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1.
J Acoust Soc Am ; 142(3): 1261, 2017 09.
Article in English | MEDLINE | ID: mdl-28964104

ABSTRACT

Emotional states can be conveyed by vocal cues such as pitch and intensity. Despite the ubiquity of cellular telephones, there is limited information on how vocal emotional states are perceived during cell-phone transmissions. Emotional utterances (neutral, happy, angry) were elicited from two female talkers and simultaneously recorded via microphone and cell-phone. Ten-step continua (neutral to happy, neutral to angry) were generated using the straight algorithm. Analyses compared reaction time (RT) and emotion judgment as a function of recording type (microphone vs cell-phone). Logistic regression revealed no judgment differences between recording types, though there were interactions with emotion type. Multi-level model analyses indicated that RT data were best fit by a quadratic model, with slower RT at the middle of each continuum, suggesting greater ambiguity, and slower RT for cell-phone stimuli across blocks. While preliminary, results suggest that critical acoustic cues to emotion are largely retained in cell-phone transmissions, though with effects of recording source on RT, and support the methodological utility of collecting speech samples by phone.


Subject(s)
Anger , Cell Phone , Happiness , Voice , Adult , Cues , Emotions , Female , Humans , Tape Recording , Young Adult
2.
Neuropsychopharmacology ; 40(4): 874-83, 2015 Mar.
Article in English | MEDLINE | ID: mdl-25267343

ABSTRACT

In addition to alleviating depression, long-term adaptive changes induced by antidepressants may regulate neural plasticity in the diseased brain, providing symptomatic and disease-modifying effects in Parkinson's disease. The present study investigated whether chronic treatment with a frequently prescribed tricyclic antidepressant was neuroprotective in a 6-hydroxydopamine (6-OHDA) rat model of parkinsonism. In lesioned animals, chronic amitriptyline (AMI; 5 mg/kg) treatment resulted in a significant sparing of tyrosine hydroxylase-immunoreactive (THir) neurons in the substantia nigra pars compacta (SNpc) compared with saline treatment. Additionally, striatal fibers were preserved and functional motor deficits were attenuated. Although 6-OHDA lesions did not induce anhedonia in our model, the dose of AMI utilized had antidepressant activity as demonstrated by reduced immobility. Recent in vitro and in vivo data provide evidence that trophic factors such as brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) may be key mediators of the therapeutic response to antidepressants. Therefore, we investigated whether AMI mediates changes in these specific trophic factors in the intact and degenerating nigrostriatal system. Chronic AMI treatment mediates an increase in nigral BDNF both before and during ongoing degeneration, suggesting it may contribute to neuroprotection observed in vivo. However, over time, AMI reduced BDNF levels in the striatum, indicating tricyclic therapy differentially regulates trophic factors within the nigrostriatal system. Combined, these results suggest that AMI treatment attenuates dopamine neuron loss and elicits significant trophic changes relevant to dopamine neuron survival.


Subject(s)
Amitriptyline/therapeutic use , Analgesics, Non-Narcotic/therapeutic use , Brain-Derived Neurotrophic Factor/metabolism , Corpus Striatum/pathology , Neurodegenerative Diseases , Parkinsonian Disorders/complications , Substantia Nigra/pathology , Adrenergic Agents/toxicity , Animals , Disease Models, Animal , Food Preferences , Gene Expression Regulation/drug effects , Hindlimb Suspension , Male , Neurodegenerative Diseases/drug therapy , Neurodegenerative Diseases/etiology , Neurodegenerative Diseases/pathology , Oxidopamine/toxicity , Parkinsonian Disorders/chemically induced , Psychomotor Performance/drug effects , Rats , Rats, Wistar , Saccharin/administration & dosage , Tyrosine 3-Monooxygenase/metabolism
3.
Neurotherapeutics ; 7(3): 250-7, 2010 Jul.
Article in English | MEDLINE | ID: mdl-20643377

ABSTRACT

Autism is a neurodevelopmental disorder characterized by dysfunction in three core symptom domains: speech and communication deficits, repetitive or compulsive behaviors with restricted interests, and social impairment. The neuropeptide oxytocin, along with the structurally similar peptide arginine vasopressin, may play a role in the etiology of autism, and especially in the social impairment domain. Oxytocin is a nonapeptide (i.e., it has nine amino acids). It is synthesized in magnocellular neurons in the paraventricular nucleus and the supraoptic nucleus of the hypothalamus and is released into the bloodstream by way of axon terminals in the posterior pituitary. Oxytocin is released both peripherally, where it is involved in milk letdown and the facilitation of uterine contractions, and centrally, where it acts as a neuromodulator along with arginine vasopressin. Here, we discuss relevant translational research pertaining to the role of oxytocin in social and repetitive behaviors and consider clinical implications. We also discuss current research limitations, review recent preliminary findings from studies involving oxytocin in autism spectrum disorder patient populations, and point to possible directions for future research.


Subject(s)
Autistic Disorder/physiopathology , Autistic Disorder/therapy , Oxytocin/physiology , Social Behavior , Animals , Arginine Vasopressin/physiology , Humans
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