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1
Herman, David Hans Keele N. Bradley. "The role of hyperpolarization-activated non-selective cation current in amygdala excitability and serotonin mediated effects". Waco, Tex. : Baylor University, 2007. http://hdl.handle.net/2104/5098.
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Holahan, Matthew R. "Amygdala involvement in aversive conditioning". Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=19529.
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Research over the past several decades has revealed that the amygdala is involved in aversive, or fear, conditioning. However, the precise nature of this involvement remains a matter of debate. One hypothesis suggests that disrupting amygdala function eliminates the storage of memories formed during aversive conditioning, eliminating the production of internal responses that alter the expression of observable behaviors. Alternatively, lesions or inactivation of the amygdala may impair the modulation of memories in other brain regions and disrupt the ability to perform certain observable behaviors. The experiments reported in the present thesis examined these arguments by making multiple behavioral measures during exposure to unconditioned (US) or conditioned (CS) aversive cues. Amygdala activity was inferred from changes in c-Fos protein expression or activity was temporarily suppressed with muscimol injections. The relationship between the behavioral measures and the role of the amygdala in producing them was examined. Amygdala neurons expressing the c-Fos protein tracked exposure to the US and CS but did not coincide with expression of freezing. Temporary inactivation of the amygdala with muscimol injections before presentation of the US or exposure to the CS attenuated the expression of freezing and active place avoidance; two incompatible behaviors. Finally, temporary inactivation of amygdala activity blocked freezing, place avoidance, and memory modulation produced by the same posttraining exposure to an aversive CS. Since amygdala activation alone was not sufficient to produce freezing and inactivation of the amygdala eliminated freezing, place avoidance, and memory modulation, the results cannot be interpreted as reflecting a direct role for the amygdala in production of observable behaviors. The results also preclude the idea that memory modulation is the only function of the amygdala. Rather, the results of all three studies suggest that the amygdala stores an aversive representation of the US which promotes the expression of various behaviors, possibly through the production of internal responses reflecting an aversive affective state.
3
Hamdani, Selma. "Effect of basolateral amygdala lesions on learning taste avoidance under various water deprivation schedules". Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116086.
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Learned taste avoidance (LTA) was studied by allowing rats to drink a novel sweet solution followed by induction of gastric malaise (training). When the solution was presented again (test), normal rats reduced their consumption. Ultrasonic vocalizations indicated that the rats experienced positive affect during training which shifted to negative affect during the test. Basolateral amygdala lesions eliminated the LTA and the negative affective shift when the rats were 23 hr water deprived during both training and test suggesting amygdala-based Pavlovian conditioning, but only attenuated the LTA and eliminated the aversive shift when the rats were 3 hr deprived on the test, suggesting instrumental learning. When rats were 3 h deprived during training the lesions had no effect on either the LTA or the negative affective shift, suggesting an amygdala-independent form of LTA based on latent learning.
4
Austin, Mason. "Is the lateral septum's inhibitory influence on the amygdala mediated by GABA-ergic neurons?" Diss., Connect to the thesis, 2004. http://hdl.handle.net/10066/741.
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Sovran, Peter. "A behavioural and anatomical investigation of amygdaloid mediation of affective memory". Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=22808.
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This thesis examined the involvement of the lateral, central and basolateral nuclei of the amygdala in both appetitive and aversive affective behavior. In Experiment I, using electrolytic lesions, it was found that damage to the lateral but not central or basolateral nuclei blocked a Conditioned Cue Preference (CCP) to food (Froot Loops) in rats that were not deprived of food. In Experiment II, also using electrolytic lesions, it was found that damage to the basolateral but not central or lateral nuclei blocked a Conditioned Cue Aversion (CCA) produced by a lithium chloride injection (42 mg/kg). In Experiment III results similar to those in Experiments I and II were obtained using axon-sparing NMDA lesions. The results of Experiments I-III demonstrate a double dissociation of affective memory with respect to the amygdala. The lateral nucleus of the amygdala mediated the memory of an appetitive affective experience and the basolateral nucleus mediated memory for an aversive affective experience.In Experiment IV the contributions of appetitive and aversive affective states to a food CCP were examined. Lesions of the lateral but not the basolateral nucleus were found to attenuate but not completely eliminate a food CCP when the rats were food deprived in the Paired compartment and sated in the Unpaired compartment. Food deprivation alone produced a CCA and lesions of the basolateral but not the lateral nucleus blocked this effect. The possibility that both the appetitive and aversive behaviours are mediated through connections from the dopamine-reward centres in the ventral striatum is discussed.
6
Blakeley, Hillary Joy Keele N. Bradley. "Functional roles of arg-vasopressin and oxytocin on cellular excitability in neurons of the rat lateral amygdala". Waco, Tex. : Baylor University, 2007. http://hdl.handle.net/2104/5127.
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Merzlyak, Irina Y. "The Role of the basolateral amygdala in affective associative learning, arousal and adaptation". Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2006. http://wwwlib.umi.com/cr/ucsd/fullcit?p3205363.
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Thesis (Ph. D.)--University of California, San Diego, 2006.Title from first page of PDF file (viewed April 4, 2006). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
8
Beaulieu, Nicole. "Behavioral investigation of the basolateral amygdala and of the pyriform cortex in rats". Thesis, McGill University, 1990. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=70179.
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The experiments reported in the present dissertation investigated the contribution of the pyriform cortex and of the basolateral amygdala to three classes of affective behavior: conditioned aversions, conditioned preferences, and neophobia. It was demonstrated that lesions of the pyriform cortex cause an impairment in the acquisition of aversions to olfactory, but not gustatory, stimuli and that this impairment is not secondary to alterations in primary olfactory function. The acquisition of a preference for a particular odor paired with reward was also shown to be impaired by such lesions. These results are discussed in terms of the rich innervation of the pyriform cortex by olfactory fibers, and of its projections to sub-cortical structures. Ibotenic-acid lesions of the basolateral amygdala caused a significant deficit in conditioned taste aversion, whereas these same lesions did not affect conditioned odor aversion. This dissociation was examined in light of the differences in anatomical projections from the olfactory and gustatory cortical areas to the basolateral region. The performance of animals with electrolytic lesions of the basolateral amygdala on a conditioned taste- and a conditioned odor-preference task raised some important questions concerning the contribution of this neural structure to stimulus-reward associations. The last two experiments demonstrated that the pyriform cortex plays an important role in neophobia, a role that is not limited to olfactory stimuli. This suggests that the analysis and subsequent transmission of olfactory information is critical to the expression of the neophobic response.
9
Lasher, Bonnie Ka Keele N. Bradley. "5,7-dihydroxytryptamine lesions of the rat amygdala increase learned fear behavior". Waco, Tex. : Baylor University, 2009. http://hdl.handle.net/2104/5302.
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Wong, Tak-hing Michael. "Brain function and structure in violent metally abnormal offenders". Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21254163.
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Young, Barbara Ann. "Anxiogenic and anxiolytic effects in the elevated plus maze produced by kindling and low frequency stimulation of the basolateral amygdala". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ62443.pdf.
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Chai, Sin-Chee 1969. "The functions of amygdala and hippocampus in conditioned cue preference learning /". Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=38470.
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The experiments in this thesis examined the roles of stimulus configuration on conditioned cue preference (CCP) learning by asking what information is processed and by which neural substrates. Results from Experiments 1 and 2 showed that lesions of the lateral nucleus of the amygdala (LNA) but not of fimbria-fornix (FF) impaired CCP learning when the cues paired with food during training were distinct from those not paired with food in either of two different apparatuses. In Experiments 3 and 4 LNA lesions increased the size of the CCP when the cues paired with food and no food were ambiguous in two different apparatuses. Learning the ambiguous cue CCP required at least one session of unreinforced pre-exposure to the cues and was eliminated by FF lesions. In the last series of experiments, a latent learning effect of unreinforced pre-exposure on ambiguous cue CCP learning on the radial maze was found in normal animals that received at least 3 sessions of unreinforced pre-exposure. FF lesions made before, but not after, pre-exposure eliminated the latent learning effect. Hippocampus lesions made either before or after pre-exposure eliminated the CCP learning. Taken together, the results are consistent with the hypothesis that distinct cue CCP learning is based on conditioned approach responses to cues paired with food, mediated by a neural system that includes the LNA. The results also suggest that ambiguous cue CCP learning takes place in two phases. First spatial learning occurs during unreinforced pre-exposure, a process that requires an intact FF. Subsequently, information about the location of the reinforcer is added to the spatial information during the reinforced training trials by a process of "reconsolidation". An intact hippocampus is required for this process. The implications of these results and interpretations for latent learning and latent inhibition are considered.
13
Mikheenko, Yevheniia. "The neural and neurochemical basis of emotion regulation : contribution of amygdala and orbitofrontal serotonin in the common marmoset (Callithrix jacchus)". Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607922.
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黃德興 i Tak-hing Michael Wong. "Brain function and structure in violent metally abnormal offenders". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31981719.
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Koh, Ming Teng. "Neural mediation of taste processing and aversion learning /". Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/9084.
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Hardee, Jillian E. "The fearful face and beyond fMRI studies of the human amygdala /". Morgantown, W. Va. : [West Virginia University Libraries], 2009. http://hdl.handle.net/10450/10653.
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Thesis (Ph. D.)--West Virginia University, 2009.Title from document title page. Document formatted into pages; contains ix, 192 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 171-190).
17
McDonald, Robert James. "Interactions among learning and memory systems : amygdala, dorsal striatum, and hippocampus". Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=28491.
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This series of experiments used the multiple learning and memory systems hypothesis of the mammalian nervous system to investigate the possibility that the amygdala, dorsal striatum, and hippocampal systems might, in certain situations, interact to produce behavior in the normal animal. Using variations of the conditioned-cue preference (CCP) task, evidence is presented showing that context-specific information acquired by the hippocampus interferes with acquisition of amygdala-based stimulus-reward learning. It was also demonstrated that there are amygdala-, dorsal striatum-, and hippocampus-based forms of place learning and that cue ambiguity and movement are important factors determining which of these learning and memory systems gain behavioral control in place learning situations. These findings provide evidence for interactions among learning and memory systems and implicate the amygdala and dorsal striatum in some types of non-hippocampal based place learning using distal cues.
18
Ramel, Wiveka. "Neural substrates of cognitive vulnerability to depression /". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2005. http://wwwlib.umi.com/cr/ucsd/fullcit?p3161971.
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Ganev, Jennifer. "The Role of the Amygdala and Other Forebrain Structures in the Immediate Fear Arousal Produced by Footshock Exposure". Thesis, University of Canterbury. Psychology, 2007. http://hdl.handle.net/10092/1503.
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When a human or animal is threatened or confronted with a stimuli signalling danger, internal defence mechanisms are activated that evoke feelings of fear and anxiety. These emotional responses promote the behaviour patterns necessary for an organism's survival. Animal research seeks to understand how these emotions affect behaviour both physiologically and neurologically in order to develop effective treatment for those suffering from severe anxiety disorders. The aim of this thesis was to examine the role of the amygdala, and dorsal and ventral hippocampus in relation to immediate fear arousal brought on by footshock. This was assessed by examining whether muscimol would interfere with the acoustic startle response before or after footshock presentation, and then comparing these reactions to a control group that received saline infusions. The results of this research are extremely important because they identify various brain structures involved in the fear-arousing effects of footshock as measured by the shock sensitization of acoustic startle. Laboratory rats received muscimol (0.1ug and 0.01ug) infusions into the basolateral amygdala, dorsal and ventral hippocampus. These three brain regions have been identified as playing a prominent role in fear neurocircuitry. The results demonstrated that the GABA A receptor agonist muscimol in doses of 0.1ug and 0.01ug reliably blocked shock sensitization of the acoustic startle response. The muscimol doses did not alter the shock reactivity amplitudes therefore indicating a normal perception of the fear arousing properties of footshock. Therefore, the present study's results suggest that a decrease of GABA activity in the amygdala, dorsal and ventral hippocampus may be essential for the neuronal basis of fear acquisition and expression of unconditioned and conditioned stimuli.
20
Masilela, Sibonisiwe Ntini. "Effects of nicotine on content of corticotropin releasing factor (CRF) in rat amygdala, hypothalamus and brain stem". Morgantown, W. Va. : [West Virginia University Libraries], 1999. http://etd.wvu.edu/templates/showETD.cfm?recnum=487.
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Thesis (M.S.)--West Virginia University, 1999.Title from document title page. Document formatted into pages; contains viii, 138 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 105-134).
21
Pontau, James R. Jr. "Neural Correlates of Deja Vu and Dissociation: The Roles of the Amygdala and Hippocampus in the Prevalence of Deja Vu Used as an Indicator for the Severity of Dissociation and Posttraumatic Stress Disorder". Cleveland State University / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=csu1232079456.
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Kalynchuk, Lisa Emily. "Effect of long term amygdala kindling on defensive behaviour in rats : a model of the interictal emotionality associated with temporal lobe epilepsy". Thesis, 1996. http://hdl.handle.net/2429/6645.
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Temporal lobe epileptics often experience interictal (i.e., between-seizure) emotional
disturbances such as fear and anxiety. Despite the problem that these disturbances present,
little progress has been made in characterizing their nature and etiology because they are not
amenable to experimental analysis in clinical populations. Accordingly, the general purpose
of the experiments in this thesis was to demonstrate the potential of long-term amygdala
kindling in rats as a model of the interictal hyperemotionality of temporal lobe epileptics.
Seven experiments comprise this thesis. Experiments 1 and 2 established that longterm
amygdala kindling (i.e., 100 stimulations) results in large and reliable increases in
emotionality. In Experiment 1, the long-term amygdala-kindled rats displayed more
resistance to capture from an open field and more open-arm activity on an elevated plus
maze than did the sham-stimulated rats; in Experiment 2, the magnitude of this
hyperemotionality was shown to be dependent on the number of amygdala stimulations that
the rats received. Experiment 3 showed that kindling-induced hyperemotionality is
enduring; the hyperemotionality present 1 day after the final stimulation did not decline
significantly over the ensuing month although some amelioration of symptoms was
observed. Experiment 4 established that kindling-induced hyperemotionality is not unique to
amygdala stimulation. Although increases in emotionality were greatest in amygdalakindled
rats, hippocampal-kindled, but not caudate-kindled, rats also displayed significant
increases. Experiments 5 and 6 showed that kindling-induced hyperemotionality is
fundamentally defensive in nature. In Experiment 5, amygdala-kindled rats displayed high
levels of emotionality in an unfamiliar, but not in a familiar, situation; in Experiment 6,
amygdala-kindled rats displayed more defensive, but less aggressive behaviour, in their
interactions with other rats. Finally, Experiment 7 showed that 8-OH-DPAT binding to
serotonin 5HT1A receptors is increased in the dentate gyrus of amygdala-kindled rats, but
not in the amygdala, periaqueductal grey, perirhinal cortex, or CA1 or CA3 hippocampal
subfields.
Together, the results of these experiments establish the potential of long-term
amygdala kindling as a useful animal model of interictal emotionality in temporal lobe
epileptics.
23
Pelletier, Marc Roger. "An investigation of the role of amygdaloid α-2 adrenoceptors in the kindling of seizures". Thesis, 1992. https://dspace.library.uvic.ca//handle/1828/9629.
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It has been reported previously that systemic administration of clonidine, an
agonist of α-2 receptors for noradrenaline, significantly retards amygdaloid kindling,
by delaying the emergence from partial seizure, Conversely, systemic administration
of α-2 antagonists has been reported to facilitate amygdaloid kindling, The
experiments I conducted attempted to discover whether α-2 adrenoceptors in the
amygdala participated in these effects, I examined the effect of either systemic
administration (i,p.) or intraamygdaloid infusions of a variety of noradrenergic drugs
on the kindling of seizures with electrical stimulation of the amygdala, Rats received
either low-frequency stimulation of the amygdala, to induce rapid kindling, or
conventional high-frequency stimulation, Drugs and electrical stimulation were
administered once every 48 hrs, I observed a significant retardation of kindling in
rats receiving i,p. injections of clonidine (0.1 mg/kg) or unilateral infusions of
clonidine in concentrations of [special characters omitted] to [special characters omitted] M, regardless of the stimulation frequency.
The prophylactic effect was due to a delay in the progression out of partial seizure. I observed similar effects with infusions of xylazine, also an α-2 adrenoceptor agonist,
The effect was specific to the amygdala/pyriform region, because infusions of
clonidine dorsal lo the amygdala were without effect. Power spectral analysis of the
AD from the stimulated and the contralateral amygdala during the initial occurrence
of bilateral AD failed to reveal differences attributable to clonidine, Therefore,
clonidine might retard kindling by modifying the propagation of AD from the
stimulated amygdala to a midbrain or pontine brainstem area critical, for the
expression of generalized seizures. Clonidine had no effect on established generalized
seizures, suggesting that it was producing a genuine prophylactic effect against
kindling. Unexpectedly, intraamygdaloid infusions of either idazoxan, yohimbine, or
SK&F 104856, antagonists of α-2 receptors, failed to accelerate kindling.
Simultaneous infusion of idazoxan blocked clonidine’s prophylactic effect, which
suggests strongly that this effect was mediated at the α-2 adrenoceptor. Blockade of
amygdaloid α-1 adrenoceptors with corynanthine failed to affect kindling.
I conclude that the population of α-2 adrenoceptors in the amygdala/pyriform
region contributes to the antiepileptogenic effect observed after systemic
administration of clonidine and that the facilitation of kindling observed after systemic
administration of α-2 antagonists reported previously may have been mediated by the
blockade of a population of α -2 adrenoceptors in addition to, or outside of, the
amygdala/pyriform region.Graduate
24
Morris, John A. "Gonadal hormone mediation of neural plasticity in the adult rodent amygdala". Diss., 2008.
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Popescu, Andrei Tiberi. "Mechanisms of amygdala facilitated cortico-striatal plasticity". 2010. http://hdl.rutgers.edu/1782.2/rucore10002600001.ETD.000052191.
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Laurent, Vincent Psychology Faculty of Science UNSW. "Role of the basolateral amygdala in learning and relearning context conditioned fear and its extinction". 2007. http://handle.unsw.edu.au/1959.4/40769.
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The basolateral complex of the amygdala (BLA) is a key component of the neuronal circuitry underlying the acquisition and the extinction of Pavlovian conditioned fear. The present series of experiments examined the role of neuronal activity and NMDA receptors (NMDAr) activation in the BLA on learning and relearning context conditioned fear and its extinction. Disruption of neuronal activity in the BLA prevented the acquisition of fear responses to a novel, a moderately familiar or a highly familiar context. It also prevented the reacquisition of fear responses to a conditioned or an extinguished context. Local blockade of NMDAr containing the NR2B subunit prior to training extinction or re-extinction impaired the short- and long-term loss of fear responses. In contrast, a similar blockade subsequent to training extinction or re-extinction left the long-term loss of fear responses unaffected. Disruption of neuronal activity in the BLA prior to training extinction and re-extinction depressed fear responses. It impaired the long-term loss of fear produced by extinction training but spared and even facilitated the long-loss of fear produced by re-extinction training when extinction had already been learned. The exact same outcome was observed when neuronal activity in the BLA was disrupted subsequent to training extinction and re-extinction. These findings suggest that the BLA is critical for both learning and relearning context conditioned fear. In contrast, the BLA is necessary for learning but not relearning extinction of conditioned fear. This implies that once extinction has been learned, others structures support the retrieval and the expression of extinction memory. This is consistent with current neural model of extinction that involves interactions between several neural substrates including the BLA and the medial prefrontal cortex.
27
Baruni, Jalal Kenji. "Mechanisms of attention in visual cortex and the amygdala". Thesis, 2016. https://doi.org/10.7916/D83T9H70.
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Spatial attention enhances perception at specific locations in the visual field, measured behaviorally as improved task performance and faster reaction times. In visual cortex, neurons with receptive fields at attended locations display enhanced responses. This neural modulation is presumed to underlie the associated behavioral benefit, although the mechanisms linking sensory cortical modulation to perceptual enhancement remain unclear. In studies of spatial attention, experimentalists persuade animals to attend to particular locations by associating them with a higher probability or magnitude of reward. Notably, these manipulations alter in tandem both the absolute expectation of reward at a particular location, as well as the expectation of reward relative to other locations in the visual field. We reasoned that independently changing absolute and relative reward expectations could provide insight into the mechanisms of attention.
We trained monkeys to discriminate the orientation of two stimuli presented simultaneously in different hemifields while independently varying the reward magnitude associated with correct discrimination at each location. Behavioral measures of attention were controlled by the relative value of each location. By contrast, neurons in visual area V4 were consistently modulated by absolute reward value, exhibiting increased firing rates, increased gamma-band power, and decreased trial-to-trial variability whenever receptive field locations were associated with large rewards. Thus, neural modulation in V4 can be robustly dissociated from the perceptual benefits of spatial attention; performance could be enhanced without neural modulation, and neural activity could be modulated without substantial perceptual improvement.
These data challenge the notion that the perceptual benefits of spatial attention rely on increased signal-to-noise in V4. Instead, these benefits likely derive from downstream selection mechanisms.
In identifying brain areas involved with attention, a distinction is generally made between sensory areas like V4— where the representation of the visual field is modulated by attentional state— and attentional “source" areas, primarily in the oculomotor system, that determine and control the locus of attention. The amygdala, long recognized for its role in mediating emotional responses, may also play a role in the control of attention. The amygdala sends prominent feedback projections to visual cortex, and recent physiological studies demonstrate that amygdala neurons carry spatial signals sufficient to guide attention. To characterize the role of the amygdala in the control of attention, we recorded neural activity in the amygdala and V4 simultaneously during performance of the orientation discrimination task. In preliminary data analysis, we note two sets of findings. First, consistent with prior work, we found that amygdala neurons combine information about space and value. Rewards both contralateral and ipsilateral to amygdala neurons modulated responses, but contralateral rewards had a larger effect. Therefore, notably distinct from known attentional control sources in the oculomotor system, spatial-reward responses in the amygdala do not reflect the relative value of locations. Second, we found signatures of functional connectivity between the amygdala and V4 during task performance. Reward cue presentation was associated with elevated alpha and beta coherence, and attention to locations contralateral to the amygdala and inside the receptive field of V4 neurons was associated with elevated inter-area gamma coherence. These results suggest that the amygdala may serve a unique role in the control of spatial attention.
Together, these experiments contribute towards an understanding of the brain-to-behavior mechanisms linking neural activity in V4 and the amygdala to the dramatic perceptual and behavioral improvement associated with attention.
28
Gore, Felicity May. "Neural circuits mediating innate and learned behavior". Thesis, 2015. https://doi.org/10.7916/D84Q7TQH.
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For many organisms the sense of smell is critical to survival. Some olfactory stimuli elicit innate responses that are mediated through hardwired circuits that have developed over long periods of evolutionary time. Most olfactory stimuli, however, have no inherent meaning. Instead, meaning must be imposed by learning during the lifetime of an organism. Despite the dominance of olfactory stimuli on animal behavior, the mechanisms by which odorants elicit learned behavioral responses remain poorly understood.
All odor-evoked behaviors are initiated by the binding of an odorant to olfactory
receptors located on sensory neurons in the nasal epithelium. Olfactory sensory neurons transmit this information to the olfactory bulb via spatially organized axonal projections such that individual odorants evoke a stereotyped map of bulbar activity. A subset of bulbar neurons, the mitral and tufted cells, relay olfactory information to higher brain structures that have been implicated in the generation of innate and learned behavioral responses, including the cortical amygdala and piriform cortex.
Anatomical studies have demonstrated that the spatial stereotypy of the olfactory
bulb is maintained in projections to the posterolateral cortical amygdala, a structure that is involved in the generation of innate odor-evoked responses. The projections of mitral and tufted cells to piriform cortex however appear to discard the spatial order of the olfactory bulb: each glomerulus sends spatially diffuse, apparently random projections across the entire cortex. This anatomy appears to constrain odor-evoked responses in piriform cortex: electrophysiological and imaging studies demonstrate that individual odorants activate sparse ensembles that are distributed across the extent of cortex, and individual piriform neurons exhibit discontinuous receptive fields such that they respond to structurally and perceptually similar and dissimilar odorants. It is therefore unlikely that olfactory representations in piriform have inherent meaning. Instead, these representations have been proposed to mediate olfactory learning. In accord with this, lesions of posterior piriform cortex prevent the expression of a previously acquired olfactory fear memory and photoactivation of a random ensemble of piriform neurons can become entrained to both appetitive and aversive outcomes. Piriform cortex therefore plays a central role in olfactory fear learning. However, how meaning is imparted on olfactory representations in piriform remains largely unknown.
We developed a strategy to manipulate the neural activity of representations of
conditioned and unconditioned stimuli in the basolateral amygdala (BLA), a downstream target of piriform cortex that has been implicated in the generation of learned responses. This strategy allowed us to demonstrate that distinct neural ensembles represent an appetitive and an aversive unconditioned stimulus (US) in the BLA. Moreover, the activity of these representations can elicit innate responses as well as direct Pavlovian and instrumental learning. Finally activity of an aversive US representation in the basolateral amygdala is required for learned olfactory and auditory fear responses. These data suggest that both olfactory and auditory stimuli converge on US representations in the BLA to generate learned behavioral responses. Having identified a US representation in the BLA that receives convergent olfactory information to generate learned fear responses, we were then able to step back into the olfactory system and demonstrate that the BLA receives olfactory input via the monosynaptic projection from piriform cortex. These data suggest that aversive meaning is imparted on an olfactory representation in piriform cortex via reinforcement of its projections onto a US representation in the BLA.
The work described in this thesis has identified mechanisms by which sensory stimuli generate appropriate behavioral responses. Manipulations of representations of unconditioned stimuli have identified a central role for US representations in the BLA in connecting sensory stimuli to both innate and learned behavioral responses. In addition, these experiments have suggested local mechanisms by which fear learning might be implemented in the BLA. Finally, we have identified a fundamental transformation through which a disordered olfactory representation in piriform cortex acquires meaning. Strikingly this transformation appears to occur within 3 synapses of the periphery. These data, and the techniques we employ, therefore have the potential to significantly impact upon our understanding of the neural origins of motivated behavior.
29
Gabard-Durnam, Laurel J. "Experience-Dependent Development of Amygdala-Prefrontal Cortex Circuitry and Function". Thesis, 2017. https://doi.org/10.7916/D8445MX3.
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Dramatic changes occur across childhood and adolescence in the activity and connectivity of an amygdala-medial prefrontal cortex circuit critical for emotional learning and regulation. However, little is currently known about how neuroplasticity within the circuit changes during development in the human. Experiences that occur during developmental sensitive periods of increased neuroplasticity have the capacity to sculpt neural function with lifelong consequences for cognition and behavior, though. This dissertation will therefore investigate when and how experience may shape amygdala-medial prefrontal cortex functional circuitry (Aim 1) and what the implications of experience-dependent circuitry development are for emotion regulation behaviors (Aim 2) across childhood, adolescence, and adulthood in three studies. Study 1 (previously published as Gabard-Durnam, Gee et al., 2016) posits and tests the long-term phasic molding hypothesis that tonic amygdala-prefrontal cortex functional connectivity, the functional architecture of the brain, is shaped during development by recurring stimulus-elicited connectivity in the circuitry using prospective examination of these connectivities’ development across childhood and adolescence. Study 1 also tests whether the ability of amygdala-prefrontal cortex stimulus-elicited connectivity to shape the amygdala-prefrontal cortex resting-state functional architecture changes across development, reflecting changing plasticity of the circuitry. Study 2 examines how the timing and duration of an early adverse experience, parental deprivation, interacts with genetically-driven differences in neuroplasticity levels indexed by the Brain-Derived Neurotrophic Factor val66met polymorphism to influence the developmental trajectory of amygdala-prefrontal cortex functional architecture using a population of previously-institutionalized children and adolescents and a never-institutionalized comparison sample. Study 2 further examines how the experience- and plasticity-related changes to the functional architecture influence both concurrent and future internalizing symptomatology across childhood and adolescence. Study 3 builds on the first two developmental studies by explicitly testing whether childhood is a sensitive period for medial prefrontal cortex-mediated regulatory signal learning through a retrospective design in adults. Study 3 additionally assesses the effects of developmental experience on adult emotion regulation behavior and physiology. My findings at the levels of brain circuitry, behavior, physiology, and genetics together delineate a period of increased sensitivity to the environment within prefrontal cortex-amygdala functional circuitry from infancy through childhood, modifiable by genetically-conferred variation in plasticity and the nature of the early environment. Moreover, experiences occurring during the sensitive period have consequences for future emotion regulation behavior both during development and lasting into young adulthood. Together, these findings demonstrate how experience-dependent development has enduring effects on amygdala-prefrontal cortex circuitry function and affective behavior.
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Stujenske, Joseph Matthew. "Prefrontal-Amygdala Circuits Regulating Fear and Safety". Thesis, 2016. https://doi.org/10.7916/D8V69JFQ.
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Switching between a state of fear and safety is a critical aspect of adaptive behavior. Aversive and non-aversive associations must be formed quickly and reliably but remain malleable as these associations change dynamically. When these associations become biased towards aversive associations by traumatic and stressful circumstances, as in PTSD, fear generalization and impaired fear extinction arise. These changes are associated with reduced activity in the medial prefrontal cortex (mPFC) and enhanced activity in the basolateral amygdala (BLA). It has been hypothesized that the mPFC mediates top-down control of the BLA to signal safety. It has previously been demonstrated that synchronous activity within the mPFC-BLA circuit is strongly engaged during fear conditioning, but it is unknown how activity in this circuit changes to mediate aversive discrimination. We investigated how the mPFC and BLA cooperate to mediate successful discrimination between aversive and non-aversive stimuli both for learned and innately-valent associations. Extracellular elecrophysiological recordings were obtained simultaneously form the mPFC and BLA in mice during innate anxiety, fear discrimination, and fear extinction. Local field potentials were recorded in both structures along with single unit recordings from the BLA. We discovered that fear was associated with enhanced theta-frequency synchrony and theta-gamma coupling within the mPFC-BLA circuit. On the other hand, safety was associated with predominant mPFC-to-BLA directionality of synchronous information flow and enhanced fast gamma frequency activity in both structures. Interestingly, gamma oscillations in the BLA were strongly coupled to theta frequency activity arising in the mPFC. This data is consistent with entrainment of inhibitory circuits in the BLA by mPFC input to mediate safety.
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Qasim, Salman Ehtesham. "In vivo electrophysiology in humans reveals neural codes for space and memory". Thesis, 2021. https://doi.org/10.7916/d8-y259-4707.
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Memory serves an integral function in every aspect of human life. Losing that function can be adevastating consequence of disease, dementia, and trauma. In order to develop treatments or prophylactics for memory disorders we must identify the neural basis of memory. Animal research has made prominent strides studying the neural correlates of memory by examining the more easily observable and manipulable neural correlates of spatial context, since the brain regions necessary for declarative memory intersect profoundly with those needed for spatial navigation. My research has two main goals. My first two studies, in Chapters 2 and 3, translate animal research relating the neural correlates of space to memory processes, and go beyond animal work to explore how internal features of experience such as goal states influence these conjunctive representations of space and memory. In Chapter 4, I expand my scope to examine how another internal feature, emotional context, affects the same brain regions on a network level to influence memory representations in the human brain. To perform these studies I recorded directly from the human brain in epilepsy patients performing a variety of memory tasks.
First, I measured single-neuron activity as subjects navigated a virtual environment, encountering various objects at unique locations. As subjects moved through the environments, they were instructed to recall the locations of specific objects they encountered—I identified neurons in the human entorhinal cortex, called “memory-trace cells”, which selectively activated near the object-location that people were instructed to retrieve from memory. This is the first evidence that neurons in the brain can be tuned to the spatial context of an event for memory, and demonstrated a direct link between memory retrieval and the spatial tuning properties of neurons. For my second study, I examined whether spatially-tuned neurons in the MTL discharge at intervals organized by theta (2–10 Hz) oscillations (which represent network level brain-activity). I identified a particular pattern that is prominent in rodents, called “phase precession”, during which spatially-tuned neurons spike slightly faster than the network oscillation, and which is theorized to hold great value throughout the brain for learning and memory. In addition to discovering this pattern for spatial sequences, I discovered that phase precession was also present during more abstract features of experience, like the specific goal a person was seeking. These findings suggest that principles of network-level brain activity for organizing spatial navigation may extend to humans, and to broader forms of cognition and memory. Finally, I examined the role of the amygdala in memory encoding during a verbal episodic memory task, finding that the emotional context of a word influenced the probability of its subsequent recall. By measuring the prevalence and coordination of brain oscillations in the amygdala-hippocampal circuit, I found that gamma oscillations (30–120 Hz) increased in both regions as a function of word arousal and encoding success, and connectivity within the amygdala-hippocampal circuit also showed significant theta-gamma coupling as a function of memory and high arousal. Furthermore, direct 50 Hz stimulation impaired memory for high arousal words. These findings suggest a causal relationship between gamma oscillations in the amygdala-hippocampal circuit for memory as a function of emotional context during encoding.
My work generalizes important neuronal principles from animal studies to humans (such as spatially-tuned neurons and phase precession), but also extends those findings more deeply to memory, and to internal/subjective aspects of memory that are difficult to directly measure in animals. Overall this work represents an important step towards understanding how the human brain enables declarative memory.
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Maller, Jerome Joseph. "Methodological factors affecting estimation of hippocampal and amygdalar volumes from brain MRI : implications for cognitive ageing". Phd thesis, 2005. http://hdl.handle.net/1885/148474.
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Delaney, Andrew James. "The central amygdala : an electrophysiological study". Phd thesis, 2000. http://hdl.handle.net/1885/146207.
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Gaskins, Denise. "ELUCIDATING MECHANISMS THAT LEAD TO PERSISTENT ANXIETY-LIKE BEHAVIOR IN RATS FOLLOWING REPEATED ACTIVATION OF CORTICOTROPIN-RELEASING FACTOR RECEPTORS IN THE BASOLATERAL AMYGDALA". Thesis, 2012. http://hdl.handle.net/1805/2738.
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Indiana University-Purdue University Indianapolis (IUPUI)Anxiety disorders are estimated to impact 1 in 4 individuals within their lifetime. For some individuals, repeated episodes of the stress response leads to pathological anxiety and depression. The stress response is linked to increased levels of corticotropin-releasing factor (CRF) in the basolateral nucleus of the amygdala (BLA), a putative site for regulating anxiety and associative processes related to aversive emotional memories, and activation of CRF receptors in the BLA of rats produces anxiety-like behavior. Mimicking repeated episodes of the stress response, sub-anxiogenic doses of urocortin 1 (Ucn1), a CRF receptor agonist, are microinjected into the BLA of rats for five consecutive days, a procedure called priming. This results in 1) behavioral sensitization, such that a previously non-efficacious dose of Ucn1 will elicit anxiety-like response after the 3rd injection and 2) the development of a persistent anxiety-like phenotype that lasts at least five weeks after the last injection without any further treatment. Therefore, the purpose of this thesis was to identify mechanisms involved in the Ucn1-priming-induced anxiogenesis. The first a set of experiments revealed that the anxiety-like behavior was not due to aversive conditioning to the context or partner cues of the testing environment. Next, Ucn1-priming-induced gene expression changes in the BLA were identified: mRNA expression for Sst2, Sst4, Chrna4, Chrma4, and Gabrr1 was significantly reduced in Ucn1-primed compared to Vehicle-primed rats. Of these, Sst2 emerged as the primary receptor of interest. Subsequent studies found that antagonizing the Sstr2 resulted in anxiety-like behavior and activation of Sstr2 blocked acute Ucn1-induced anxiety-like responses. Furthermore, pretreatment with a Sstr2 agonist delayed the behavioral sensitization observed in Ucn1-induced priming but did not stop the development of persistent anxiety-like behavior or the Ucn1-priming-induced decrease in the Sstr2 mRNA. These results suggest that the decrease in Sstr2 mRNA is associated with the expression of persistent anxiety-like behavior but dissociated from the mechanisms causing the behavioral sensitization. Pharmacological studies confirmed that a reduced Sstr2 mediated effect in the BLA is likely to play a role in persistent anxiety and should be investigated further.