various aspects of affect processing and mood regulation by its rich anatomical connections to other limbic and cortical regions. It is plausible that depressive disorders, and response to antidepressant drugs, may reflect changes in the physiological coupling between the amygdala and other components of affect-related large-scale brain systems. We explored this hypothesis by mapping the functional coupling of right and left amygdalae in functional magnetic resonance imaging data acquired from 19 patients with major depressive disorder and 19 healthy volunteers, each scanned twice (at baseline and 8 weeks later) during performance of an implicit facial affect processing task. Between scanning sessions, the patients received treatment with an antidepressant drug, fluoxetine 20 mg/day. We found that the amygdala was positively coupled bilaterally with medial temporal and ventral occipital regions, and negatively coupled with the anterior cingulate cortex. Antidepressant treatment was associated with significantly increased coupling between the amygdala and right frontal and cingulate cortex, striatum, and thalamus. Treatment-related increases in functional coupling to frontal and other regions were greater for the left amygdala than for the right amygdala. These results indicate that antidepressant drug effects can be measured in terms of altered coupling between components of cortico-limbic systems and that these effects were most clearly demonstrated by enhanced functional coupling of the left amygdala.

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Section: Positive and Negative Functional Coupling Of The Amygdalasupporting

confidence: 57%

Functional Coupling of the Amygdala in Depressed Patients Treated with Antidepressant Medication

Chen

Suckling

Ooi

et al. 2007

Neuropsychopharmacol

202

150

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“…These observations suggest that mPFC KORs may shape glutamatergic synaptic transmission by inhibiting presynaptic glutamate terminals, but the source of the inputs being modulated is not known. As anatomical studies indicate the mPFC receives glutamatergic inputs from the BLA (Bacon et al, 1996;McDonald, 1996) and the BLA has a rich density of KOR receptor mRNA and immunoreactivity (DePaoli et al, 1994;Meng et al, 1993;Van't Veer et al, 2013a), it is conceivable that mPFC KORs are expressed in BLA terminals, thereby modulating glutamatergic inputs from this limbic structure. Here, we utilized in vivo electrophysiological techniques combined with optogenetics to determine whether KORs negatively regulate glutamatergic inputs from the BLA to the mPFC.…”

Section: Introductionmentioning

confidence: 99%

Prefrontal Cortical Kappa Opioid Receptors Attenuate Responses to Amygdala Inputs

Tejeda

Hanks

Scott

et al. 2015

Neuropsychopharmacol

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Kappa opioid receptors (KORs) have been implicated in anxiety and stress, conditions that involve activation of projections from the basolateral amygdala (BLA) to the medial prefrontal cortex (mPFC). Although KORs have been studied in several brain regions, their role on mPFC physiology and on BLA projections to the mPFC remains unclear. Here, we explored whether KORs modify synaptic inputs from the BLA to the mPFC using in vivo electrophysiological recordings with electrical and optogenetic stimulation. Systemic administration of the KOR agonist U69,593 inhibited BLA-evoked synaptic responses in the mPFC without altering hippocampus-evoked responses. IntramPFC U69,593 inhibited electrical and optogenetic BLA-evoked synaptic responses, an effect blocked by the KOR antagonist nor-BNI. Bilateral intra-mPFC injection of the KOR antagonist nor-BNI increased center time in the open field test, suggesting an anxiolytic effect. The data demonstrate that mPFC KORs negatively regulate glutamatergic synaptic transmission in the BLA-mPFC pathway and anxiety-like behavior. These findings provide a framework whereby KOR signaling during stress and anxiety can regulate the flow of emotional state information from the BLA to the mPFC.

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“…The vmPFC-amygdala circuit also plays an integral role in the regulation of fear memory (Quirk and Beer, 2006). The vmPFC and amygdala are reciprocally innervated (Canteras et al, 1992;Bacon et al, 1996;McDonald et al, 1996;Smith et al, 2000;Berretta et al, 2005), and the vmPFC likely participates in modulation of learned fear via input to amygdaloid nuclei (Sotres-Bayon et al, 2004), perhaps by activation of inhibitory neurons in the intercalated nuclei (Berretta et al, 2005). Lesions (Quirk et al, 2000), neurochemical inactivation (Santini et al, 2001;Santini et al, 2004), or stress-induced dendritic retraction in this region produces deficits in fear extinction and/or the recall of extinction (Izquierdo et al, 2006;Miracle et al, 2006) resulting from dysregulation of PFC modulation of the amygdala (Canteras et al, 1992;McDonald et al, 1996;Smith et al, 2000;Berretta et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Impaired Stress-Coping and Fear Extinction and Abnormal Corticolimbic Morphology in Serotonin Transporter Knock-Out Mice

Wellman¹,

Izquierdo²,

Garrett³

et al. 2007

J. Neurosci.

339

278

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A lesser-expressing form of the human 5-HT transporter (5-HTT) gene has been associated with increased fear and anxiety and vulnerability to the effects of stress. These phenotypic abnormalities are linked to functional and anatomical disturbances in a neural pathway connecting the prefrontal cortex (PFC) and amygdala. Likewise, rodent and nonhuman primate studies indicate a major role for PFC and amygdala in the mediation of fear-and stress-related behaviors. We used a 5-HTT knock-out (KO) mouse to examine the effects of genetically driven loss of 5-HTT function for the following: (1) depression-related behavior in response to repeated stress, and pavlovian fear conditioning, extinction, and extinction recall; and (2) dendritic morphology and spine density of Golgi-stained pyramidal neurons in the infralimbic cortex (IL) and the basolateral amygdala (BLA). 5-HTT KO mice exhibited increased depressive-like immobility after repeated exposure to forced swim stress, compared with wild-type (WT) controls. Whereas fear conditioning and fear extinction was normal, 5-HTT KO mice exhibited a significant deficit in extinction recall. The apical dendritic branches of IL pyramidal neurons in 5-HTT KO mice were significantly increased in length relative to WT mice. Pyramidal neurons in BLA had normal dendritic morphology but significantly greater spine density in 5-HT KO mice compared with WT mice. Together, the present findings demonstrate a specific phenotypic profile of fear-and stress-related deficits in 5-HTT KO mice, accompanied by morphological abnormalities in two key neural loci. These data provide insight into the behavioral sequelae of loss of 5-HTT gene function and identify potential neural substrates underlying these phenotypes.

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Amygdala input to medial prefrontal cortex (mPFC) in the rat: A light and electron microscope study

Cited by 164 publications

References 18 publications

Functional Coupling of the Amygdala in Depressed Patients Treated with Antidepressant Medication

Functional Coupling of the Amygdala in Depressed Patients Treated with Antidepressant Medication

Prefrontal Cortical Kappa Opioid Receptors Attenuate Responses to Amygdala Inputs

Impaired Stress-Coping and Fear Extinction and Abnormal Corticolimbic Morphology in Serotonin Transporter Knock-Out Mice

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