Autonomic and somatomotor effects of amygdala central N. stimulation in awake rabbits☆

Applegate, Craig D.; Kapp, Bruce S.; Underwood, Mark D.; McNall, Carol L.

doi:10.1016/0031-9384(83)90201-9

Cited by 216 publications

(132 citation statements)

References 31 publications

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“…Previous studies have shown that electrical stimulation of the amygdala evokes fear-associated responses such as cardiovascular changes (24,25), potentiated startle (26), and freezing (27). Contemporary fear models posit that the basolateral amygdalar (basal and lateral nuclei) complex is interconnected with the central nucleus (CeA), which is thought to be the main amygdaloid output structure sending efferent fibers to various autonomic and somatomotor centers involved in mediating specific fear responses (7,28,29).…”

Section: Discussionmentioning

confidence: 99%

Dorsal periaqueductal gray-amygdala pathway conveys both innate and learned fear responses in rats

Kim¹,

Horovitz

Pellman³

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

157

132

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The periaqueductal gray (PAG) and amygdala are known to be important for defensive responses, and many contemporary fearconditioning models present the PAG as downstream of the amygdala, directing the appropriate behavior (i.e., freezing or fleeing). However, empirical studies of this circuitry are inconsistent and warrant further examination. Hence, the present study investigated the functional relationship between the PAG and amygdala in two different settings, fear conditioning and naturalistic foraging, in rats. In fear conditioning, electrical stimulation of the dorsal PAG (dPAG) produced unconditional responses (URs) composed of brief activity bursts followed by freezing and 22-kHz ultrasonic vocalization. In contrast, stimulation of ventral PAG and the basolateral amygdalar complex (BLA) evoked freezing and/or ultrasonic vocalization. Whereas dPAG stimulation served as an effective unconditional stimulus for fear conditioning to tone and context conditional stimuli, neither ventral PAG nor BLA stimulation supported fear conditioning. The conditioning effect of dPAG, however, was abolished by inactivation of the BLA. In a foraging task, dPAG and BLA stimulation evoked only fleeing toward the nest. Amygdalar lesion/inactivation blocked the UR of dPAG stimulation, but dPAG lesions did not block the UR of BLA stimulation. Furthermore, in vivo recordings demonstrated that electrical priming of the dPAG can modulate plasticity of subiculum-BLA synapses, providing additional evidence that the amygdala is downstream of the dPAG. These results suggest that the dPAG conveys unconditional stimulus information to the BLA, which directs both innate and learned fear responses, and that brain stimulation-evoked behaviors are modulated by context. fear circuitry | learning and memory | long-term depression | long-term potentiation | synaptic plasticity D ecades of research involving various techniques have identified that the amygdala is essential for both innate and learned fear (1). Evidence indicates that neurons in the basolateral amygdalar complex (BLA) (basal and lateral nuclei) (2) are responsive to both the conditional stimulus (CS) and unconditional stimulus (US) (3, 4), undergo plastic changes during fear conditioning (5), and are necessary for producing fear responses (6, 7). Indeed, a recent study has shown that optogenetically induced depolarization of pyramidal neurons in the lateral amygdala (LA) can elicit a fear unconditional response (UR) and, when repeatedly paired with auditory CS, supports fear conditioning via Hebbian-like synaptic plasticity (8).However, stimulation-induced fear conditioning is not only achievable through the amygdala. Other studies have found that stimulation of the dorsal periaqueductal gray (dPAG) is an effective US in fear conditioning (9, 10). The PAG has long been implicated in generating defensive behaviors (11), and it has been suggested that its stimulation can support fear conditioning to a CS because it transmits the aversive US information to the LA (9, 12). Some have a...

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Section: Discussionmentioning

confidence: 99%

Dorsal periaqueductal gray-amygdala pathway conveys both innate and learned fear responses in rats

Kim¹,

Horovitz

Pellman³

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

157

132

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“…In rats, amygdala stimulation produces freezing (Weingarten and White, 1978), cardiovascular changes (Iwata et al, 1987), and enhanced startle responses (Rosen and Davis, 1988). In rabbits, CeA stimulation induces bradycardia, pupillodilation, arrest of ongoing behavior (such as mouth and tongue movements), and enhanced amplitude of the nictitating membrane reflex (Applegate et al, 1983;Whalen and Kapp, 1991). Stimulation of the lateral hypothalamus, an efferent target of the amygdala, generates cardiovascular responses in anesthetized rabbits (Gellman et al, 1981).…”

Section: Evidence From Stimulation and Recording Studiesmentioning

confidence: 99%

“…Unit recording studies reveal that neurons in the CeA respond to both CS and US (Pascoe and Kapp, 1985) and undergo learning-related changes during fear conditioning (Applegate et al, 1983). Using a differential conditioning paradigm, Pascoe and Kapp (1985) reported that CeA neurons exhibited selective increases in single unit activity to a tone (CS+) that signaled the US, but not to a different tone (CS−) that did not signal the US.…”

Section: Evidence From Stimulation and Recording Studiesmentioning

confidence: 99%

Neural circuits and mechanisms involved in Pavlovian fear conditioning: A critical review

Kim

Jung

2006

Neuroscience & Biobehavioral Reviews

538

438

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Pavlovian or classical fear conditioning is recognized as a model system to investigate the neurobiological mechanisms of learning and memory in the mammalian brain and to understand the root of fear-related disorders in humans. In recent decades, important progress has been made in delineating the essential neural circuitry and cellular-molecular mechanisms of fear conditioning. Converging lines of evidence indicate that the amygdala is necessarily involved in the acquisition, storage and expression of conditioned fear memory, and long-term potentiation (LTP) in the lateral nucleus of the amygdala is often proposed as the underlying synaptic mechanism of associative fear memory. Recent studies further implicate the prefrontal cortexamygdala interaction in the extinction (or inhibition) of conditioned fear. Despite these advances, there are unresolved issues and findings that challenge the validity and sufficiency of the current amygdalar LTP hypothesis of fear conditioning. The purpose of this review is to critically evaluate the strengths and weaknesses of evidence indicating that fear conditioning depend crucially upon the amygdalar circuit and plasticity. KeywordsFear conditioning; Amygdala; Prefrontal cortex; LTP; NMDA Fear is considered a defensive mechanism that evolved because of its evolutionary success in protecting animals from danger. While fear to certain kinds of stimuli is innately hardwired (e.g. a loud noise evoking fear in newborn infants, a cat inducing fear in naïve laboratory-reared rats), fear can also be acquired rapidly and lastingly to different stimuli allowing animals to respond adaptively to new or changing environmental situations. In the laboratory setting, Pavlovian or classical fear conditioning has become the par excellence task for studying the anatomical, cellular and molecular bases of fear memory formation in the brain.

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“…The fact that IC stimulation elicits cardiovascular responses is also not unique for the IC. In fact, electrical stimulation of the amygdala induces stress-related responses, including tachycardia and elevated arterial pressure as well as renal, intestine and skin vasoconstriction [229], while the stimulation of the CeA produces bradycardia, dilation of the pupils and movements of the mouth and tongue [230]. Furthermore, a study using single cell recordings of the amygdala in the cat reported that 46% of cells responded to carotid sinus nerve stimulation and that half of them responded to selective baroreceptor or chemoreceptor activation [231].…”

Section: Insular Cortex and Amygdala Interactionsmentioning

confidence: 99%

The Insular Cortex and the Amygdala: Shared Functions and Interactions

Moraga-Amaro¹,

Stehberg²

2012

The Amygdala - A Discrete Multitasking Manager

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Autonomic and somatomotor effects of amygdala central N. stimulation in awake rabbits☆

Cited by 216 publications

References 31 publications

Dorsal periaqueductal gray-amygdala pathway conveys both innate and learned fear responses in rats

Dorsal periaqueductal gray-amygdala pathway conveys both innate and learned fear responses in rats

Neural circuits and mechanisms involved in Pavlovian fear conditioning: A critical review

The Insular Cortex and the Amygdala: Shared Functions and Interactions

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