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The effects of epilepsy and its treatments on affect and emotion
Published in Howard J. Rosen, Robert W. Levenson, Neurocase, 2020
John D. Hixson, Heidi E. Kirsch
Either due to the loss of mesial temporal structures on the side of surgery or due to an abnormal contralateral amygdala, a temporal lobectomy also can create impairments in tasks specific to the amygdala. Multiple investigators have found evidence of impaired fear conditioning in patients who have had an ATL (LaBar et al., 1995; Weike et al., 2005); intriguingly, this impairment occurred despite an intact psychophysical response to the stimuli as measured by skin conductance discrimination. In addition, when memory for these stimuli was tested, patients were shown to have intact declarative memory of the contingencies despite impairment of the fear-potentiated startle response (Weike et al., 2005). This supports the idea that declarative learning and the conditioned fear response occur via distinct systems, and that the latter depends critically on proper amygdalar functioning.
Animal Models of Anxiety and Anxiolytic Drug Action
Published in Siegfried Kasper, Johan A. den Boer, J. M. Ad Sitsen, Handbook of Depression and Anxiety, 2003
Dallas Treit, Aldemar Degroot, Akeel Shah
In contrast, fear-potentiated startle is reliably suppressed by 5HT1A-type anxiolytics. Buspirone, gepirone, and ipsapirone each blocked potentiated startle across a wide range of doses [46,121,145,161]. In addition, the magnitude of these anxiolytic effects were similar to those of benzodiazepine anxiolytics. The selective 5HT1A agonists flesinoxan and 8-OH-DPAT also produced dose-dependent anxiolytic effects on fear-potentiated startle [119,120].
Synthesis, Enzyme Localization, and Regulation of Neurosteroids
Published in Sheryl S. Smith, Neurosteroid Effects in the Central Nervous System, 2003
Behav. Brain Res., 58, 123, 1993. Stanford, S.C., Central adrenoceptors in response and adaptation to stress, in The Pharmacology of Noradrenaline in the Central Nervous System, Heal, D.J. and Marsden, C.A., Eds., Oxford University Press, Oxford, 1990, p. 379.Charney, D.S. and Heninger, G.R., Abnormal regulation of noradrenergic function in panic disorders: effects of clonidine in healthy subjects and patients with agoraphobia and panic disorder, Am. J. Psychiatry, 43, 1042, 1986.Redmond, D.E., Jr., The possible role of locus coeruleus noradrenergic activity in anxietγ-panic, Clin. Neuropharmacol., 9 (Suppl. 4), 40, 1986.Davis, M., The role of the amygdala in fear-potentiated startle: implications for animal models of anxiety, Trends Pharmacol. Sci., 13, 35, 1992.Akwa, Y. et al., The amygdala mediates the anxiolytic-like effect of the neurosteroid allopregnanolone in rat, Behav. Brain Res., 106, 119, 1999.Gray, J.A., The neuropsychology of anxiety: an enquiry into the functions of the septo-hippocampal system, Behav. Brain Sci., 5, 469, 1982.Gabriel, M., Discriminative avoidance learning: a model system, in Neurobiology of Cingulate Cortex and Limbic Thalamus: A Comprehensive Handbook, Vogt, B.A.
Pharmacological treatment of anxiety disorders in adults with epilepsy
Published in Expert Opinion on Pharmacotherapy, 2018
In general terms, anxiety is a set of preformed cognitive and behavioral patterns in response to threat or stress and, from an evolutionary perspective, represents a normal adaptive response [22]. The Pavlovian-fear conditioning and fear-potentiated startle response are well-known animal models of anxiety and they have been extensively used to study the neurobiology of anxiety, identifying an extended neuroanatomical network which centers on the amygdala and a number of connected structures including the limbic system, the sensory thalami, the orbital, and medial prefrontal cortex, the anterior insula, the hypothalamus, and multiple brainstem nuclei [23]. The amygdala is a key structure in the experience of fear and its autonomic and endocrine response (through the output to the hypothalamus). The output to the periaqueductal grey nuclei mediates avoidance behavior while the hippocampi play a role in the re-experiencing of fear [24,25]. The spontaneous activation of these networks is the major neurobiological hypothesis for anxiety disorders and the reduction of such an excessive output from these neurons represents the main target of antianxiety treatments. In this regard, it is interesting to note that such a mechanism has a number of similarities with the excessive outburst typical of epileptic neurons and easily explain why some of the agents used in the treatment of epilepsy are also effective in anxiety and vice versa [26,27].
Enhanced innate fear and altered stress axis regulation in VGluT3 knockout mice
Published in Stress, 2018
Diána Balázsfi, Anna Fodor, Bibiána Török, Szilamér Ferenczi, Krisztina J. Kovács, József Haller, Dóra Zelena
In addition to the elevated resting CRH mRNA levels, the lack of VGluT3 decreased the stressor-induced corticosterone rise. Previous studies connected enhanced fear to decreased corticosterone elevation not only in the shock-associated environment several days after foot shock trauma (Verma, Bali, Singh, & Jaggi, 2015), but also in the FST test (Browne et al., 2014), similarly to the mechanisms found in principal fear disorders or PTSD. Even the high alcohol preferring mice, showing greater fear-potentiated startle, a model used to study PTSD, showed lower corticosterone rise after different stimuli (Chester, Kirchhoff, & Barrenha, 2014). Indeed, it is widely accepted that low cortisol response to trauma (Yehuda, McFarlane, & Shalev, 1998) may be a risk factor for PTSD and PTSD patients react to new stimuli with reduced stress-hormone level elevation (Daskalakis, Lehrner, & Yehuda, 2013). These facts suggest that reduced stress-hormone reaction in VGluT3 KO mice might be an important contributor to their exaggerated emotional state.
Fear Learning in Genital Pain: Toward a Biopsychosocial, Ecologically Valid Research and Treatment Model
Published in The Journal of Sex Research, 2023
Second, latent constructs such as fear need to be measured explicitly and throughout the conditioning procedure. Fear can be measured directly via fear-potentiated startle responses or verbal reports of fear learning after each (block of) CS presentations (e.g., ratings of US-expectancy, contingency, and risk as well as ratings of affect and fear; Beckers et al., 2013; Bradley & Lang, 2000). Note that Both and colleagues did include continuous reports of fear, affect, and US-expectancy in several of their studies on sexual conditioning (Brom et al., 2015a, 2015b; Pawłowska et al., 2020).