Unique Neural Mechanisms Research Articles

Distinct Neural Plasticity Enhancing Visual Perception.

The developed human brain shows remarkable plasticity following perceptual learning, resulting in improved visual sensitivity. However, such improvements commonly require extensive stimuli exposure. Here we show that efficiently enhancing visual perception with minimal stimuli exposure recruits distinct neural mechanisms relative to standard repetition-based learning. Participants (n = 20, 12 women, 8 men) encoded a visual discrimination task, followed by brief memory reactivations of only five trials each performed on separate days, demonstrating improvements comparable with standard repetition-based learning (n = 20, 12 women, 8 men). Reactivation-induced learning engaged increased bilateral intraparietal sulcus (IPS) activity relative to repetition-based learning. Complementary evidence for differential learning processes was further provided by temporal-parietal resting functional connectivity changes, which correlated with behavioral improvements. The results suggest that efficiently enhancing visual perception with minimal stimuli exposure recruits distinct neural processes, engaging higher-order control and attentional resources while leading to similar perceptual gains. These unique brain mechanisms underlying improved perceptual learning efficiency may have important implications for daily life and in clinical conditions requiring relearning following brain damage.

Distinct ACC Neural Mechanisms Underlie Authentic and Transmitted Anxiety Induced by Maternal Separation in Mice.

It is known that humans and rodents are capable of transmitting stress to their naive partners via social interaction. However, a comprehensive understanding of transmitted stress, which may differ from authentic stress, thus revealing unique neural mechanisms of social interaction resulting from transmitted stress and the associated anxiety, is missing. We used, in the present study, maternal separation (MS) as a stress model to investigate whether MS causes abnormal behavior in adolescence. A key concern in the analysis of stress transmission is whether the littermates of MS mice who only witness MS stress ("Partners") exhibit behavioral abnormalities similar to those of MS mice themselves. Of special interest is the establishment of the neural mechanisms underlying transmitted stress and authentic stress. The results show that Partners, similar to MS mice, exhibit anxiety-like behavior and hyperalgesia after witnessing littermates being subjected to early-life repetitive MS. Electrophysiological analysis revealed that mice subjected to MS demonstrate a reduction in both the excitatory and inhibitory synaptic activities of parvalbumin interneurons (PVINs) in the anterior cingulate cortex (ACC). However, Partners differed from MS mice in showing an increase in the number and excitability of GABAergic PVINs in the ACC and in the ability of chemogenetic PVIN inactivation to eliminate abnormal behavior. Furthermore, the social transfer of anxiety-like behavior required intact olfactory, but not visual, perception. This study suggests a functional involvement of ACC PVINs in mediating the distinct neural basis of transmitted anxiety.SIGNIFICANCE STATEMENT The anterior cingulate cortex (ACC) is a critical brain area in physical and social pain and contributes to the exhibition of abnormal behavior. ACC glutamatergic neurons have been shown to encode transmitted stress, but it remains unclear whether inhibitory ACC neurons also play a role. We evaluate, in this study, ACC neuronal, synaptic and network activities and uncover a critical role of parvalbumin interneurons (PVINs) in the expression of transmitted stress in adolescent mice who had witnessed MS of littermates in infancy. Furthermore, inactivation of ACC PVINs blocks transmitted stress. The results suggest that emotional contagion has a severe effect on brain function, and identify a potential target for the treatment of transmitted anxiety.

Neural substrates of behavioral inhibitory control during the two-choice oddball task: functional neuroimaging evidence.

Behavioral inhibitory control (BIC) depicts a cognitive function of inhibiting inappropriate dominant responses to meet the context requirement. Despite abundant research into neural substrates of BIC during the go/no-go and stop signal tasks, these tasks were consistently shown hard to isolate neural processes of response inhibition, which is of primary interest, from those of response generation. Therefore, it is necessary to explore neural substrates of BIC using the two-choice oddball (TCO) task, whose design of dual responses is thought to produce an inhibition effect free of the confounds of response generation. The current study aims at depicting neural substrates of performing behavioral inhibitory control in the two-choice oddball task, which designs dual responses to balance response generation. Also, neural substrates of performing BIC during this task are compared with those in the go/no-go task, which designs a motor response in a single condition. The present study integrated go/no-go (GNG) and TCO tasks into a new Three-Choice BIC paradigm, which consists of standard (75%), deviant (12.5%), and no-go (12.5%) conditions simultaneously. Forty-eight college students participated in this experiment, which required them to respond to standard (frequent) and deviant stimuli by pressing different keys, while inhibiting motor response to no-go stimuli. Conjunction analysis and ROI (region of interest) analysis were adopted to identify the unique neural mechanisms that subserve the processes of BIC. Both tasks are effective in assessing BIC function, reflected by the significantly lower accuracy of no-go compared to standard condition in GNG, and the significantly lower accuracy and longer reaction time of deviant compared to standard condition in TCO. However, there were no significant differences between deviant and no-go conditions in accuracy. Moreover, functional neuroimaging has demonstrated that the anterior cingulate cortex (ACC) activation was observed for no-go vs. standard contrast in the GNG task, but not in deviant vs. standard contrast in the TCO task, suggesting that ACC involvement is not a necessary component of BIC. Second, ROI analysis of areas that were co-activated in TCO and GNG showed co-activations in the right inferior frontal cortex (triangle and orbital), with the signals in the TCO task significantly higher than those in the GNG task. These findings show that the designed responses to both standard and deviant stimuli in the TCO task, compared to the GNG task, produced a more prominent prefrontal inhibitory processing and extinguished an unnecessary component of ACC activation during BIC. This implies that prefrontal involvement, but not that of ACC, is mandatory for the successful performance of inhibiting prepotent behaviors.

Common and unique neural mechanisms of social and nonsocial conflict resolving and adaptation.

Humans often need to deal with various forms of information conflicts that arise when they receive inconsistent information. However, it remains unclear how we resolve them and whether the brain may recruit similar or distinct brain mechanisms to process different domains (e.g. social vs. nonsocial) of conflicts. To address this, we used functional magnetic resonance imaging and scanned 50 healthy participants when they were asked to perform 2 Stroop tasks with different forms of conflicts: social (i.e. face-gender incongruency) and nonsocial (i.e. color-word incongruency) conflicts. Neuroimaging results revealed that the ventral lateral prefrontal cortex was generally activated in processing incongruent versus congruent stimuli regardless of the task type, serving as a common mechanism for conflict resolving across domains. Notably, trial-based and model-based results jointly demonstrated that the dorsal and rostral medial prefrontal cortices were uniquely engaged in processing social incongruent stimuli, suggesting distinct neural substrates of social conflict resolving and adaptation. The findings uncover that the common but unique brain mechanisms are recruited when humans resolve and adapt to social conflicts.

Menstrual Pain and Visual Sensitivity Are Related to Different Neural Mechanisms in Adolescent Girls

A substantial body of evidence exists demonstrating central pain mechanisms involved in the experience of menstrual pain. Yet, the neurobiological underpinnings are not yet known and have not yet been studied in adolescents. Further, no study has investigated the relationship of menstrual pain to non-physical pain (i.e., noxious visual stimuli) and examined brain connectivity in networks commonly associated with pain. Forty-six adolescent girls (ages 14 to 18) completed a 6-min resting state MRI scan and then completed a visual sensitivity task involving viewing a blue and yellow checkerboard stimulus. Visual unpleasantness ratings and self-reported average menstrual pain ratings were collected. Thirty-five resting-state networks was estimated using a multivariate data-driven method for group Independent Component Analysis (GICA). Cingulo-opercular (CN), prefrontal salience (pfSN) and default mode (DMN) networks were selected as a priori, as they are often associated with pain. Using dual regression approach, we extracted subject-specific network maps corresponding to each a priori network. Statistical models were analyzed using Randomise in FSL to investigate the association of menstrual pain and visual sensitivity scores with the connectivity of these networks. Menstrual pain was negatively associated with connectivity of wide-spread prefrontal areas within the DMN, thalamus, insula, and striatum. In contrast, visual sensitivity was positively associated with connectivity of the medial temporal subnetwork of the DMN. These data suggest that different pain experiences may result from unique neural mechanisms. For visual sensitivity, increased connectivity of medial temporal lobe DMN regions with anterior DMN may be a mechanism in which affective experience of noxious stimuli is linked with self-reported pain. For menstrual pain, dysregulated connectivity within the DMN and between the DMN and pain-related regions might lead to impaired regulation of other pain constructs and put some individuals at risk for chronic pain. Grant support from NIH/NICHD R01 HD093680.

Threat Neurocircuitry Predicts the Development of Anxiety and Depression Symptoms in a Longitudinal Study

BackgroundOwing to high heterogeneity and comorbidity, the shared and unique neural mechanisms underlying the development of anxiety and major depressive disorders remain unclear. Using a dimensional model describing shared versus unique symptoms associated with anxiety and depression, this study investigated how longitudinal changes in symptom dimensions relate to threat neurocircuitry. MethodsParticipants were 18- to 19-year-olds (N = 279, 186 females) who completed self-report measures of anxiety and depression at baseline and at 10, 20, and 30 months. Linear slopes of symptom dimensions of general distress, fear, and anhedonia-apprehension were estimated through a trilevel factorial model. In addition, functional magnetic resonance imaging scans were obtained while participants performed Pavlovian fear conditioning tasks at baseline and 30 months, including three phases of fear acquisition, extinction, and extinction recall. Neural responses in regions of interest related to threat neural circuitry (e.g., amygdala, ventromedial prefrontal cortex, and subgenual anterior cingulate cortex) were extracted. ResultsLinear mixed models used to estimate relationships between changes of symptom dimensions and neural responses revealed two major findings: 1) greater neural responses to threatening stimuli during fear acquisition at baseline were associated with a greater increase in fear symptoms during the 30-month prospective period; and 2) elevated neural responses to the extinguished stimulus during extinction recall at 30 months were negatively associated with changes in general distress, suggesting that greater increases in general distress are associated with larger deficits in extinction memory. ConclusionsThese findings improve our understanding of pathophysiological pathways underlying the development of anxiety and depression, while separating symptom dimensions that are shared versus unique between the two disorders.

Aberrant Development of Cross-Frequency Multiplex Functional Connectome in First-Episode, Drug-Naive Major Depressive Disorder and Schizophrenia.

Introduction: Both major depressive disorder (MDD) and schizophrenia (SCH) are characterized by neurodevelopmental abnormalities; however, transdiagnostic and diagnosis-specific patterns of such abnormalities have rarely been examined, particularly in large-scale functional brain networks via advanced multilayer network models. Methods: Here, we collected resting-state functional magnetic resonance imaging data from 45 MDD patients, 64 SCH patients, and 48 healthy controls (HCs; 13-45 years old), and we constructed functional networks in different frequency intervals. The frequency-dependent networks were then fused by multiplex network models, followed by graph-based topological analyses. Results: We found that functional networks of the patients showed common neurodevelopmental abnormalities in the right ventromedial parietooccipital sulcus (opposite correlations with age to HCs), whereas functional networks of the MDD patients exhibited specific alterations in the left superior parietal lobule and right precentral gyrus with respect to cross-frequency interactions. These findings were quite different from those from brain networks within each frequency interval, which revealed SCH-specific neurodevelopmental abnormalities in the right superior temporal gyrus (opposite correlations with age to the other two groups) in 0.027-0.073 Hz, and SCH-specific alterations in the left superior temporal gyrus and bilateral insula in 0.073-0.198 Hz. Finally, multivariate analysis of age prediction revealed that the subcortical network lost prediction ability in both patient groups, whereas the visual network exhibited additional prediction ability in the MDD patients. Discussion and Conclusion: Altogether, these findings demonstrate transdiagnostic and diagnosis-specific neurodevelopmental abnormalities and alterations in large-scale functional brain networks between MDD and SCH, which have important implications for understanding shared and unique neural mechanisms underlying the diseases.

Slower dispositional respiration is associated with lower pain sensitivity, higher mindfulness and multiple unique neural mechanisms

The relationship between non-volitionally controlled breathing and pain remains unknown. The psychological mechanisms supporting this relationship are also poorly characterized. Anxiety and dispositional mindfulness, two antithetical constructs, are postulated to mediate the relationship between pain and respiration. Anxiety increases breathing and pain. In contrast, dispositional mindfulness is associated with lower anxiety and pain. Importantly, the neural correlates of respiration rate have not been identified. Seventy-four pain-free participants were administered the Five Faceted Mindfulness Questionnaire (FFMQ) and the Spielberger State Anxiety Inventory (SAI) before scanning. Two innocuous (35°C) and noxious (49°C; right calf) stimulation series during pseudo-continuous arterial spin labeling functional MRI and continuous respiratory were then acquired. Subjects were instructed to “remain still and close their eyes” and visual analogue scale (0 = “no pain” – 10 = “worst pain imaginable”) pain intensity ratings were collected after each series. Slower respiration was associated with lower pain intensity ratings during noxious (r = .26, p = .03) and innocuous (r = .28, p = .02) stimulation. Higher mindfulness scores were associated with slower respiration (r = -.28, p = .02) and lower pain (r = -.25, p = .03). State anxiety did not significantly co-vary with pain or respiration (ps > .18). When compared to 35°C, 49°C stimulation produced significant activation in the primary somatosensory cortex corresponding to the stimulation site, bilateral thalamus, secondary somatosensory cortex, anterior/posterior insula, and dorsal anterior cingulate cortex (dACC). Slower respiration was associated with greater activation in the subcallosal cortex, subgenual ACC, right-lateralized dorsolateral prefrontal cortex (dlPFC), putamen, anterior insula, and left caudate. Faster breathing was associated with greater activation in respiratory control centers within the pons, medulla, and cerebellum. These findings suggest that individuals who naturally breathe slower report lower pain and engage multiple unique executive-level processes supporting psychological resilience and self-regulation of affect. This work was supported by the National Center for Complementary and Integrative Health (R21-AT007247, F32-AT006949, K99/R00-AT008238, R01-AT009693; F32 AT010843) and the Mind and Life Institute's Francisco J. Varela Award.

Shared and unique neural mechanisms underlying pediatric trichotillomania and obsessive compulsive disorder

BackgroundLittle is known about the neural underpinnings of pediatric trichotillomania (TTM). We examined error-related negativity (ERN)-amplitude and theta-EEG power differences among youth with TTM, OCD, and healthy controls (HC). MethodsForty channel EEG was recorded from 63 pediatric participants (22 with TTM, 22 with OCD, and 19 HC) during the Eriksen Flanker Task. EEG data from inhibitory control were used to derive estimates of ERN amplitude and event-related spectral power associated with motor inhibition. ResultsTTM and HC were similar in brain activity patterns in frontal and central regions and TTM and OCD were similar in the parietal region. Frontal ERN-amplitude was significantly larger in OCD relative to TTM and HC, who did not differ from each other. The TTM group had higher theta power compared to OCD in frontal and central regions, and higher theta than both comparison groups in right motor cortex and superior parietal regions. Within TTM, flanker task performance was correlated with EEG activity in frontal, central, and motor cortices whereas global functioning and impairment were associated with EEG power in bilateral motor and parietal cortices. ConclusionsFindings are discussed in terms of shared and unique neural mechanisms in TTM and OCD and treatment implications.

A Review of Default Mode Network Connectivity and Its Association With Social Cognition in Adolescents With Autism Spectrum Disorder and Early-Onset Psychosis.

Recent studies have demonstrated substantial phenotypic overlap, notably social impairment, between autism spectrum disorder (ASD) and schizophrenia. However, the neural mechanisms underlying the pathogenesis of social impairments across these distinct neuropsychiatric disorders has not yet been fully examined. Most neuroimaging studies to date have focused on adults with these disorders, with little known about the neural underpinnings of social impairments in younger populations. Here, we present a narrative review of the literature available through April 2020 on imaging studies of adolescents with either ASD or early-onset psychosis (EOP), to better understand the shared and unique neural mechanisms of social difficulties across diagnosis from a developmental framework. We specifically focus on functional connectivity studies of the default mode network (DMN), as the most extensively studied brain network relevant to social cognition across both groups. Our review included 29 studies of DMN connectivity in adolescents with ASD (Mean age range = 11.2–21.6 years), and 14 studies in adolescents with EOP (Mean age range = 14.2–24.3 years). Of these, 15 of 29 studies in ASD adolescents found predominant underconnectivity when examining DMN connectivity. In contrast, findings were mixed in adolescents with EOP, with five of 14 studies reporting DMN underconnectivity, and an additional six of 14 studies reporting both under- and over-connectivity of the DMN. Specifically, intra-DMN networks were more frequently underconnected in ASD, but overconnected in EOP. On the other hand, inter-DMN connectivity patterns were mixed (both under- and over-connected) for each group, especially DMN connectivity with frontal, sensorimotor, and temporoparietal regions in ASD, and with frontal, temporal, subcortical, and cerebellar regions in EOP. Finally, disrupted DMN connectivity appeared to be associated with social impairments in both groups, less so with other features distinct to each condition, such as repetitive behaviors/restricted interests in ASD and hallucinations/delusions in EOP. Further studies on demographically well-matched groups of adolescents with each of these conditions are needed to systematically explore additional contributing factors in DMN connectivity patterns such as clinical heterogeneity, pubertal development, and medication effects that would better inform treatment targets and facilitate prediction of outcomes in the context of these developmental neuropsychiatric conditions.

Attention to breath sensations does not engage endogenous opioids to reduce pain.

The endogenous opioidergic system is critically involved in the cognitive modulation of pain. Slow-breathing-based techniques are widely used nonpharmacological approaches to reduce pain. Yet, the active mechanisms of actions supporting these practices are poorly characterized. Growing evidence suggest that mindfulness-meditation, a slow-breathing technique practiced by nonreactively attending to breathing sensations, engages multiple unique neural mechanisms that bypass opioidergically mediated descending pathways to reduce pain. However, it is unknown whether endogenous opioids contribute to pain reductions produced by slow breathing. The present double-blind, placebo-controlled crossover study examined behavioral pain responses during mindfulness-meditation (n = 19), sham-mindfulness meditation (n = 20), and slow-paced breathing (n = 20) in response to noxious heat (49°C) and intravenous administration (0.15 mg/kg bolus + 0.1 mg/kg/hour maintenance infusion) of the opioid antagonist, naloxone, and placebo saline. Mindfulness significantly reduced pain unpleasantness ratings across both infusion sessions when compared to rest, but not pain intensity. Slow-paced breathing significantly reduced pain intensity and unpleasantness ratings during naloxone but not saline infusion. Pain reductions produced by mindfulness-meditation and slow-paced breathing were insensitive to naloxone when compared to saline administration. By contrast, sham-mindfulness meditation produced pain unpleasantness reductions during saline infusion but this effect was reversed by opioidergic antagonism. Sham-mindfulness did not lower pain intensity ratings. Self-reported "focusing on the breath" was identified as the operational feature particularly unique to the mindfulness-meditation and slow paced-breathing, but not sham-mindfulness meditation. Across all individuals, attending to the breath was associated with naloxone insensitive pain-relief. These findings provide evidence that slow breathing combined with attention to breath reduces pain independent of endogenous opioids.

Discrete electrocortical predictors of anxiety and anxiety-related treatment response in youth with autism spectrum disorder

There are two established electroencephalogram (EEG) indices that putatively relate to anxiety symptoms: a) the error-related negativity (ERN), which reflects endogenous threat sensitivity, and b) resting-state EEG relative right frontal activity (rRFA), which relates to approach/withdrawal motivation. We examined these indices conjointly to better elucidate differential mechanisms underlying the common anxiety phenotype in youth with autism spectrum disorder (ASD), in relation to subjective reports of symptomatology and treatment response. EEG was recorded from 53 youth with ASD who participated in a 10-week social skills intervention (SSI). More negative ERN related to higher self-reported social anxiety symptoms at baseline, and predicted improvements in self-reported social anxiety symptoms following SSI. Although rRFA did not relate to anxiety symptoms at baseline, more rRFA predicted improvement in parent-reported anxiety domains but worsening in self-reported anxiety symptoms. This study provides evidence for unique neural mechanisms of anxiety symptoms and changes in anxiety after SSI in youth with ASD.

4.30 Shared and Unique Neural Mechanisms Underlying Inhibitory Control in Trichotillomania and OCD

Trichotillomania (TTM) is typified by recurrent hair pulling, hair loss, and significant distress or impairment. TTM is classified in DSM-5 as an OCD and related disorder on the basis of related diagnostic validators with OCD. Here we examine shared and unique neural mechanisms of inhibitory control in TTM and OCD.

Aggression in Women: Behavior, Brain and Hormones.

We review the literature on aggression in women with an emphasis on laboratory experimentation and hormonal and brain mechanisms. Women tend to engage in more indirect forms of aggression (e.g., spreading rumors) than other types of aggression. In laboratory studies, women are less aggressive than men, but provocation attenuates this difference. In the real world, women are just as likely to aggress against their romantic partner as men are, but men cause more serious physical and psychological harm. A very small minority of women are also sexually violent. Women are susceptible to alcohol-related aggression, but this type of aggression may be limited to women high in trait aggression. Fear of being harmed is a robust inhibitor of direct aggression in women. There are too few studies and most are underpowered to detect unique neural mechanisms associated with aggression in women. Testosterone shows the same small, positive relationship with aggression in women as in men. The role of cortisol is unclear, although some evidence suggests that women who are high in testosterone and low in cortisol show heightened aggression. Under some circumstances, oxytocin may increase aggression by enhancing reactivity to provocation and simultaneously lowering perceptions of danger that normally inhibit many women from retaliating. There is some evidence that high levels of estradiol and progesterone are associated with low levels of aggression. We highlight that more gender-specific theory-driven hypothesis testing is needed with larger samples of women and aggression paradigms relevant to women.

Neural mechanism of placebo effects and cognitive reappraisal in emotion regulation

The present study compared learning-based placebo effect and cognition-based reappraisal, to reveal the common and unique neural mechanisms between the two emotion regulations. First, the anxiety-relieving effect was tested by conducting a behavioral experiment. Next, the participants with the highest placebo or reappraisal effect were selected for the functional magnetic resonance imaging experiments. The results indicated that: (1) they both attenuated activity in the right amygdala and right insula, and (2) placebo effect activated the left subgenual cingulate whereas reappraisal activated the right dorsal prefrontal cortex (PFC) and the left inferior PFC. Our results show that learning-based placebo effect and cognition-based reappraisal have common anxiety-relieving effects. The placebo effect mainly depends on direct pathway subgenual cingulate-amygdala to regulate emotions, whereas the reappraisal may rely on both indirect pathways, such as the dorsal PFC-subgenual cingulate-amygdala, and direct pathways, such as the ventral lateral PFC-amygdala to regulate emotions.

Cognitive-Affective Neural Plasticity following Active-Controlled Mindfulness Intervention

Mindfulness meditation is a set of attention-based, regulatory, and self-inquiry training regimes. Although the impact of mindfulness training (MT) on self-regulation is well established, the neural mechanisms supporting such plasticity are poorly understood. MT is thought to act through interoceptive salience and attentional control mechanisms, but until now conflicting evidence from behavioral and neural measures renders difficult distinguishing their respective roles. To resolve this question we conducted a fully randomized 6 week longitudinal trial of MT, explicitly controlling for cognitive and treatment effects with an active-control group. We measured behavioral metacognition and whole-brain blood oxygenation level-dependent (BOLD) signals using functional MRI during an affective Stroop task before and after intervention in healthy human subjects. Although both groups improved significantly on a response-inhibition task, only the MT group showed reduced affective Stroop conflict. Moreover, the MT group displayed greater dorsolateral prefrontal cortex responses during executive processing, consistent with increased recruitment of top-down mechanisms to resolve conflict. In contrast, we did not observe overall group-by-time interactions on negative affect-related reaction times or BOLD responses. However, only participants with the greatest amount of MT practice showed improvements in response inhibition and increased recruitment of dorsal anterior cingulate cortex, medial prefrontal cortex, and right anterior insula during negative valence processing. Our findings highlight the importance of active control in MT research, indicate unique neural mechanisms for progressive stages of mindfulness training, and suggest that optimal application of MT may differ depending on context, contrary to a one-size-fits-all approach.

Developmental emergence of fear learning corresponds with changes in amygdala synaptic plasticity

Mother–infant attachment is facilitated in altricial rodents through unique neural mechanisms that include impaired neonatal fear conditioning until the time that pups first begin to leave the nest (sensitive period). Here, we confirmed the developmental emergence of odor fear conditioning in neonatal rat pups, and examined synaptic plasticity of inputs to the basolateral amygdala in vitro. Coronal slices through the amygdala were obtained from sensitive (< 10 days) and post-sensitive (> 10, < 19 days) period pups. Field potentials were recorded in the basolateral amygdala in response to stimulation of either the external capsule (neocortical inputs) or fibers from the cortical nucleus of the amygdala (olfactory inputs). The effects of tetanic stimulation were examined in each pathway. In both pathways, tetanic stimulation induce significant long-term synaptic plasticity in post-sensitive period pups, but no significant plasticity in sensitive period pups incapable of learning odor aversions. GABA A receptor blockade in post-sensitive period slices reverts synaptic plasticity to sensitive period characteristics. The results suggest that sensitive period deficits in fear conditioning may be related to impaired amygdala synaptic plasticity and the immature state of GABAergic inhibition and/or its modulation in the neonatal amygdala.

Neural mechanisms regulating neurohypophysial resistance arteries.

We defined the extent of vasoactive intestinal polypeptide (VIP) and noradrenergic influences on isolated 100- to 200-microns-diameter vessels from the resistance arterial circulation of the neurohypophysis. A dual extracranial (inferior hypophysial) and intracranial (superior hypophysial) arterial supply to the neurohypophysis was confirmed. The inferior hypophysial artery demonstrates noradrenergic and VIP-like perivascular nerves, whereas the superior hypophysial artery shows primarily VIP-like innervation. Pharmacological sensitivity of the inferior hypophysial to VIP [mean effective dose (ED50) = 10(-8.2) M] and to norepinephrine (ED50 = 10(-5.7) M) was demonstrated. The superior hypophysial reacted only to VIP (ED50 = 10(-8.6) M). The physiological relevance of these findings was tested with transmural nerve stimulation. Frequency-dependent vasodilation of both inferior and superior hypophysial arteries was demonstrated. This dilation could not be blocked with atropine or propranolol. Frequency-dependent vasoconstriction was identified in extracranial vessels including the inferior hypophysial artery. This constriction is only partially blocked by prazosin, phentolamine, and guanethidine. When neurohypophysial resistance vessels are compared with larger circle of Willis arteries and similar-size pial vessels of other cerebral regions, they appear to have regionally unique neural mechanisms for regulating blood flow. Specifically whether controlled by periarterial nerves or other tissue influences, the inferior hypophysial artery appears to meet anatomic, pharmacological, and physiological definitions of neural control for both dilator and constrictor activities of flow to the neurohypophysis.

The evolution of neural circuits controlling feeding behavior in frogs.

Our approach to understanding motor systems is a phylogenetic, 'outside-in' approach, the goal of which is to identify behavioral transitions during phylogenesis and elucidate their neurological basis. In this paper, we review the results of recent behavioral, biomechanical and neurological studies on frog feeding behavior. These studies show that highly protrusible tongues have evolved numerous times independently among frogs, and that the biomechanics and neuromuscular control of feeding behavior have been transformed repeatedly during frog evolution. Many of the independent lineages possess unique biomechanical mechanisms for protracting their tongues and unique neural mechanisms for coordinating feeding behavior. In frogs, there has been considerable evolution at the interface between reticular central pattern generators (CPGs) associated with feeding and sensory feedback circuits that modulate feeding motor output. In particular, the roles of hypoglossal and glossopharyngeal sensory feedback appear to have been relatively plastic in their evolution. Prey-type dependence of hypoglossal sensory feedback in Rana suggests that the interaction between descending visual control and sensory feedback also may be evolutionarily plastic. Comparative studies have found that motor systems sometimes evolve conservatively across morphological and behavioral transitions (i.e., the shoulder in birds) or, alternatively, they may be subject to considerably more evolutionary change than is reflected in morphological characteristics (i.e., feeding in cichlids). We hypothesize that the CPG circuits for feeding behavior in the reticular formation may evolve conservatively because they are highly integrated, multifunctional networks which cannot be optimized for one function without compromising others. In contrast, the interfaces between the CPG, sensory feedback and descending control should be less constrained. When changes in motor patterns occur during evolution, it is likely that sensory feedback or descending control may be involved.