Abstract
We have previously reported that lactating rats, unlike cycling rats, are refractory to N-methyl-d,l-aspartic acid (NMA), but not kainate, in terms of behavioral responses and activation of cFos expression in the neocortex and hippocampus. To study the factors involved in the suppression of cortical activation in lactating rats in response to NMA, we examined the effects of removing either the suckling stimulus and/or progesterone. The degree of cFos expression was used as a marker for cortical activation. Whereas control suckled animals exhibited little or no cFos activation in the piriform cortex in response to NMA, cycling rats showed a high degree of activation. Blockade of the effects of progesterone or removal of the pups for 24 h, resulted in a moderate level of cFos intensity in response to NMA. Total recovery was observed only in animals who had their pups removed for 24 h and the effects of progesterone were blockad. In general, similar results were obtained in the hippocampus except that the total recovery of hippocampal activation took longer than the cortex. Thus, the deficits in cortical activation depend on the presence of both the suckling stimulus and progesterone. However, progesteron alone cannot induced these cortical deficits since pregnant rats showed no deficits in cortical activation in response to NMA when compared to cycling rats. Therefore, the suckling stimulus is required for the inhibition of NMDA-receptor mediated activation of the cortex and hippocampus. The effects of progesterone appear to act synergistically with the effects of suckling.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 16-23 |
| Number of pages | 8 |
| Journal | Brain Research |
| Volume | 604 |
| Issue number | 1-2 |
| DOIs | |
| State | Published - Feb 26 1993 |
| Externally published | Yes |
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Keywords
- CFos expression
- Cortical activation
- Lactation
- N-Methyl-d,l-aspartic acid
- N-Methyl-d-aspartate receptor inactivation
- progesterone
ASJC Scopus subject areas
- Developmental Biology
- Molecular Biology
- Clinical Neurology
- Neuroscience(all)
Cite this
Cortical refractoriness to N-methyl-d, l-aspartic acid (NMA) stimulation in the lactating rat : recovery after pup removal and blockade of progesterone receptors. / Abbud, Rula; Hoffman, Gloria E.; Smith, M (Susan).
In: Brain Research, Vol. 604, No. 1-2, 26.02.1993, p. 16-23.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Cortical refractoriness to N-methyl-d, l-aspartic acid (NMA) stimulation in the lactating rat
T2 - recovery after pup removal and blockade of progesterone receptors
AU - Abbud, Rula
AU - Hoffman, Gloria E.
AU - Smith, M (Susan)
PY - 1993/2/26
Y1 - 1993/2/26
N2 - We have previously reported that lactating rats, unlike cycling rats, are refractory to N-methyl-d,l-aspartic acid (NMA), but not kainate, in terms of behavioral responses and activation of cFos expression in the neocortex and hippocampus. To study the factors involved in the suppression of cortical activation in lactating rats in response to NMA, we examined the effects of removing either the suckling stimulus and/or progesterone. The degree of cFos expression was used as a marker for cortical activation. Whereas control suckled animals exhibited little or no cFos activation in the piriform cortex in response to NMA, cycling rats showed a high degree of activation. Blockade of the effects of progesterone or removal of the pups for 24 h, resulted in a moderate level of cFos intensity in response to NMA. Total recovery was observed only in animals who had their pups removed for 24 h and the effects of progesterone were blockad. In general, similar results were obtained in the hippocampus except that the total recovery of hippocampal activation took longer than the cortex. Thus, the deficits in cortical activation depend on the presence of both the suckling stimulus and progesterone. However, progesteron alone cannot induced these cortical deficits since pregnant rats showed no deficits in cortical activation in response to NMA when compared to cycling rats. Therefore, the suckling stimulus is required for the inhibition of NMDA-receptor mediated activation of the cortex and hippocampus. The effects of progesterone appear to act synergistically with the effects of suckling.
AB - We have previously reported that lactating rats, unlike cycling rats, are refractory to N-methyl-d,l-aspartic acid (NMA), but not kainate, in terms of behavioral responses and activation of cFos expression in the neocortex and hippocampus. To study the factors involved in the suppression of cortical activation in lactating rats in response to NMA, we examined the effects of removing either the suckling stimulus and/or progesterone. The degree of cFos expression was used as a marker for cortical activation. Whereas control suckled animals exhibited little or no cFos activation in the piriform cortex in response to NMA, cycling rats showed a high degree of activation. Blockade of the effects of progesterone or removal of the pups for 24 h, resulted in a moderate level of cFos intensity in response to NMA. Total recovery was observed only in animals who had their pups removed for 24 h and the effects of progesterone were blockad. In general, similar results were obtained in the hippocampus except that the total recovery of hippocampal activation took longer than the cortex. Thus, the deficits in cortical activation depend on the presence of both the suckling stimulus and progesterone. However, progesteron alone cannot induced these cortical deficits since pregnant rats showed no deficits in cortical activation in response to NMA when compared to cycling rats. Therefore, the suckling stimulus is required for the inhibition of NMDA-receptor mediated activation of the cortex and hippocampus. The effects of progesterone appear to act synergistically with the effects of suckling.
KW - CFos expression
KW - Cortical activation
KW - Lactation
KW - N-Methyl-d,l-aspartic acid
KW - N-Methyl-d-aspartate receptor inactivation
KW - progesterone
UR - http://www.scopus.com/inward/record.url?scp=0027450907&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0027450907&partnerID=8YFLogxK
U2 - 10.1016/0006-8993(93)90347-P
DO - 10.1016/0006-8993(93)90347-P
M3 - Article
C2 - 8457843
AN - SCOPUS:0027450907
VL - 604
SP - 16
EP - 23
JO - Brain Research
JF - Brain Research
SN - 0006-8993
IS - 1-2
ER -