Memories for habits and skills ("implicit or procedural memory") and memories for facts ("explicit or episodic memory") are built up in different brain systems and are vulnerable to different neurodegenerative disorders in humans. So that the striatum-based mechanisms underlying habit formation could be studied, chronic recordings from ensembles of striatal neurons were made with multiple tetrodes as rats learned a T-maze procedural task. Large and widely distributed changes in the neuronal activity patterns occurred in the sensorimotor striatum during behavioral acquisition, culminating in task-related activity emphasizing the beginning and end of the automatized procedure. The new ensemble patterns remained stable during weeks of subsequent performance of the same task. These results suggest that the encoding of action in the sensorimotor striatum undergoes dynamic reorganization as habit learning proceeds.

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1 Ejaculatory problems and anorgasmia are well-known side-e ects of the SSRI antidepressants, and a pharmacologically induced increase in serotonergic neurotransmission inhibits ejaculatory behaviour in the rat. In the present study the role of 5-HT 1A and 5-HT 1B receptors in the mediation of male rat ejaculatory behaviour was examined by use of selective agonists and antagonists acting at these 5-HT receptor subtypes. 2 The 5-HT 1A receptor agonist 8-OH-DPAT (0.25 ± 4.00 mmol kg 71 s.c.) produced an expected facilitation of the male rat ejaculatory behaviour, and this e ect was fully antagonized by pretreatment with the new selective 5-HT 1A receptor antagonist (R)-3-N,N-dicyclobutylamino-8-¯uoro-3,4-dihydro-2H-1-benzopyran-5-carboxamide hydrogen (2R,3R) tartrate monohydrate (NAD-299) (1.0 mmol kg 71 s.c.). NAD-299 by itself (0.75 ± 3.00 mmol kg 71 s.c.) did not a ect the male rat ejaculatory behaviour. 3 The 5-HT 1B receptor agonist anpirtoline (0.25 ± 4.00 mmol kg 71 s.c.) produced a dose-dependent inhibition of the male rat ejaculatory behaviour, and this e ect was fully antagonized by pretreatment with the 5-HT 1B receptor antagonist isamoltane (16 mmol kg 71 s.c.) as well as by the new and selective antagonist (R)-(+)-2-(3-morpholinomethyl-2H-chromene-8-yl)oxymethylmorpholino methansulphonate (NAS-181) (16 mmol kg 71 s.c.). Isamoltane (1.0 ± 16.0 mmol kg 71 s.c.) and NAD-181 (1.0 ± 16.0 mmol kg 71 s.c.) had no, or weakly facilitatory e ects on the male rat ejaculatory behaviour. The non-selective 5-HT 1 receptor antagonist (7)-pindolol (8 mmol kg 71 s.c.), did not antagonize the inhibition produced by anpirtoline.4 The present results demonstrate opposite e ects, facilitation and inhibition, of male rat ejaculatory behaviour by stimulation of 5-HT 1A and 5-HT 1B receptors, respectively, suggesting that the SSRIinduced inhibition of male ejaculatory dysfunction is due to 5-HT 1B receptor stimulation.

The nonapeptide oxytocin is released into systemic circulation in situations of psychosocial interaction, and has been shown to be involved in mechanisms of social bonding and social recognition in laboratory studies. In view of disturbances in psychosocial relationships being a triggering factor for depression and anxiety, it is interesting to note that experimental studies have shown oxytocin to possess antidepressant- and anxiolytic-like actions. Thus. in the present study we examined effects of the SSRI citalopram (20 mg/kg i.p.) on plasma oxytocin, acutely and upon repeated administration, in adult male Sprague-Dawley rats. Plasma oxytocin, and some functionally related peptides (CCK, gastrin, somatostatin and insulin), were measured by standard radioimmunoassay techniques. Acute citalopram administration produced a statistically significant increase in plasma oxytocin and CCK levels. Administration of citalopram for 14 days did not attenuate the oxytocin-releasing effect to a challenge dose of the SSRI zimeldine (20 mg/kg s.c.), whereas CCK levels were not increased after the subchronic citalopram treatment. Thus, the SSRI citalopram produces increased plasma oxytocin levels acutely, and there appears to be no or little tolerance to this effect upon repeated administration. There were no, or variable, effects on plasma levels of gastrin, somatostatin or insulin. It is suggested that oxytocin release is an important aspect of the pharmacological actions of SSRIs, and this could be an important contributory factor for the clinical profile of this group of antidepressants with particular efficacy in disorders of psychosocial origin.

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