sfn2007

Cai L, Johnson DA (2007) Poster: Recognition of novel objects and their location in rats with selective cholinergic lesion of the medial septum. Neuroscience 2007 Abstracts 92.21/TT2. Society for Neuroscience, San Diego, CA.

Summary: The goal of this project was to determine whether cholinergic neurons projecting from the medial septum (MS) to the hippocampus play a role in novel object recognition or location. The specific aim was to determine whether lesion of cholinergic neurons in MS by the selective cholinergic neurotoxin 192IgG-saporin (SAP) would induce retrograde amnesia and/or anterograde amnesia for a novel object and/or its location. Male SD rats were tested in an object recognition paradigm. The time the rats spent examining old and novel objects was measured. Infusion of SAP into medial septum was performed 2 days after a one week pre-surgery training. Fourteen days after surgery post-surgery retention testing for retrograde object memory was carried out. Then 3 days later, a new acquisition training and retention testing for anterograde memory was started. One-way ANOVA and Fisher’s exact test were used for statistical analysis. There were no significant differences in the exploration ratios between the control group without surgery and the CSF surgical group. The mean exploration ratios for both groups demonstrated retention of memory for the novel object and its placement. SAP infusion into the MS failed to induce a deficit in retrograde amnesia 2 days after training, but did show a strong trend for anterograde amnesia for novel object recognition and a significant association with anterograde amnesia for object location. Conclusions were that cholinergic neurons of MS were not involved in retrograde object memory 2 days before the infusion of SAP and may or may not be necessary for anterograde object memory formation, but cholinergic neurons of the MS were involved in anterograde spatial memory formation for novel objects.

Related Products: 192-IgG-SAP (Cat. #IT-01)

Coons KD, Wilson RE, Sengelaub DR (2007) Protection from dendritic atrophy with testosterone following partial motoneuron depletion: dose-dependence in males and efficacy in females. Neuroscience 2007 Abstracts 56.11/S5. Society for Neuroscience, San Diego, CA.

Summary: Partial depletion of motoneurons from the highly androgen-sensitive spinal nucleus of the bulbocavernosus (SNB), or the more typical somatic motoneuron population innervating the quadriceps muscles, induces dendritic atrophy in remaining motoneurons. Treatment with testosterone (T) is neuroprotective, and dendritic atrophy following partial motoneuron depletion is attenuated in both populations. In the present study, we examined the dose-dependency of T effects in male rats, as well as its potential efficacy in females. Motoneurons innervating the bulbocavernosus/levator ani (BC/LA) or vastus medialis muscles were selectively killed by intramuscular injection of cholera toxin-conjugated saporin. Simultaneously, saporin-injected rats were given T implants designed to produce plasma titers ranging from 0.75 to 5.0 ng/ml or left untreated. Four weeks later, motoneurons innervating the contralateral BC or the ipsilateral vastus lateralis muscles were labeled with cholera toxin-conjugated HRP, and dendritic arbors were reconstructed in 3 dimensions. Partial motoneuron depletion resulted in dendritic atrophy in remaining SNB and quadriceps motoneurons (40% and 36% of normal length, respectively). T treatment attenuated this atrophy in a dose-dependent manner, with maximum effectiveness at 2.0-2.5 ng/ml (the normal adult physiological level). This dosage of T resulted in SNB dendritic lengths that did not differ from those of intact control males. In contrast, although dendritic atrophy in quadriceps motoneurons was attenuated by the same dosage of T, resultant dendritic lengths were 60% of normal length, and did not improve further with higher levels of T. Neuroprotective effects of T treatment were also assessed in quadriceps motoneurons in female rats (adult female rats lack the SNB neuromuscular system). As described above, motoneurons innervating the vastus medialis muscles were selectively killed by saporin injection, and females were given T implants (resulting in plasma levels of 2.0-2.5 ng/ml) or left untreated. Four weeks later, motoneurons innervating the ipsilateral vastus lateralis muscles were labeled with cholera toxin-conjugated HRP, and dendritic arbors were reconstructed. As in males, partial motoneuron depletion in females resulted in dendritic atrophy (52% of normal length) in remaining quadriceps motoneurons, and this atrophy was attenuated (70% of normal length) with T treatment. Together, these findings suggest that the neuroprotective effects of T on dendrites are achieved with dosages within the normal physiological range, and furthermore can be observed in motoneurons of both male and female rats.

Related Products: CTB-SAP (Cat. #IT-14)

Ferguson AS, Sengelaub DR (2007) Dendritic atrophy following partial motoneuron depletion: time course of recovery and protection with testosterone. Neuroscience 2007 Abstracts 56.24/S18. Society for Neuroscience, San Diego, CA.

Summary: In male rats, motoneurons of the spinal nucleus of the bulbocavernosus (SNB) project to the bulbocavernosus and levator ani (BC/LA) muscles, and both the motoneurons and their target muscles are highly androgen-sensitive. We have previously demonstrated that partial depletion of motoneurons from the SNB induces dendritic atrophy in remaining motoneurons, and that treatment with testosterone (T) is neuroprotective against this atrophy. In the present study, we assessed dendritic atrophy after partial motoneuron depletion in SNB motoneurons at a variety of time points, to determine its time course and pattern with and without T treatment. Motoneurons innervating the BC/LA muscles in gonadally intact males were selectively killed by intramuscular injection of cholera toxin-conjugated saporin. Simultaneously, saporin-injected males were given T implants (45mm) or left untreated. At 2, 4, 6, or 10 weeks after motoneuron depletion, motoneurons innervating the contralateral BC were labeled with cholera toxin-conjugated HRP, and dendritic arbors were reconstructed in 3 dimensions. As previously reported, partial motoneuron depletion resulted in dendritic atrophy in remaining SNB motoneurons. While motoneuron depletion occurs within 7 days after saporin injection, dendritic atrophy in remaining SNB motoneurons progresses linearly over several weeks, with a decrease of 32% present at 2 weeks after motoneuron depletion, and a decrease to 66% at 4 weeks. Evidence of recovery in dendritic lengths was observed at 6 weeks post depletion (only 43% decreased), and by 10 weeks SNB dendritic lengths had returned to those of normal, intact males. Treatment with T altered the pattern of dendritic atrophy. While initial dendritic atrophy was similar to that of untreated saporin-injected males (29% decreased at 2 weeks post motoneuron depletion), T treatment attenuated dendritic atrophy. Four weeks after motoneuron depletion, SNB dendritic lengths had not declined further in T-treated males (32% decreased), and were now 102% longer than those of untreated, saporin-injected males. These findings suggest that SNB dendrites undergo a protracted atrophy and subsequent recovery following partial motoneuron depletion, and that the neuroprotective effects of T attenuate the magnitude of the induced atrophy.

Related Products: CTB-SAP (Cat. #IT-14)