Using Clickers to Teach Biology-Based Material in a Developmental Psychology Class

This talk will describe a study designed to assess if clicker technology during a lesson can improve learning relative to traditional lecture alone. A control group was exposed to the stages of prenatal development via traditional lecture, and an experimental group was exposed to the material via an exercise that used clickers. A pretest showed no difference before the intervention. A posttest showed that the clicker group had significant gains indicating clickers may facilitate learning of science-based material.

Prenatal augmented auditory stimulation and visual system development: Effects of timing on intersensory organization

This study investigated the effects of augmented prenatal auditory stimulation on postnatal visual responsivity and neural organization in bobwhite quail (Colinus virginianus). I delivered conspecific embryonic vocalizations before, during, or after the development of a multisensory, midbrain audiovisual area, the optic tectum. Postnatal simultaneous choice tests revealed that hatchlings receiving augmented auditory stimulation during optic tectum development as embryos failed to show species-typical visual preferences for a conspecific maternal hen 72 hours after hatching. Auditory simultaneous choice tests showed no hatchlings had deficits in auditory function in any of the groups, indicating deficits were specific to visual function. ZENK protein expression confirmed differences in the amount of neural plasticity in multiple neuroanatomical regions of birds receiving stimulation during optic tecturn development, compared to unmanipulated birds. The results of these experiments support the notion that the timing of augmented prenatal auditory stimulation relative to optic tectum development can impact postnatal perceptual organization in an enduring way.^

Relationships of impulsivity and physical fighting history to alcohol -induced aggression in women

Research suggests women respond to the aggression-inducing effects of alcohol in a manner similar to men. Highly aggressive men are more prone to alcohol-induced aggression, but this relationship is less clear for women. This study examined whether alcohol consumption would differentially affect laboratory-measured aggression in a sample of aggressive and non-aggressive women and how those differences might be related to components of impulsive behavior. In 39 women recruited from the community (two groups: with and without histories of physical fighting) ages 21–40, laboratory aggressive behavior was assessed following placebo and 0.80 g/kg alcohol consumption (all women experienced both conditions). Baseline laboratory impulsive behavior of three impulsivity models was later assessed in the same women. In the aggression model (PSAP), participants were provoked by periodic subtractions of money, which were blamed on a fictitious partner. Aggression was operationalized as the responses the participant made to subtract money from that partner. The three components of impulsivity that were tested included: (1) response initiation (IMT/DMT), premature responses made prior to the completion of stimulus processing, (2) response inhibition (GoStop), a failure to inhibit an already initiated response, and (3) consequence sensitivity (SKIP and TCIP), the choice for a smaller-sooner reward over a larger-later reward. I hypothesized that, compared to women with no history of physical fighting, women with a history of physical fighting would exhibit higher rates of alcohol-induced laboratory aggression and higher rates of baseline impulsive responding (particularly for the IMT/DMT), which would also be related to the alcohol-induced increases aggression. Consistent with studies in men, the aggressive women showed strong associations between laboratory aggression and self-report measures, while the non-aggressive women did not. However, unlike men, following alcohol consumption it was the non-aggressive women's laboratory aggression that was related to their self-reports of aggression and impulsivity. Additionally, response initiation measures of impulsivity distinguished the two groups, while response inhibition and consequence sensitivity measures did not; commission error rates on the IMT/DMT were higher in the aggressive women compared to the non-aggressive women. Regression analyses of the behavioral measures showed no relationship between the aggression and impulsivity performance of the two groups. These results suggest that the behavioral (and potentially biological) mechanism underlying aggressive behavior of women is different than that of men. ^

Aggression, impulsivity and serotonin in drug dependence

Aggression, impulsivity, and central serotonergic function were evaluated in two groups of human volunteers; one group having a history of substance dependence (DRUG+) and another group with no drug use history (DRUG$-$). The hypothesis was that DRUG+ subjects would be more aggressive, more impulsive, and have attenuated serotonergic function. Results showed that DRUG+ subjects behaved more aggressively in a computer paradigm of aggression and also reported more aggression on questionnaires than DRUG$-$ subjects. In a computer paradigm of impulsivity, the DRUG+ group showed a lesser ability to delay gratification than the DRUG$-$ group in the last session of testing. The DRUG+ subjects also reported more venturesomeness and problems associated with low impulse control on questionnaires. Serotonergic function was measured through the neuroendocrine and hypothermic response to an orally administered serotonin (5-HT) agonist specific to the 5-HT$\rm\sb{1A}$ receptor subtype (ipsapirone). The neuroendocrine responses did not differ between DRUG$\pm$ groups, indicating no difference in the sensitivity of the presynaptic or postsynaptic 5-HT$\rm\sb{1A}$ receptors. An unexpected result was that the indicator hormone, cortisol, was at a lower baseline level in the DRUG+ group than the DRUG$-$ group. Lowered cortisol levels have been previously noted in children at high risk foul antisociality and future drug use. A principal components analysis including impulsivity, aggression, and serotonergic function measures produced three unique factors. The factors, Antisocial Tendency and Self-Control and Serotonergic Function combined to produce a significant regression equation explaining 36% of variability in the DRUG$\pm$ groups. These factors included measures of aggression, impulsivity, mood, and educational attainment. These results suggest that the current measures of aggression and impulsivity were predictive of a drug dependence disorder but that neuroendocrine function is not yet a useful indicator of drug dependence status. ^

Behavioral effects of plasma tryptophan depletion in aggressive and nonaggressive men

Serotonin (5-HT) neurotransmission deficits have been implicated in impulsive aggression. A Trp-free beverage of amino acids competitively inhibits Trp uptake into the brain for 5-HT synthesis and also lowers endogenous plasma Trp for several hours. This has worsened mood and/or increased aggressive behavior, especially in hostile persons or those with histories of depression. In 24 community-recruited men (12 each with and without significant aggression histories), aggressive and impulsive behavior in the laboratory was assessed before and after plasma Trp depletion and Trp loading. In the aggression model, subjects were provoked by periodic subtractions of participation earnings, and these subtractions were blamed on a ficitious other participant. Aggression was measured as the responses the subject made to subtract money from his antagonist. Impulsiveness was operationalized as: (1) the choice of smaller reward after a shorter delay over having to wait longer to receive a larger reward, and (2) “false alarm” commission errors in a modified Continuous Performance Task, which represent a failure to inhibit responding to stimuli similar (but not identical) to target stimuli. Finally, plasma cortisol and Trp were measured under each condition immediately following a aggression testing session when subjects were highly provoked. I hypothesized that 5-HT may tonically modulate (inhibit) the hypothalmnic-pituitary-adrenal stress response, such that Trp depletion may enhance the cortisol response to high provocation in aggressive men. ^ Trp depletion had no effect in the laboratory tasks purported to measure impulsive behavior, and failed to cause increases in aggressive behavior under low provocation conditions. Under higher provocation, however, aggressive responses we re elevated under Trp-depleted conditions relative to Trp-loaded conditions in aggressive men, whereas the reverse was true in nonaggressive men. Cortisol levels nonsignificantly paralled the group differences in aggression under Trp-depleted and Trp-loaded conditions. Aggressive men achieved lower plasma Trp levels after Trp loading than did nonaggressive men, possibly due to heavy alcohol use histories. The high post-loading plasma Trp levels in nonaggressive men tended also to correlate with their aggressive responding rates, due perhaps to increases in other psychoactive Trp metabolites. ^

Learning in the cerebellar nucleus is necessary for acquisition of Pavlovian eyelid conditioning

The cumulative work presented here supports the hypothesis that plasticity in the cerebellar cortex and cerebellar nuclei mediates a simple associative form of motor teaming-Pavlovian eyelid conditioning. It was previously demonstrated that focal ablative lesions of cerebellar anterior lobe or pharmacological block of the cerebellar cortex output disrupted the timing of the conditioned eyeblink response, unmasking a response with a relatively fixed and very short latency to onset. The results of this thesis demonstrate that the short-latency responses are due to associative learning. Unpaired training does not support the acquisition of short-latency responses while the rate of acquisition of short-latency responses during paired training is approximately the same as that of timed conditioned responses. The acquisition of short-latency responses is dependent on an intact cerebellar cortex. Both ablative lesions of the cerebellar cortex and inactivation of cerebellar cortex output with picrotoxin block the acquisition of short-latency responses. However, once the short-latency responses are acquired neither disconnection of cerebellar cortex nor inactivation of the cerebellar nucleus block reacquisition. The results are consistent with the proposal that plasticity in the cerebellar cortex is necessary for learning the timing of conditioned responses, plasticity in the interpositus nucleus mediates the short latency responses, and cerebellar cortical output and mossy fiber input are necessary for the acquisition of short latency responses. ^

Proactive aggression: A two part study

Aggressive behavior can be divided into the subtypes: reactive and proactive. Reactive aggressive acts occur in response to a stimulus or provocation. Proactive aggressive acts occur without provocation and are goal-directed. A number of findings have suggested that individuals displaying proactive aggression may be discerned from individuals not displaying proactive aggression on measures of personality, psychopathology and psychopathy, as well as on aggressive histories and type and severity of aggressive behaviors committed. The current study was conducted in two phases; phase 1 and 2. This was because phase 1 compared proactive aggressive, reactive aggressive and non-aggressive subjects on questionnaire measures, while phase 2 observed the acute effects of the benzodiazepine alprazolam on only proactive aggressive subjects. The phase 1 hypotheses were that proactive aggressive subjects would show greater numbers of personality disorders and have greater psychopathy relative to reactive and non-aggressive subjects. To verify these hypotheses subjects were recruited from the community and classified as proactive (n = 20), reactive (n = 20) or non-aggressive (n = 10) via laboratory behavioral testing. Classified subjects were administered a battery of questionnaires pertaining to personality disorders (SCID-II, OMNI-IV), psychopathy (PCL-R) and aggression history. The results of these questionnaire measures were subjected to statistical analyses, which confirmed the hypotheses. In the second phase, the acute effects of three doses of the benzodiazepine alprazolam were evaluated in proactive aggressive subjects on proactive aggressive responding in the computer-based Point Subtraction Aggression Paradigm (PSAP). In phase 2 it was hypothesized that alprazolam would produce dose dependent decreases in aggressive responding. Subjects were never provoked in this phase, and aggressive responding was classified as proactive. Studies of drugs acting on the GABA system have frequently found decreases in aggression in animals and humans, although there have also been findings of increased (paradoxical) aggression. The hypothesis was tested by statistical analysis of proactive aggressive responding under placebo vs. under alprazolam. The hypothesis was supported by six of seven subjects. Aggressive responding was significantly, decreased under alprazolam relative to placebo in six subjects. One subject showed increases in aggressive responding.^

Blood-oxygen-level-dependent (BOLD) signal changes in total cortex and subcortex, pain, reward, and vigilance regions during mechanical pressure pain after morphine administration

Morphine is the most common clinical choice in the management of severe pain. Although the molecular mechanisms of morphine have already been characterized, the cerebral circuits by which it attenuates the sensation of pain have not yet been studied in humans. The objective of this two-arm (morphine versus placebo), between-subjects study was to examine whether morphine affects pain via pain-related cortical circuits, but also via reward regions that relate to the motivational state, as well as prefrontal regions that relate to vigilance as a result of morphine's sedative effects. Cortical activity was measured by the blood-oxygen-level-dependent (BOLD) signal changes using functional magnetic resonance imaging (fMRI). ^ The novelty of this study is at three levels: (i) to develop a methodology that will assess the average BOLD signal across subjects for the pain, reward, and vigilance cortical systems; (ii) to examine whether the reward and/or sedative effects of morphine are contributing factors to cortical regions associated with the motivational state and vigilance; and (iii) to propose a neuroanatomical model related to the opioid-sensitive effects of reward and sedation as a function of cortical activity related to pain in an effort to assess future analgesics. ^ Consistent with our hypotheses, our findings showed that the decrease in total pain-related volume activated between the post- and the pre-treatment morphine group was about 78%, while the post-treatment placebo group displayed only a 5% decrease when compared to pre-treatment levels of activation. The volume increase in reward regions was 451% in the post-treatment compared to the pre-treatment morphine condition. Finally, the volumetric decrease in vigilance regions was 63% in the posttreatment compared to the pre-treatment morphine condition. ^ These findings imply that changes in the blood flow of the reward and vigilance regions may be contributing factors in producing the analgesic effect under morphine administration. Future studies need to replicate this study in a higher resolution fMRI environment and to assess the proposed neuroanatomical model in patient populations. The necessity of pain research is apparent, since pain cuts across different diseases especially chronic ones, and thus, is recognized as a vital public health developing area. ^

A commentary on the current and future status of educational and developmental psychology in Australia

Educational and developmental psychology faces a number of current and future challenges and opportunities in Australia. In this commentary we consider the identity of educational and developmental psychology in terms of the features that distinguish it from other specialisations, and address issues related to training, specialist endorsement, supervision and rebating under the Australian government's Medicare system. The current status of training in Australia is considered through a review of the four university programs in educational and developmental psychology currently offered, and the employment destinations of their graduates. Although the need for traditional services in settings such as schools, hospitals, disability and community organisations will undoubtedly continue, the role of educational and developmental psychologists is being influenced and to some extent redefined by advances in technology, medicine, genetics, and neuroscience. We review some of these advances and conclude with recommendations for training and professional development that will enable Australian educational and developmental psychologists to meet the challenges ahead.

Novelty and Habituation: the Driving Forces in Early Stage Learning for Developmental Robotics

Meng, Q., & Lee, M. (2005). Novelty and Habituation: the Driving Forces in Early Stage Learning for Developmental Robotics. Wermter, S., Palm, G., & Elshaw, M. (Eds.), In: Biomimetic Neural Learning for Intelligent Robots: Intelligent Systems, Cognitive Robotics, and Neuroscience. (pp. 315-332). (Lecture Notes in Computer Science). Springer Berlin Heidelberg.

Genetic psychology monographs.

Developmental and clinical psychology (varies)

Archives of psychology [microform]

Microopaque.

Biology of sensory systems

A comprehensive and highly illustrated text providing a broad and invaluable overview of sensory systems at the molecular, cellular and neurophysiological level of vertebrates, invertebrates and prokaryotes. It retains a strong focus on human systems, and takes an evolutionary and comparative approach to review the mechanosenses, chemosenses, photosenses, and other sensory systems including those for detecting pain, temperature electric and magnetic fields etc. It incorporates exciting and significant new insights provided by molecular biology which demonstrate how similar the molecular architecture and physiology of sensory cells are across species and across sensory modality, often indicationg a common ancestry dating back over half a billion years. Written by a renowned author, with extensive teaching experience in the biology of sensory systems, this book includes: - Over 400 illustrations - Self–assessment questions - Full bibliography preceded by short bibliographical essays - Boxes containing useful supplementary material. It will be invaluable for undergraduates and postgraduates studying biology, zoology, animal physiology, neuroscience, anatomy, molecular biology, physiological psychology and related courses.

Contingency, contiguity, and development: The ontogeny of contingency learning in northern bobwhite (Colinus virginianus) chicks

The purpose of this study was to investigate the ontogeny of auditory learning via operant contingency in Northern bobwhite (Colinus virginianus ) hatchlings and possible interaction between attention, orienting and learning during early development. Chicks received individual 5 min training sessions in which they received a playback of a bobwhite maternal call at a single delay following each vocalization they emitted. Playback was either from a single randomly chosen speaker or switched back and forth semi-randomly between two speakers during training. Chicks were tested 24 hrs later in a simultaneous choice test between the familiar and an unfamiliar maternal call. It was found that day-old chicks showed a significant time-specific decrement in auditory learning when trained with delays in the range of 470–910 ms between their vocalizations and call playback only when training involved two speakers. Two-day-old birds showed an even more sustained disruption of learning than day-old chicks, whereas three-day-old chicks showed a pattern of intermittent interference with their learning when trained at such delays. A similar but less severe decrement in auditory learning was found when chicks were provided with motor training in which playback was contingent upon chicks entering and exiting one of two colored squares placed on the floor of the arena. Chicks provided with playback of the call at randomly chosen delays each time they vocalized exhibited large fluctuations in their responsivity to the auditory stimulus as a function of delay—fluctuations which were correlated significantly with measures of chick learning, particularly at two-days-of-age. When playback was limited to a single location chicks no longer showed a time-specific disruption of their learning of the auditory stimulus. Sequential analyses revealed several patterns suggesting that an attentional process similar or analogous to attentional blink may have contributed both to the observed fluctuations in chick responsivity to the auditory stimulus as a function of delay and to the time-specific learning deficit shown by chicks provided with two-speaker training. The study highlights that learning can be substantially modulated by processes of orienting and attention and has a number of important implications for research within cognitive neuroscience, animal behavior and learning.

Developmental Neural Correlates of Social Interaction

Children develop in a sea of reciprocal social interaction, but their brain development is predominately studied in non-interactive contexts (e.g., viewing photographs of faces). This dissertation investigated how the developing brain supports social interaction. Specifically, novel paradigms were used to target two facets of social experience—social communication and social motivation—across three studies in children and adults. In Study 1, adults listened to short vignettes—which contained no social information—that they believed to be either prerecorded or presented over an audio-feed by a live social partner. Simply believing that speech was from a live social partner increased activation in the brain’s mentalizing network—a network involved in thinking about others’ thoughts. Study 2 extended this paradigm to middle childhood, a time of increasing social competence and social network complexity, as well as structural and functional social brain development. Results showed that, as in adults, regions of the mentalizing network were engaged by live speech. Taken together, these findings indicate that the mentalizing network may support the processing of interactive communicative cues across development. Given this established importance of social-interactive context, Study 3 examined children’s social motivation when they believed they were engaged in a computer-based chat with a peer. Children initiated interaction via sharing information about their likes and hobbies and received responses from the peer. Compared to a non-social control, in which children chatted with a computer, peer interaction increased activation in mentalizing regions and reward circuitry. Further, within mentalizing regions, responsivity to the peer increased with age. Thus, across all three studies, social cognitive regions associated with mentalizing supported real-time social interaction. In contrast, the specific social context appeared to influence both reward circuitry involvement and age-related changes in neural activity. Future studies should continue to examine how the brain supports interaction across varied real-world social contexts. In addition to illuminating typical development, understanding the neural bases of interaction will offer insight into social disabilities such as autism, where social difficulties are often most acute in interactive situations. Ultimately, to best capture human experience, social neuroscience ought to be embedded in the social world.