Observation model and parameter partials for the JPL VLBI parameter estimation software MASTERFIT-1987

This report is a revision of the document of the same title (1986), dated August 1, which it supersedes. Model changes during 1986 and 1987 included corrections for antenna feed rotation, refraction in modelling antenna axis offsets, and an option to employ improved values of the semiannual and annual nutation amplitudes. Partial derivatives of the observables with respect to an additional parameter (surface temperature) are now available. New versions of two figures representing the geometric delay are incorporated. The expressions for the partial derivatives with respect to the nutation parameters have been corrected to include contributions from the dependence of UTI on nutation. The authors hope to publish revisions of this document in the future, as modeling improvements warrant

The Deep Space Network capabilities for radio interferometry

The very long baseline interferometry capability as well as the planned capability of the deep space network (DSN) are described. Major emphasis is placed on the following: VLBI development; operational VLBI for DSN calibration; and VLBI for spacecraft navigation

Determination of intercontinental baselines and Earth orientation using VLBI

A series of experiments was conducted during the last decade to explore the capability of very long baseline interferometry (VLBI) to measure the crustal and rotational motions of the Earth with accuracies at the centimeter level. The observing stations are those of NASA's Deep Space Network in California, Spain and Australia. A multiparameter fit to the observed values of delay and delay rate yields radio source positions, polar motion, universal time, the precession constant, baseline vectors, and solid Earth tides. Source positions are obtained with formal errors of the order of 0''.01. UT1-UTC and polar motion are determined at 49 epochs, with formal error estimates for the more recent data of 0.5 msec for UT1-UTC and 2 to 6 mas for polar motion. Intercontinental baseline lengths are determined with formal errors of 5 to 10 cm. The Love numbers and Earth tide phase lag agree with the commonly accepted values

VLBI measurements of radio source positions at the Jet Propulsion Laboratory

The results of approximately 1300 observations of 67 radio sources are presented. Most of the measurements were made at the stations of the Deep Space Network in California, Spain, and Australia at wavelengths of 13.1 and 3.6 cm, between 1971 and 1978. The formal errors in the derived source positions are generally in the neighborhood of 0.01 seconds of arc and the positions agree fairly well with those previously published

Chronic opioid pretreatment potentiates the sensitization of fear learning by trauma.

Despite the large comorbidity between PTSD and opioid use disorders, as well as the common treatment of physical injuries resulting from trauma with opioids, the ability of opioid treatments to subsequently modify PTSD-related behavior has not been well studied. Using the stress-enhanced fear learning (SEFL) model for PTSD, we characterized the impact of chronic opioid regimens on the sensitization of fear learning seen following traumatic stress in mice. We demonstrate for the first time that chronic opioid pretreatment is able to robustly augment associative fear learning. Highlighting aversive learning as the cognitive process mediating this behavioral outcome, these changes were observed after a considerable period of drug cessation, generalized to learning about multiple aversive stimuli, were not due to changes in stimulus sensitivity or basal anxiety, and correlated with a marker of synaptic plasticity within the basolateral amygdala. Additionally, these changes were not observed when opioids were given after the traumatic event. Moreover, we found that neither reducing the frequency of opioid administration nor bidirectional manipulation of acute withdrawal impacted the subsequent enhancement in fear learning seen. Given the fundamental role of associative fear learning in the generation and progression of PTSD, these findings are of direct translational relevance to the comorbidity between opioid dependence and PTSD, and they are also pertinent to the use of opioids for treating pain resulting from traumas involving physical injuries

Engram size varies with learning and reflects memory content and precision

Memories are rarely acquired under ideal conditions, rendering them vulnerable to profound omissions, errors, and ambiguities. Consistent with this, recent work using context fear conditioning has shown that memories formed after inadequate learning time display a variety of maladaptive properties, including overgeneralization to similar contexts. However, the neuronal basis of such poor learning and memory imprecision remains unknown. Using c-fos to track neuronal activity in male mice, we examined how these learning-dependent changes in context fear memory precision are encoded in hippocampal ensembles. We found that the total number of c-fos-encoding cells did not correspond with learning history but instead more closely reflected the length of the session immediately preceding c-fos measurement. However, using a c-fos-driven tagging method (TRAP2 mouse line), we found that the degree of learning and memory specificity corresponded with neuronal activity in a subset of dentate gyrus cells that were active during both learning and recall. Comprehensive memories acquired after longer learning intervals were associated with more double-labeled cells. These were preferentially reactivated in the conditioning context compared with a similar context, paralleling behavioral discrimination. Conversely, impoverished memories acquired after shorter learning intervals were associated with fewer double-labeled cells. These were reactivated equally in both contexts, corresponding with overgeneralization. Together, these findings provide two surprising conclusions. First, engram size varies with learning. Second, larger engrams support better neuronal and behavioral discrimination. These findings are incorporated into a model that describes how neuronal activity is influenced by previous learning and present experience, thus driving behavior.SIGNIFICANCE STATEMENT Memories are not always formed under ideal circumstances. This is especially true in traumatic situations, such as car accidents, where individuals have insufficient time to process what happened around them. Such memories have the potential to overgeneralize to irrelevant situations, producing inappropriate fear and contributing to disorders, such as post-traumatic stress disorder. However, it is unknown how such poorly formed fear memories are encoded within the brain. We find that restricting learning time results in fear memories that are encoded by fewer hippocampal cells. Moreover, these fewer cells are inappropriately reactivated in both dangerous and safe contexts. These findings suggest that fear memories formed at brief periods overgeneralize because they lack the detail-rich information necessary to support neuronal discrimination

Maladaptive Properties of Context-Impoverished Memories.

The context in which sudden fearful events occur can be poorly encoded into memory. Yet, the consequences of the resulting context-impoverished memories remain unknown. We demonstrate that restricting the time available for context encoding during contextual fear conditioning causes maladaptively overgeneralized and inextinguishable fear. However, post-conditioning context exposure enables further context encoding through hippocampal reconsolidation-dependent memory updating. Updating in the conditioning context alleviates overgeneralization and restores capacity for extinction. However, updating in a similar safe context erroneously shifts fear from the dangerous to the safe context. We argue that these phenomena can be explained by uncertainty about where events occurred. Moreover, we show that a hippocampal-neocortical neurocomputational model based on this assumption successfully simulates and explains our observations. These findings reveal that context-impoverished memories are maladaptive and can be improved or distorted after recall, with implications for basic memory theory, memory distortion, and treatment of disorders like post-traumatic stress disorder

The alpha1 subunit of the GABA(A) receptor modulates fear learning and plasticity in the lateral amygdala.

Synaptic plasticity in the amygdala is essential for emotional learning. Fear conditioning, for example, depends on changes in excitatory transmission that occur following NMDA receptor activation and AMPA receptor modification in this region. The role of these and other glutamatergic mechanisms have been studied extensively in this circuit while relatively little is known about the contribution of inhibitory transmission. The current experiments addressed this issue by examining the role of the GABA(A) receptor subunit alpha1 in fear learning and plasticity. We first confirmed previous findings that the alpha1 subunit is highly expressed in the lateral nucleus of the amygdala. Consistent with this observation, genetic deletion of this subunit selectively enhanced plasticity in the lateral amygdala and increased auditory fear conditioning. Mice with selective deletion of alpha1 in excitatory cells did not exhibit enhanced learning. Finally, infusion of a alpha1 receptor antagonist into the lateral amygdala selectively impaired auditory fear learning. Together, these results suggest that inhibitory transmission mediated by alpha1-containing GABA(A) receptors plays a critical role in amygdala plasticity and fear learning

NF-kB functions in synaptic signaling and behavior

Ca^(2+)-regulated gene transcription is essential to diverse physiological processes, including the adaptive plasticity associated with learning. We found that basal synaptic input activates the NF-kB transcription factor by a pathway requiring the Ca^(2+)/calmodulin-dependent kinase CaMKII and local submembranous Ca^(2+) elevation. The p65:p50 NF-kB form is selectively localized at synapses; p65-deficient mice have no detectable synaptic NF-kB. Activated NF-kB moves to the nucleus and could directly transmute synaptic signals into altered gene expression. Mice lacking p65 show a selective learning deficit in the spatial version of the radial arm maze. These observations suggest that long-term changes to adult neuronal function caused by synaptic stimulation can be regulated by NF-kB nuclear translocation and gene activation

Inverse temporal contributions of the dorsal hippocampus and medial prefrontal cortex to the expression of long-term fear memories

Retrograde amnesia following disruptions of hippocampal function is often temporally graded, with recent memories being more impaired. Evidence supports the existence of one or more neocortical long-term memory storage/retrieval site(s). Neurotoxic lesions of the medial prefrontal cortex (mPFC) or the dorsal hippocampus (DH) were made 1 day or 200 days following trace fear conditioning. Recently encoded trace fear memories were most disrupted by DH lesions, while remotely encoded trace and contextual memories were most disrupted by mPFC lesions. These data strongly support the consolidation theory of hippocampus function and implicate the mPFC as a site of long-term memory storage/retrieval