Wallacerhodes9751

A 41 years-old male patient presented acutely with severe right testicular pain, and fever for 48 hours. Patient had a backround of previous left orchidectomy for epididymo-orchitis and sexually-transmitted disease. A clinical diagnosis of right epididymo-orchitis was made and patient was treated with intravenous broad-spectrum antibiotic. However subsequent ultrasound revealed imminent testicular ischaemia. Given the challenging nature of the case, i.e. single testicle with testicular ischaemia, surgical exploration, fasciotomy and tunica vaginalis grafting was performed to the patient. The patient recovered fully post-operatively with ultrasound proving restoration of end-diastolic flow to the testicle.

We examined how acute ethanol (EtOH) exposure affects long term depression (LTD) in the dentate gyrus (DG) of the hippocampus in juvenile rats. EtOH is thought to directly modulate n-methyl-D-aspartate receptor (NMDAr) currents, which are believed important for LTD induction. LTD in turn is believed to play an important developmental role in the hippocampus by facilitating synaptic pruning.

Hippocampal slices (350

m) were obtained at post-natal day (PND) 14, 21, or 28. Field EPSPs (excitatory post-synaptic potential) or whole-cell EPSCs (excitatory post-synaptic conductance) were recorded from the DG (dentate gyrus) in response to medial perforant path activation. Low-frequency stimulation (LFS; 900 pulses; 120 s pulse) was used to induce LTD.

Whole-cell recordings indicated that EtOH exposure at 50mM did not significantly impact ensemble NMDAr EPSCs in slices obtained from animals in the PND14 or 21 groups, but it reliably produced a modest inhibition in the PND28 group. read more Increasing the concentration to 100 mM resulted in a modest inhibition of NMDAr EPSCs in all three groups. LTD induction and maintenance was equivalent in magnitude in all three age groups in control conditions, however, and surprisingly, NMDA antagonist AP5 only reliably blocked LTD in the PND21 and 28 age groups. The application of 50 mM EtOH attenuated LTD in all three age groups, however increasing the concentration to 100 mM did not reliably inhibit LTD.

These results indicate that the effect of EtOH on NMDAr-EPSCs recorded from DGCs is both age and concentration dependent in juveniles. Low concentrations of EtOH can attenuate, but did not block LTD in the DG. The effects of EtOH on LTD do not align well with it's effects on NNMDA receptors.

These results indicate that the effect of EtOH on NMDAr-EPSCs recorded from DGCs is both age and concentration dependent in juveniles. Low concentrations of EtOH can attenuate, but did not block LTD in the DG. The effects of EtOH on LTD do not align well with it's effects on NNMDA receptors.

Acute (

) and chronic (

) alcohol exposure induces neuroplastic changes in the dorsal striatum, a critical region implicated in instrumental learning.

Sex differences are evident in alcohol reward and reinforcement, with female rats consuming higher amount of alcohol in operant paradigms compared to male rats. However, sex differences in the neuroplastic changes produced by acute alcohol in the dorsal striatum have been unexplored.

Using electrophysiological recordings from dorsal striatal slices obtained from adult male and female rats, we investigated the effects of

ethanol exposure on synaptic transmission and synaptic plasticity. Ethanol (44 mM) enhanced basal synaptic transmission in both sexes. Ethanol also enhanced long-term potentiation in both sexes. Other measures of synaptic plasticity including paired-pulse ratio were unaltered by ethanol in both sexes.

The results suggest that alterations in synaptic plasticity induced by acute ethanol, at a concentration associated with intoxication, could play an important role in alcohol-induced experience-dependent modification of corticostriatal circuits underlying the learning of goal-directed instrumental actions and formation of habits mediating alcohol seeking and taking.

Taken together, understanding the mechanism(s) underlying alcohol induced changes in corticostriatal function may lead to the development of more effective therapeutic agents to reduce habitual drinking and seeking associated with alcohol use disorders.

Taken together, understanding the mechanism(s) underlying alcohol induced changes in corticostriatal function may lead to the development of more effective therapeutic agents to reduce habitual drinking and seeking associated with alcohol use disorders.Alcohol is one of the oldest pharmacological agents used for its sedative/hypnotic effects, and alcohol abuse and alcohol use disorder (AUD) continues to be major public health issue. AUD is strongly indicated to be a brain disorder, and the molecular and cellular mechanism/s by which alcohol produces its effects in the brain are only now beginning to be understood. In the brain, synaptic plasticity or strengthening or weakening of synapses, can be enhanced or reduced by a variety of stimulation paradigms. Synaptic plasticity is thought to be responsible for important processes involved in the cellular mechanisms of learning and memory. Long-term potentiation (LTP) is a form of synaptic plasticity, and occurs via N-methyl-D-aspartate type glutamate receptor (NMDAR or GluN) dependent and independent mechanisms. In particular, NMDARs are a major target of alcohol, and are implicated in different types of learning and memory. Therefore, understanding the effect of alcohol on synaptic plasticity and transmission mediated by glutamatergic signaling is becoming important, and this will help us understand the significant contribution of the glutamatergic system in AUD. In the first part of this review, we will briefly discuss the mechanisms underlying long term synaptic plasticity in the dorsal striatum, neocortex and the hippocampus. In the second part we will discuss how alcohol (ethanol, EtOH) can modulate long term synaptic plasticity in these three brain regions, mainly from neurophysiological and electrophysiological studies. Taken together, understanding the mechanism(s) underlying alcohol induced changes in brain function may lead to the development of more effective therapeutic agents to reduce AUDs.