Amygdaloid region for defence reactions and its efferent pathway to the brain stem

Hilton, S. M.; Zbrożyna, A. W.

doi:10.1113/jphysiol.1963.sp007049

Cited by 395 publications

(95 citation statements)

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“…Electrical stimulation in anesthetized animals of the areas from which defensive behavior is evoked in awake animals produces a pattern of sympathetic excitation characteristically evoked by threatening stimuli. Thus, electrical stimulation of sites in the amygdala, hypothalamus, and central gray evokes the cardiovascular defense pattern (Hilton and Zbrozyna, 1963;Hilton 1975;Yardley and Hilton, 1986). We recently found that microinjection of excitatory amino acids into the amygdala of freely behaving, conscious rats evokes increases in arterial pressure and heart rate, responses indicative of sympathetic excitation (Iwata et al, 1987).…”

Section: Discussionmentioning

confidence: 99%

“…In fact, the term, "defense reaction," was first used to describe the behavioral response evoked by electrical stimulation of the hypothalamus and other areas of the brain stem in the awake cat (Hess and Brtigger, 1943). Since that time, many studies have been conducted using electrical brain stimulation to map the neural pathways mediating defensive behavior and the associated pattern of sympathetic activation (Abrahams et al, 1960;Hilton and Zbrozyna, 1963;Flynn, 1967;Kaada, 1967;Fonberg, 1972Fonberg, , 1973Reis, 1972;Clemente and Chase, 1973;Hilton, 1975;Siegel and Edinger, 198 1). It is assumed in such work that the neural pathways underlying defense reactions elicited by brain stimulation overlap considerably, if not completely, with the pathways through which defense is expressed in response to natural (sensory) stimuli.…”

Section: Discussionmentioning

confidence: 99%

“…Since the major projection from the acoustic thalamus terminates in the lateral nucleus and the amygdalostriatal zone (LeDoux et al, 1985), one of these regions probably serves as the sensory interface of the amygdala during conditioning (Cicchetti et al, 1987). In contrast, the amygdaloid output pathway is likely to involve the central nucleus, a structure implicated in the expression of the autonomic and behavioral correlates of emotional arousal by lesion (Kapp et al, 1979;Gentile et al, 1986;Hitchcock and Davis, 1986;Iwata et al, 1986a), electrical stimulation (Ursin and Kaada, 1960;Hilton and Zbrozyna, 1963;Reis and Oliphant, 1964;Heinemann et al, 1973;Kapp et al, 1982;Galeno and Brody, 1983;Iwata et al, 1987), and unit recording (Applegate et al, 1982;Pascoe and Kapp, 1985a, b) studies in several species. If the central amygdaloid nucleus (ACE) is an essential link in the pathway mediating the autonomic and behavioral correlates of conditioned fear, it should be possible to disrupt conditioned fear responses by destroying areas to which the central nucleus projects.…”

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confidence: 99%

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Different projections of the central amygdaloid nucleus mediate autonomic and behavioral correlates of conditioned fear

et al. 1988

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The purpose of the present study was to determine whether lesions of areas projected to by the central amygdaloid nucleus (ACE) would disrupt the classical conditioning of autonomic and/or behavioral emotional responses. The areas studied included 3 projection targets of the ACE: the lateral hypothalamic area (LH), midbrain central gray (CG) region, and bed nucleus of the stria terminalis (BNST). Lesions were made either electrolytically or by microinjection of ibotenic acid, which destroys local neurons without interrupting fibers of passage. Two weeks later, the animals were classically conditioned by pairing an acoustic stimulus with footshock. The next day, conditioned changes in autonomic activity (increases in arterial pressure) and emotional behavior (“freezing,” or the arrest of somatomotor activity) evoked by the acoustic conditioned stimulus (CS) were measured during extinction trials. Electrolytic and ibotenic acid lesions of the LH interfered with the conditioned arterial pressure response, but did not affect conditioned freezing. Electrolytic lesions of the rostral CG disrupted conditioned freezing but not conditioned changes in arterial pressure. Ibotenic acid injected into the rostral CG reduced neither the arterial pressure nor the freezing response. Injection of ibotenic acid in the caudal CG, like electrolytic lesions of the rostral CG, disrupted the freezing, but not the arterial pressure response. Injection of ibotenic acid into the BNST had no effect on either response. These data demonstrate that neurons in the LH are involved in the autonomic, but not the behavioral, conditioned response pathway, whereas neurons in the caudal CG are involved in the behavioral, but not the autonomic, pathway. Different efferent projections of the central amygdala thus appear to mediate the behavioral and autonomic concomitants of conditioned fear.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Different projections of the central amygdaloid nucleus mediate autonomic and behavioral correlates of conditioned fear

et al. 1988

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“…However, it was very difficult to test the hypothesis more fully because the common anaesthetics of the time, including chloralose, barbituates and halothane were found to block afferent activation of the brain stem defence areas. In other words, noxious stimuli that were known to evoke defensive or aggressive behaviour with the characteristic autonomic changes in conscious animals could not evoke the autonomic components of the response in animals anaesthetised with these agents (31,32).…”

Section: The Alerting or Defence Responsementioning

confidence: 99%

Chemoreceptors and cardiovascular control in acute and chronic systemic hypoxia

Jm¹

1998

Braz J Med Biol Res

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This review describes the ways in which the primary bradycardia and peripheral vasoconstriction evoked by selective stimulation of peripheral chemoreceptors can be modified by the secondary effects of a chemoreceptor-induced increase in ventilation. The evidence that strong stimulation of peripheral chemoreceptors can evoke the behavioural and cardiovascular components of the alerting or defence response which is characteristically evoked by novel or noxious stimuli is considered. The functional significance of all these influences in systemic hypoxia is then discussed with emphasis on the fact that these reflex changes can be overcome by the local effects of hypoxia: central neural hypoxia depresses ventilation, hypoxia acting on the heart causes bradycardia and local hypoxia of skeletal muscle and brain induces vasodilatation. Further, it is proposed that these local influences can become interdependent, so generating a positive feedback loop that may explain sudden infant death syndrome (SIDS). It is also argued that a major contributor to these local influences is adenosine. The role of adenosine in determining the distribution of O 2 in skeletal muscle microcirculation in hypoxia is discussed, together with its possible cellular mechanisms of action. Finally, evidence is presented that in chronic systemic hypoxia, the reflex vasoconstrictor influences of the sympathetic nervous system are reduced and/or the local dilator influences of hypoxia are enhanced. In vitro and in vivo findings suggest this is partly explained by upregulation of nitric oxide (NO) synthesis by the vascular endothelium which facilitates vasodilatation induced by adenosine and other NO-dependent dilators and attenuates noradrenaline-evoked vasoconstriction. Correspondence

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“…Electrical stimulation in animals of the areas from which defensive behaviour is evoked produced a pattern of sympathetic excitation characteristically evoked by threatening stimuli. Thus, electrical stimulation of sites in the Bright-field photomicrographs showing a low-magnification overview of the PAG in sagittal section ( (Hilton, 1975, Hilton and Zbrozyna, 1963, Thornton, et al, 2002, Yang and Coote, 1998.…”

Section: Hypothalamusmentioning

confidence: 99%

The Periaqueductal Gray: From Longitudinal columns to defensive behaviour

Lim¹,

Blokland²,

Wandevalle³

et al. 2009

jecm

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Recent findings on the different functional properties of the neuroanatomical columnar subdivision of the Periaqueductal Gray (PAG) have provided a fundamental understanding for the pathophysiology of panic and anxiety disorder. In this review, we focus mainly on the prominent role of the PAG in defensive behaviour by combining both the behavioural and neuroanatomical data. We have applied the theoretical model of the "two dimensional defence system" by McNaughton and Corr (2004), and thereby constituted an organizational structure on the neuronal circuitry of the different brain regions in relation with this panic-and fearlike behaviour. It has become clear that the dorsal and lateral PAG are involved in the active emotional coping (fight and flight reaction), whereas the ventrolateral PAG is responsible for the passive emotional coping (quiescence/freezing). In this regard, the PAG and other related brain structures are working in concert with different neurotransmitters providing animals with defensive strategies in response to predatory threats. The functional roles of the PAG in these behaviours as characterized in animals warrants further translational studies in humans which may eventually lead to novel approaches in anxiety-and panic-related disorders.

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Amygdaloid region for defence reactions and its efferent pathway to the brain stem

Cited by 395 publications

References 14 publications

Different projections of the central amygdaloid nucleus mediate autonomic and behavioral correlates of conditioned fear

Different projections of the central amygdaloid nucleus mediate autonomic and behavioral correlates of conditioned fear

Chemoreceptors and cardiovascular control in acute and chronic systemic hypoxia

The Periaqueductal Gray: From Longitudinal columns to defensive behaviour

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