Dendritic morphology changes in neurons from the ventral hippocampus, amygdala and nucleus accumbens in rats with neonatal lesions into the prefrontal cortex

Abstract

Neonatal prefrontal cortex (nPFC) lesions in rats could be a potential animal model to study the early neurodevelopmental abnormalities associated with the behavioral and morphological brain changes observed in schizophrenia. Morphological alterations in pyramidal neurons from the ventral hippocampus (VH) have been observed in post-mortem schizophrenic brains, mainly because of decreased dendritic arbor and spine density. We assessed the effects of nPFC-lesions on the dendritic morphology of neurons from the VH, basolateral-amygdala (BLA) and the nucleus accumbens (NAcc) in rats. nPFC lesions were made on postnatal day 7 (PD7), after dendritic morphology was studied by the Golgi-Cox stain procedure followed by Sholl analysis at PD35 (prepubertal) and PD60 (adult) ages. We also evaluated the effects of PFC-lesions on locomotor activity caused by a novel environment. Adult animals with nPFC lesions showed a decreased spine density in pyramidal neurons from the VH and in medium spiny cells from the NAcc. An increased locomotion was observed in a novel environment for adult animals with a PFC-lesion. Our results indicate that PFC-lesions alter the neuronal dendrite morphology of the NAcc and the VH, suggesting a disconnection between these limbic structures. The locomotion paradigms suggest that dopaminergic transmission is altered in the PFC lesion model. This could help to understand the consequences of an earlier PFC dysfunction in schizophrenia. To evaluate possible dendritic changes in neonatal prefrontal cortex lesions in schizophrenia-related regions including nucleus accumbens, ventral hippocampus and basolateral amygdala, we used the Golgi-Cox stain samples at PD35 and PD70. Our results suggest that neonatal prefrontal cortex damage alters dendritic parameters in limbic regions, and this has potential implications for schizophrenia.

L-DOPA Oppositely Regulates Synaptic Strength and Spine Morphology in D1 and D2 Striatal Projection Neurons in Dyskinesia

“…Although dopamine denervation increases MSN firing rate ( Calabresi et al 1993 ; Azdad et al 2009 ; Suarez et al 2014 ), the specific electrophysiological changes that occur in each type of MSN in PD and after chronic L-DOPA treatment remain to be fully characterized. Additionally, studies in animal models of other disorders, including schizophrenia or drug-addiction, suggest that alterations in striatal synaptic function are mediated by changes not only in the number of dendritic spines, but also in spine morphology ( Robinson and Kolb 2004 ; Lazcano et al 2015 ). Dendritic spines are usually classified into three categories based on their morphology: mushroom, thin, and stubby.…”

The neuropeptide‐12 improves recognition memory and neuronal plasticity of the limbic system in old rats

“…After the treatment with N‐PEP‐12 or vehicle, the animals developed the locomotor activity in a novel environment as proposed Flores, Wood, Liang, Quirion, & Srivastava (), Lazcano et al () and Diaz et al (). Locomotor activity was monitored in boxes of locomotion (20 × 40 × 30 cm), which were equipped with an eight‐photo‐beam detector connected to a computer counter (Technology Digital, Mexico).…”

The aminoestrogen prolame increases recognition memory and hippocampal neuronal spine density in aged mice

“…Twenty‐four hours after the last administration of the prolame (Day 60 of the treatment with prolame), spontaneous locomotor activity for the prolame and control mice was assessed in a novel environment. Assays were performed as described previously (Lazcano et al, ). Locomotor activity was monitored in 10 individual cages (20 × 40 × 30 cm), each of which was equipped with an eight‐photo‐beam detector connected to a computer counter (Technology Digital, Mexico).…”