Ejaculation latency determines susceptibility to stress in the male rat.

Stress induces diverse effects on sexual behavior, ranging from enhanced execution to the complete abolishment of sexual interaction. However, it is not clear whether some characteristics intrinsic to the individual that experiences stress could also explain this differential effect. This study seeks to relate sexual execution to susceptibility to stress (as post-stress sexual motivation). To this end, we designed a three-session experimental paradigm. In the first session, male rats were allowed to copulate with a female. In the second, the male rats received electric foot shocks as they attempted to approach the female. The third and final session was used to determine the effects of stress on sexual behavior by separating the rats into two groups: a motivation-impaired group (rats that did not cross to achieve copulation), and an unimpaired group (rats that did cross). Mount latency was affected immediately by stress in both groups, though only the non-crossing group presented a reduced number of copulatory events. The rats that did not cross showed slower-paced sexual execution even before stress was applied compared to the rats that crossed. These results show that rats that are more susceptible to stress present higher ejaculation latency even before the application of stress.

Effects of inactivation of the ventral tegmental area on prefronto-accumbens activity and sexual motivation in male rats.

Sexual motivation requires the processing of sexual stimuli. The prefrontal cortex (PFC) and nucleus accumbens (NAcc) receive dopaminergic innervation from the ventral tegmental area (VTA). Both structures participate in processing stimuli, and their adequate functioning is modulated by dopamine and other neurotransmitters. This study was designed to determine the effect of inactivation of the VTA on sexual motivation, relative power (RP) and electroencephalographic (EEG) correlation of the PFC and NAcc in male rats. A total of 20 rats implanted with electrodes in the left medial prefrontal cortex (mPFC) and NAcc, and with bilateral cannulae in the VTA, were divided into two groups of 10 rats each, one injected with tetrodotoxin (TTX), the other with a vehicle solution (VEH). EEGs from the mPFC and NAcc were recorded during the awake-quiet state in the presence of either a receptive or non-receptive female. The TTX group showed a lower preference for the receptive female accompanied by a lower RP of the 8-13 and 14-30 Hz bands in the mPFC. Also, in the presence of the receptive female, the TTX group had a lower RP of the 8-13 Hz band in the NAcc, but a higher prefronto-accumbens correlation in the same band. These results provide evidence that VTA activity is necessary for the adequate functioning of the mPFC and NAcc and, therefore, also for the adequate processing of sexually-relevant stimuli that allows the induction and maintenance of sexual motivation in male rats.

Inhibition of transcription and translation in the striatum after memory reactivation: Lack of evidence of reconsolidation.

It has been found that interference with neural activity after a consolidated memory is retrieved produces an amnestic state; this has been taken has indicative of destabilization of the memory trace that would have been produced by a process of reconsolidation (allowing for maintenance of the original trace). However, a growing body of evidence shows that this is not a reliable effect, and that it is dependent upon some experimental conditions, such as the age of the memory, memory reactivation procedures, the predictability of the reactivation stimulus, and strength of training. In some instances, where post-retrieval treatments induce a retention deficit (which would be suggestive of interference with reconsolidation), memory is rescued by simple passing of time or by repeated retention tests. We now report that post-training and post-retrieval inhibition of transcription and translation in dorsal striatum, a structure where both of these manipulations have not been studied, produce interference with consolidation and a transitory retention deficit, respectively. These results do not give support to the reconsolidation hypothesis and lead to the conclusion that the post-activation deficiencies are due to interference with retrieval of information.

Nicotine uses neuron-glia communication to enhance hippocampal synaptic transmission and long-term memory.

Nicotine enhances synaptic transmission and facilitates long-term memory. Now it is known that bi-directional glia-neuron interactions play important roles in the physiology of the brain. However, the involvement of glial cells in the effects of nicotine has not been considered until now. In particular, the gliotransmitter D-serine, an endogenous co-agonist of NMDA receptors, enables different types of synaptic plasticity and memory in the hippocampus. Here, we report that hippocampal long-term synaptic plasticity induced by nicotine was annulled by an enzyme that degrades endogenous D-serine, or by an NMDA receptor antagonist that acts at the D-serine binding site. Accordingly, both effects of nicotine: the enhancement of synaptic transmission and facilitation of long-term memory were eliminated by impairing glial cells with fluoroacetate, and were restored with exogenous D-serine. Together, these results show that glial D-serine is essential for the long-term effects of nicotine on synaptic plasticity and memory, and they highlight the roles of glial cells as key participants in brain functions.