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Lecture 4

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David Haley

PSYC23 Lecture 4  Hunger and Memory: o Severe hunger (24-hr food-deprivation in Drosophila)  Switched off aversive long-term memory, which involves costly synthesis of new proteins and neural activity in dopaminergic neurons o Enhance appetitive learning Hard to form new synapses and connections in brain because theres no energy o Mild hunger (9-16hr food-deprivation) o Enhanced long-term memory Mild starvation= enhance memory  Threat Detection done by the amygdala= threat detector o Fear is elicited by amygdala and it detects threats that are fearful o Patient SM: Urbach Wiethe disease, a congenital calcification of the amygdala bilaterally  Disease that prevents their amygdala from working= it gets calcified and they don’t hv an amygdala  Explicit dislike of spiders and snakes  Demonstrated approach behavior to spiders and snakes  The Stress System: o Once the amygdala detects a threat, its outputs lead to the activation of a variety of target areas that control both behavioral and physiological responses designed to address the threat. In addition to the expression of defensive behaviors, such as freezing , amygdala activation leads to responses in the brain and the body that support the fear reaction. In the brain, monoaminergic systems are activated, resulting in the release of neurotransmitters such as NE, acetylcholine, serotonin, and dopamine throughout the brain. These neurotransmitters lead to an increase in arousal and vigilance and, in general, an enhancement in the processing of external cues. o Detection of threat by the amygdala also has endocrine consequences (i.e., activation of the HPA-axis). Amygdaloid signaling causes secretion of corticotropin-releasing hormone (CRH) from the periventricular nucleus of the hypothalamus. CRH, along with other hypothalamic secretagogs, causes the release of adrenocorticotropic hormone from the pituitary, which in turn stimulates the secretion of GCs from the adrenal cortex. o Circulating GCs bind to the high-affinity mineralocorticoid receptor (MR) and the low- affinity glucocorticoid receptor (GR) in tissues throughout the body and the brain (de Kloet 2004, Korte 2001). o Finally, detection of threat by the amygdala has autonomic consequences. o Thus, the detection of threat and the consequent activation of the fear system elicit a variety of effects that feed back onto the system that initiates and modulates emotional processing.  Example of study done with neonatal rat pups Good Memories of Bad Events in Infancy (Sullivan et al., Nature, 407, 38-39, 2000) FIND AND READ  Sullivan et al subjected neonatal rats to a fear-conditioning paradigm that involved odor–shock pairings. They envisioned this aversive conditioning paradigm as a model for early attachment to an abusive caregiver. They found that very young rat pups exposed to odors associated with electric shocks were attracted to that odor-- i.e., they learned an approach response to that odor. In contrast, older pups learned odor avoidance.  Postnatal day 10, older rat pups secrete CORT--> activate amygdala--> avoid odor  Before postnatal day 10, younger rat pups didn’t secrete CORT--> didn’t activate amygdala--> approach odor  Although younger rat pups show the same behavioral response as older rat pups -- > they show no CORT= no activation of amygdala= approach it o If the younger rat pups were injected with cortisol or dopamine then they would show amygdala activation, and then they would learn to avoid rather than be attracted to the odor. o However, if they were injected with cortisol but given a dopamine blocker....then they wouldn’t activate the amygdala and so continue to be attracted to the odor. o Interestingly, if older rat pups had their adrenals removed so they couldn’t secrete cortisol in response to the shock then they would also be attracted and not avoid the odor. o More importantly, the presence of the mother had a profound effect on whether the older rat pups would secrete cortisol. If the mother was present then they wouldn’t secrete cortisol and so not activate the amygdala and so learned to approach the odor but as soon as they were exposed to cortisol then the amygdala was activated and they learned to avoid the odor. o This is consistent with the idea that the amygdala is the location of many stress hormone receptors. o IN the BARr et al study, it was shown that GC induced changes in the amygdala caused upregulation of dopamine  Barr et al. write, “attachment [by such an infant] to the caretaker has evolved to ensure that the infant forms a bond to that caregiver regardless of the quality of care received”.  The younger rats don’t do avoidance since they don’t secrete cortisol  Cortisol acting on dopamine recepter is what produces fearful learning or avoidance  (Transitions in Infant Learning Are Modulated By Dopamine in the Amygdala (Barr, G. et al. Nat. Neurosci. 12, 1367–136, 2009 FIND AND READ  Glucocorticoids o Chronic Stress Triggers Social Aversion Via Glucocorticoid Receptor in Dopaminoceptive Neurons (Barik et al., Science, 339, 332, Jan 18, 2013) find and read o Social defeat is correlated to aggression =Elevation in GC + Activation of Dopaminergic system= anxiety, avoidance, stress and fear showed a deterioiration in fur state, thymys weight, body weight and adrenal hypertrophy (increase in size of adrenal gland= more cortisol released) o Glucocorticoids and brain circuitry.(A) Social stress acts, in a glucocorticoid-dependent manner, on two dopamine-dependent pathways—the ventral tegmental area–to–nucleus accumbens and ventral tegmental area–to–frontal cortex—in the rodent brain to influence behavior (human brain shown). (B) Glucocorticoid actions on neurons are direct genomic, indirect genomic, and nongenomic, affecting the release of signaling factors, calcium buffering, and structural plasticity. mGR, membrane-associated glucocorticoid receptor. o Barik et al (2013) found that deletion of gene for mGR in dopamine neurons selectively eliminated the avoidance response but ma
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