PMID- 22170567
OWN - NLM
STAT- MEDLINE
DCOM- 20120709
LR  - 20141120
IS  - 1098-2396 (Electronic)
IS  - 0887-4476 (Linking)
VI  - 66
IP  - 5
DP  - 2012 May
TI  - Dendritic morphology of neurons in prefrontal cortex and ventral hippocampus of 
      rats with neonatal amygdala lesion.
PG  - 373-82
LID - 10.1002/syn.21517 [doi]
AB  - Neonatal basolateral amygdala (nBLA) lesions in rats have been widely used as a 
      neurodevelopmental model that mimics schizophrenia-like behaviors. Recently, we 
      reported that nBLA lesions result in significant decreases in the dendritic spine 
      number of layer 3 prefrontal cortex (PFC) pyramidal cells and medium spiny 
      neurons of the nucleus accumbens (NAcc), which all changes after puberty. At 
      present, we aimed to evaluate the effect of this lesion in pyramidal neurons of 
      CA1 of the ventral hippocampus (VH) and layer 5 of the PFC. In order to assess 
      the effects of nBLA lesions on the dendritic morphology of the PFC and VH 
      neurons, we carried out nBLA lesions in rats on postnatal day (PD) 7, and then we 
      studied the dendritic morphology of these two limbic subregions at prepubertal 
      (PD35) and postpubertal (PD60) ages. Dendritic characteristics were measured by 
      Golgi-Cox procedure followed by Sholl analysis. We also evaluated the effects of 
      nBLA lesions on the prepulse inhibition (PPI) and acoustic startle responses. The 
      nBLA lesion induced a significant increase in dendritic length of layer 5 
      pyramidal neurons of the PFC at both ages, with a decrease in the dendritic 
      spines density after puberty. The spine density of CA1 VH pyramidal neurons 
      showed significant decreases at both ages. PPI was decreased in adulthood in the 
      animals with an nBLA lesion. These results show that an nBLA lesion alters the 
      dendritic morphology at the level of the PFC and VH in distinct ways before 
      puberty, suggesting a disconnection between these limbic structures at an early 
      age, and increasing our understanding of the implications of the VH in early 
      amygdala dysfunction in schizophrenia.
CI  - Copyright (c) 2011 Wiley Periodicals, Inc.
FAU - Vazquez-Roque, Ruben Antonio
AU  - Vazquez-Roque RA
AD  - Laboratorio de Neuropsiquiatria, Instituto de Fisiologia, Universidad Autonoma de 
      Puebla. 14 Sur 6301, CP: 72570 Puebla, Mexico.
FAU - Solis, Oscar
AU  - Solis O
FAU - Camacho-Abrego, Israel
AU  - Camacho-Abrego I
FAU - Rodriguez-Moreno, Antonio
AU  - Rodriguez-Moreno A
FAU - Cruz, Fidel De La
AU  - Cruz Fde L
FAU - Zamudio, Sergio
AU  - Zamudio S
FAU - Flores, Gonzalo
AU  - Flores G
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120215
PL  - United States
TA  - Synapse
JT  - Synapse (New York, N.Y.)
JID - 8806914
SB  - IM
MH  - Amygdala/*injuries
MH  - Animals
MH  - Animals, Newborn
MH  - CA1 Region, Hippocampal/*pathology
MH  - Dendritic Spines/*pathology
MH  - Models, Animal
MH  - Prefrontal Cortex/*pathology
MH  - Pyramidal Cells/*pathology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reflex, Startle/physiology
MH  - Schizophrenia/pathology
EDAT- 2011/12/16 06:00
MHDA- 2012/07/10 06:00
CRDT- 2011/12/16 06:00
PHST- 2011/09/06 00:00 [received]
PHST- 2011/11/21 00:00 [accepted]
PHST- 2011/12/16 06:00 [entrez]
PHST- 2011/12/16 06:00 [pubmed]
PHST- 2012/07/10 06:00 [medline]
AID - 10.1002/syn.21517 [doi]
PST - ppublish
SO  - Synapse. 2012 May;66(5):373-82. doi: 10.1002/syn.21517. Epub 2012 Feb 15.