- •Development of locomotion in the rat: the significance of early movements.
- •Abstract
- •Role of gravity in the development of posture and locomotion in the neonatal rat.
- •Abstract
- •Development of receptors for dopamine and noradrenaline in rat brain.
- •Abstract
- •Locomotor-rotational movements in the ontogeny and play of the laboratory rat Rattus norvegicus.
- •Abstract
- •The maturation of locomotor networks.
- •Abstract
- •Delayed effects of neonatal hippocampal damage on haloperidol-induced catalepsy and apomorphine-induced stereotypic behaviors in the rat.
- •Abstract
- •Early walking in the neonatal rat: a kinematic study.
- •Abstract
- •The activation of back muscles during locomotion in the developing rat.
- •Abstract
- •The development of locomotor kinematics in neonatal rats: an agent-based modeling analysis in group and individual contexts.
- •Abstract
- •Effect of precocious locomotor activity on the development of motoneurones and motor units of slow and fast muscles in rat.
- •Abstract
- •Results:
- •Conclusions:
- •Delayed effects of neonatal hippocampal damage on haloperidol-induced catalepsy and apomorphine-induced stereotypic behaviors in the rat.
- •Abstract
Results:
A motor performance score detected the functional differences between the control and the recovered rats. Muscle-evoked potentials of hind limbs after electrical stimulation to the brain were recorded in some of the recovered rats, but never in the unrecovered rats. Moreover, the muscle-evoked potentials of the recovered rats disappeared after spinal cord retransection that resulted in loss of voluntary movement. Morphologic studies in two rats provided evidence that reconnection of rubrospinal, vestibulospinal, and reticulospinal tracts had occurred, whereas corticospinal regeneration was not detected.
Conclusions:
It can be concluded that the hind limb function of rats that underwent spinal cord transection in infancy was partially regained; that axonal regeneration of the rubrospinal, vestibulospinal, or reticulospinal tracts was demonstrated, whereas the reconnection of the corticospinal tract was not observed; and that the axonal regeneration of these tracts is involved in the functional recovery.
PMID:
11389386
[PubMed - indexed for MEDLINE]
Brain Res Dev Brain Res. 1993 Oct 15;75(2):213-22.
Delayed effects of neonatal hippocampal damage on haloperidol-induced catalepsy and apomorphine-induced stereotypic behaviors in the rat.
Lipska BK, Weinberger DR.
Source
Clinical Brain Disorders Branch, National Institute of Mental Health, NIH, Neuroscience Center, St. Elizabeths, Washington, DC 20032.
Abstract
The developmental effects of neonatal excitotoxic ventral hippocampal (VH) damage on behaviors related to dopaminergic (DA) transmission in the basal ganglia were investigated in the rat. Ibotenic acid (in Lesion) or artificial cerebrospinal fluid (in Sham) was infused into the VH of 7-day-old (PD7) rat pups. Haloperidol-induced (1 mg/kg, i.p.) catalepsy and apomorphine-induced (0.75 mg/kg, s.c.) stereotypic behaviors as well as locomotion were assessed in Sham and Lesion rats prior to (PD35) and after puberty (PD56). On PD35, Lesion and Sham animals did not differ in induced catalepsy or stereotypy. On PD56, however, Lesion animals were less cataleptic following haloperidol injection and manifested supersensitivity to apomorphine as compared to Sham rats. At both, PD35 and PD56, locomotor activity after apomorphine was significantly increased in Lesion animals as compared with controls. These results indicate that the neonatal excitotoxic VH lesion results in a unique time-dependent pattern of behavioral changes related to striatal DA transmission. Moreover, the response to apomorphine differs qualitatively from that previously reported after the analogous lesion induced in adult animals in which stereotypy was reduced. These findings suggest that early hippocampal deafferentation affects the development of other brain regions, such as the medial prefrontal cortex, that are also involved in the regulation of striatal DA function.
PMID: 7903225
[PubMed - indexed for MEDLINE]