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Thomas A Stalnaker

Publications and source records attributed to Thomas A Stalnaker.

7 recordsLinked to original sources
PubMed2006

Associative encoding in posterior piriform cortex during odor discrimination and reversal learning.

Recent proposals have conceptualized piriform cortex as an association cortex, capable of integrating incoming olfactory information with descending input from higher order associative regions such as orbitofrontal cortex and basolateral amygdala (ABL). If true, encoding in piriform cortex should reflect associative features prominent in these areas during associative learning involving olfactory cues. We recently reported that neurons in anterior piriform cortex (APC) in rats exhibited significant plasticity in their responses to odor cues during associative learning. Here, we have repeated this study, recording from neurons in posterior piriform cortex (PPC), a region of piriform cortex that receives much stronger input from ABL. If associative encoding in piriform cortex is driven by inputs from ABL, then we should see more plasticity in PPC neurons than we observed in APC. Consistent with this hypothesis, we found that PPC neurons were highly associative and appeared to be somewhat more likely than neurons recorded in APC to alter their responses to the odor cues after reversal of the odor-outcome associations in the task. Further, odor-selective PPC populations exhibited markedly different firing patterns based on the valence of the odor cue. These results suggest associative encoding in piriform cortex is represented in a topographical fashion, reflecting the stronger and more specific input from olfactory bulb concerning the sensory features of odors in anterior regions and stronger input from ABL concerning the meaning of odors in posterior regions.

Amygdala↗
PubMed2006

Associative encoding in anterior piriform cortex versus orbitofrontal cortex during odor discrimination and reversal learning.

Recent proposals have conceptualized piriform cortex as an association cortex, capable of integrating incoming olfactory information with descending input from higher order associative regions such as orbitofrontal cortex (OFC). If true, encoding in piriform cortex should reflect associative features prominent in these areas during associative learning involving olfactory cues. To test this hypothesis, we recorded from neurons in OFC and anatomically related parts of the anterior piriform cortex (APC) in rats, learning and reversing novel odor discriminations. Findings in OFC were similar to what we have reported previously, with nearly all the cue-selective neurons exhibiting substantial plasticity during learning and reversal. Also, many of the cue-selective neurons were originally responsive in anticipation of the outcomes early in learning, thereby providing a single-unit representation of the cue-outcome associations. Some of these features were also evident in firing activity in APC, including some plasticity across learning and reversal. However, APC neurons failed to reverse cue selectivity when the associated outcome was changed, and the cue-selective population did not include neurons that were active prior to outcome delivery. Thus, although representations in APC are substantially more associative than expected in a purely sensory region, they do appear to be somewhat more constrained by the sensory features of the odor cues than representations in downstream areas of OFC.

Animals↗
PubMed2006

Orbitofrontal cortex, decision-making and drug addiction.

The orbitofrontal cortex, as a part of prefrontal cortex, is implicated in executive function. However, within this broad region, the orbitofrontal cortex is distinguished by its unique pattern of connections with crucial subcortical associative learning nodes, such as basolateral amygdala and nucleus accumbens. By virtue of these connections, the orbitofrontal cortex is uniquely positioned to use associative information to project into the future, and to use the value of perceived or expected outcomes to guide decisions. This review will discuss recent evidence that supports this proposal and will examine evidence that loss of this signal, as the result of drug-induced changes in these brain circuits, might account for the maladaptive decision-making that characterizes drug addiction.

Animals↗
PubMed2006

Abnormal associative encoding in orbitofrontal neurons in cocaine-experienced rats during decision-making.

Recent evidence has linked exposure to addictive drugs to an inability to employ information about adverse consequences, or outcomes, to control behavior. For instance, addicts and drug-experienced animals fail to adapt their behavior to avoid adverse outcomes in gambling and reversal tasks or after changes in the value of expected rewards. These deficits are similar to those caused by damage to the orbitofrontal cortex, suggesting that addictive drugs may cause long-lasting changes in the representation of outcome associations in a circuit that includes the orbitofrontal cortex. Here we test this hypothesis by recording from orbitofrontal neurons in a discrimination task in rats previously exposed to cocaine (30 mg/kg i.p. for 14 days). We found that orbitofrontal neurons recorded in cocaine-experienced rats failed to signal the adverse outcome at the time a decision was made in the task. The loss of this signal was associated with abnormal changes in response latencies on aversive trials. Furthermore, upon reversal of the cue-outcome associations, orbitofrontal neurons in cocaine-treated rats with enduring reversal impairments failed to reverse their cue-selectivity, while orbitofrontal neurons in cocaine-treated rats with normal performance showed an increase in the plasticity of cue-selective firing after reversal. These results provide direct neurophysiological evidence that exposure to cocaine can cause behaviorally relevant changes in the processing of associative information in a circuit that includes the orbitofrontal cortex.

Animals↗
PubMed2003

AMPA receptor stimulation within the central nucleus of the amygdala elicits a differential activation of central dopaminergic systems.

Appetitive and aversive arousing stimuli increase rates of dopamine (DA) release, particularly within the prefrontal cortex (PFC). Evidence suggests an activating influence of both the central (CeA) and basolateral (BlA) nuclei of the amygdala on DA neurotransmission. For example, lesions of CeA block stressor-induced increases in DA release. Additionally, electrical stimulation of BlA increases DA release in select terminal fields. Previous studies indicate that glutamatergic AMPA receptors modulate CeA and BlA output. However, the extent to which AMPA receptors participate in amygdala-dependent activation of DA neurotransmission is unknown. The current studies examined the effects of bilateral AMPA infusions within CeA or BlA on post-mortem and in vivo microdialysis indices of DA release. Additionally, stress is associated with moderate increases in serotonin (5-HT) neurotransmission that are also blocked by CeA lesions. Thus, the current studies also examined the impact of AMPA infusions on post-mortem indices of 5-HT utilization. AMPA infusion into CeA, but not BlA, increased post-mortem indices of DA and 5-HT release in a pattern comparable to that observed under appetitive/aversive conditions. In vivo microdialysis studies confirmed that AMPA infusions into CeA, but not BlA, increase extracellular PFC DA levels. When infused into sleeping animals, CeA-AMPA infusion also elicited a rapid-onset transition into waking. Thus, CeA-AMPA receptors exert an excitatory influence on DA and 5-HT neurotransmission and on behavioral state. Combined, these results suggest that CeA-AMPA receptors may participate in the coordination of neural systems involved in the regulation of behavioral state under high-arousal conditions.

Amygdala↗
PubMed2002

Relationship between low-dose amphetamine-induced arousal and extracellular norepinephrine and dopamine levels within prefrontal cortex.

Despite the well-known and potent arousal-enhancing effects of amphetamine (AMPH)-like stimulants, the neurobiological substrates of AMPH-induced arousal have rarely been examined explicitly. Available evidence suggests the possible participation of noradrenergic and/or dopaminergic systems in the arousal-enhancing actions of AMPH-like stimulants. The current studies examined the extent to which low-dose AMPH-induced increases in waking are related to AMPH-induced increases in extracellular norepinephrine (NE) and dopamine (DA) levels within the prefrontal cortex (PFC), as measured by in vivo microdialysis. Vehicle injections elicited brief epochs of waking. Vehicle-induced waking was closely associated with a brief and moderate (50% above baseline) increase in NE levels. DA levels were less sensitive to the arousing actions of vehicle injections, with maximal increases of approximately 25% above baseline observed. 0.15 mg/kg and 0.25 mg/kg AMPH increased time spent awake, which resulted primarily from increases in quiet waking. Although the magnitude of the waking response did not differ substantially between the two doses across time, a trend for a more rapid recovery to baseline waking levels was observed at the higher dose, possibly suggesting the development of a relatively rapid-onset tolerance to the wake-promoting actions of AMPH at this dose. At the 0.15 mg/kg dose, AMPH elicited maximum increases of approximately 175% and 125% above baseline levels for NE and DA, respectively. The time course of AMPH-induced increases in waking closely paralleled the time course of AMPH-induced increases in both NE and DA efflux. These observations are consistent with the hypothesis that both increased DA and NE efflux contribute to the low-dose behavioral effects of AMPH-like stimulants, including the arousal-enhancing actions of these drugs. Additionally, these observations also suggest a possibly greater sensitivity of NE efflux, relative to DA, to moderately arousing conditions including low-dose AMPH-like stimulant administration.

Amphetamine↗