Alterations in neuropeptide Y levels and Y1 binding sites in the Flinders Sensitive Line rats, a genetic animal model of depression. Rx drugs

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Neurosci Lett. 1999 Apr 23;265(3):191-4.
Alterations in neuropeptide Y levels and Y1 binding sites in the Flinders Sensitive Line rats, a genetic animal model of depression.

Caberlotto L, Jimenez P, Overstreet DH, Hurd YL, Mathe AA, Fuxe K.

Department of Neuroscience, Karolinska Institute, Stockholm, Sweden.

Previously, we observed specific alterations of neuropeptide Y (NPY) and Y1 receptor mRNA expression in discrete regions of the Flinders Sensitive Line rats (FSL), an animal model of depression. In order to clarify the correlation between mRNA expression and protein content, radioimmunoassay and receptor autoradiography were currently performed. In the FSL rats, NPY-like immunoreactivity (NPY-LI) was decreased in the hippocampal CA region, while Y1 binding sites were increased; NPY-LI was increased in the arcuate nucleus. Fluoxetine treatment elevated NPY-LI in the arcuate and anterior cingulate cortex and increased Y1 binding sites in the medial amygdala and occipital cortex in both strains. No differences were found regarding the Y2 binding sites. The results demonstrate a good correlation between NPY peptide and mRNA expression, and sustain the possible involvement of NPY and Y1 receptors in depression.

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Serotonin transporters (SERTs), sites of psychostimulant action, display multiple conducting states in expression systems. These include a substrate-independent transient conductance, two separate substrate-independent leak conductances associated with Na(+) and H(+), and a substrate-dependent conductance of variable stoichiometry, which exceeds that predicted from electroneutral substrate transport. The present data show that the SNARE protein syntaxin 1A binds the N-terminal tail of SERT, and this interaction regulates two SERT-conducting states. First, substrate-induced currents are absent because Na(+) flux becomes strictly coupled to 5HT transport. Second, Na(+)-mediated leak currents are eliminated. These two SERT-conducting states are present endogenously in thalamocortical neurons, act to depolarize the membrane potential, and are modulated by molecules that disrupt SERT and syntaxin 1A interactions. These data show that protein interactions govern SERT activity and suggest that both cell excitability and psychostimulant-mediated effects will be dependent upon the state of association among SERT and its interacting partners.

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BACKGROUND: Primates reared in captivity may display stereotypic behaviors. These behaviors are arguably reminiscent of human obsessive-compulsive or posttraumatic symptoms, which respond to selective serotonin reuptake inhibitors (SSRIs). Captive primates with marked stereotypic behaviors were entered into a randomized controlled study of the SSRI, fluoxetine. METHODS: A sample of 10 vervet monkeys with behaviors such as marked saluting, somersaulting, weaving, or head tossing was selected. Subjects were randomized to receive fluoxetine 1 mg/kg for 6 weeks (n=5) or no treatment (n=5). A rater blind to the medication status of subjects noted the frequency of the stereotypic behaviors. RESULTS: Repeated-measures analysis of variance (RM-ANOVA) demonstrated a significant GroupxTime difference with significantly fewer stereotypic symptoms in the fluoxetine group by endpoint. At this time, three of the five fluoxetine-treated subjects (but none of the no-treatment subjects) were responders on the Clinical Global Impressions (CGI) change item (CGI < or =2). CONCLUSIONS: Stereotypic behaviors in captive vervets gradually and partially decrease in response to administration of an SSRI, paralleling research on human anxiety symptoms. Further research on animal stereotypies may be useful in providing appropriate veterinary care, and in exploring the underlying neurobiology of certain psychiatric disorders.

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