Behavioral Disinhibition

Cross references: 
 

Searching PubMed for "behavioral disinhibition" found 2,360 references:   
http://www.ncbi.nlm.nih.gov/pubmed/?term=behavioral+disinhibition  
    This is too many.  I need another search term.  



1987    1141<1206   (1175<1240) 
Defense reaction elicited by injection of GABA antagonists and synthesis inhibitors into the posterior hypothalamus in rats.   
http://www.ncbi.nlm.nih.gov/pubmed/3037412   
    "These results suggest that both the physiological and locomotor components of the hypothalamic defense reaction may be under tonic GABAergic inhibition in the region of the posterior hypothalamus."  
    Abstract
    "Blockade of gamma-aminobutyric acid (GABA) in the posterior hypothalamic nucleus elicits cardiorespiratory stimulation in anesthetized rats. The present study was conducted to test the hypothesis that blockade of GABA in this cardiostimulatory area of the posterior hypothalamus in conscious animals would elicit a defense reaction characterised by a "fight or flight" response.  
    Blockade of GABA was achieved by injecting bicuculline methiodide (BMI 1-25 ng) and picrotoxin (4-100 ng), two post-synaptic GABA antagonists and isoniazid (INH 35 and 70 micrograms), an inhibitor of the synthesis of GABA, bilaterally into the posterior hypothalamus through chronically implanted microinjection cannulae.  
    All three drugs produced dose-dependent increases in locomotor activity, suggesting an "escape" reaction which was quantified as number of crossings and rearings. The effects of bicuculline and picrotoxin appeared immediately after the injection while those of isoniazid appeared much more slowly, attaining peak effects 24 +/- 1 min after injection. Injection of either strychnine (38 ng) into the posterior hypothalamus or bicuculline into the lateral hypothalamic area (LHA) or the dorso-medial/ventro-medial hypothalamus (DMH/VMH) did not elicit a significant increase in locomotor behavior.  
    These results suggest that both the physiological and locomotor components of the hypothalamic defense reaction may be under tonic GABAergic inhibition in the region of the posterior hypothalamus."  
    See:  Fear for  Related citations and Cited by's.   
The motor programs which are referred to  Defense reaction 
    My comment
Perhaps my mother's Sadism  was a deeply ingrained, habituated defense reaction.   
    See:  My Dysfunctional Family  and  Anger


1996    (from a different search)
Neural networks for vertebrate locomotion     
http://www.ncbi.nlm.nih.gov/pubmed/8533066
    No PubMed Abstract, but full length paper on Google
http://neuromajor.ucr.edu/courses/Grillner_Sci-Am-1996.pdf

    " Under resting conditions, the basal ganglia continuously inhibit the brain’s sundry motor centers so that no movements occur. But when the active inhibition is released, coordinated motions may begin. "
    See:  GABA/Glycine Inhibition 
for full-length article and Related citations.    
The motor programs which are  referred to  vertebrate locomotion 
 

2001    843<1206  (875<1240) 
GABA(B) receptor inhibition causes locomotor stimulation in mice   
http://www.ncbi.nlm.nih.gov/pubmed/11755139   
    "These results suggest the existence of a GABA(B) receptor-mediated tonic inhibition of dopamine neurons."
    Abstract
    "The present study investigated the effect of the administration of the GABA(B) receptor antagonists,
    SCH 50911 [(2S)(+)-5,5-dimethyl-2-morpholineacetic acid], 
    CGP 46381 [(3-aminopropyl)(cyclohexylmethyl)phosphinic acid] and 
    CGP 52432 (3-[[(3,4-dichlorophenyl)methyl]amino]propyl]diethoxymethyl)phosphinic acid),
on spontaneous locomotor activity in mice. All drugs were acutely administered at the doses of 10 and 30 mg/kg (i.p.).  The dose of 30 mg/kg of all drugs resulted in a significant stimulation of locomotor activity.  
    The locomotor stimulation elicited by SCH 50911 was completely blocked by haloperidol (0.1 mg/kg, i.p.), suggesting that hyperactivity induced by blockade of the GABA(B) receptor is mediated by enhanced dopamine release.
    These results suggest the existence of a GABA(B) receptor-mediated tonic inhibition of dopamine neurons."   
See:  GABA Metabotropic Receptor  for  Related citations and Cited by's.    
    The motor programs which are  referred to locomotor stimulation 


2007    557<1206 
GABAergic output of the basal ganglia.   
http://www.ncbi.nlm.nih.gov/pubmed/17499116    
    "Using GABAergic outputs from the SNr or GP(i), the basal ganglia exert inhibitory control over several motor areas in the brainstem which in turn control the central pattern generators for the basic motor repertoire including eye-head orientation, locomotion, mouth movements, and vocalization. These movements are by default kept suppressed by tonic rapid firing of SNr/GP(i) neurons, but can be released by a selective removal of the tonic inhibition. ...
    To summarize, an essential function of the basal ganglia is to select, sort, and integrate innate movements and learned movements, together with cognitive and emotional mental operations, to achieve purposeful behaviors. Intricate hand-finger movements do not occur in isolation; they are always associated with appropriate motor sets, such as eye-head orientation and posture."   
    See:  Basal Ganglia  for full Abstract, Related citations and Cited by's. 

The motor programs which are referred to    GABAergic output of the basal ganglia.   
    "
Intricate hand-finger movements do not occur in isolation; they are always associated with appropriate motor sets, such as eye-head orientation and posture
    See:  Early Behavior  
 

2008   491<1206   
Diencephalic locomotor region in the lamprey--afferents and efferent control. 
http://www.ncbi.nlm.nih.gov/pubmed/18596192      
    "These findings suggest that
GABAergic projections provide tonic inhibition that once turned off can release locomotion. Double-labeling experiments were carried out to identify GABAergic projections to the DLR."
    Abstract
    "In vertebrates, locomotion can be initiated by stimulation of the diencephalic locomotor region (DLR). Little is known of the different forebrain regions that provide input to the neurons in DLR.
    In the lamprey, it had been shown previously that DLR provides monosynaptic input to reticulospinal neurons, which in turn elicit rhythmic ventral root activity at the spinal level.  
    To show that actual locomotor movements are produced from DLR, we use a semi-intact preparation in which the brain stem is exposed and the head fixed, while the body is left to generate actual swimming movements. DLR stimulation induced symmetric locomotor movements with an undulatory wave transmitted along the body.  
    To explore if DLR is under tonic GABAergic input under resting conditions, as in mammals, GABAergic antagonists and agonists were locally administered into DLR. 
    Injections of GABA agonists inhibited locomotion, whereas GABA antagonists facilitated the induction of locomotion. These findings suggest that GABAergic projections provide tonic inhibition that once turned off can release locomotion.  
    Double-labeling experiments were carried out to identify GABAergic projections to the DLR. Populations of GABAergic projection neurons to DLR originated in the caudoventral portion of the medial pallium, the lateral and dorsal pallium, and the striatal area.  
    These different GABAergic projection neurons, which also project to other brain stem motor centers, may represent the basal ganglia output to DLR. Moreover, electrical stimulation of striatum induced long-lasting plateau potentials in reticulospinal cells and associated locomotor episodes dependent on DLR being intact, suggesting that striatum may act via the basal ganglia output identified here."  
    See:  GABA/Glycine Inhibition for Related citations, Cited by's and
Free Article 
    The motor programs which are referred to:   Tonic Inhibition  


2008    489<1206  
Gabaergic mechanisms of hypothalamic nuclei in the expression of conditioned fear. 
http://www.ncbi.nlm.nih.gov/pubmed/18634894       
    "The amygdala, the dorsal periaqueductal gray (dPAG), and the medial hypothalamus have long been recognized to be a neural system responsible for the generation and elaboration of unconditioned fear in the brain. It is also well known that this neural substrate is under a tonic inhibitory control exerted by GABA mechanisms."

    Abstract
    "The amygdala, the dorsal periaqueductal gray (dPAG), and the medial hypothalamus have long been recognized to be a neural system responsible for the generation and elaboration of unconditioned fear in the brain.  It is also well known that this neural substrate is under a tonic inhibitory control exerted by GABA mechanisms.  
    However, whereas there is a growing body of evidence to suggest that the amygdala and dPAG are also able to integrate conditioned fear, it is still unclear, however, how the distinct hypothalamic nuclei participate in fear conditioning.  
    In this work we aimed to examine the extent to which the gabaergic mechanisms of this brain region are involved in conditioned fear using the fear-potentiated startle (FPS).  
    Muscimol, a GABA-A receptor agonist, and semicarbazide, an inhibitor of the GABA synthesizing enzyme glutamic acid decarboxylase (GAD), were used as an enhancer and inhibitor of the GABA mechanisms, respectively. Muscimol and semicarbazide were injected into the anterior hypothalamus (AHN), the dorsomedial part of the ventromedial nucleus (VMHDM), the dorsomedial (DMH) or the dorsal premammillary (PMD) nuclei of male Wistar rats before test sessions of the fear conditioning paradigm.  
    The injections into the DMH and PMD did not produce any significant effects on FPS. On the other hand, muscimol injections into the AHN and VMHDM caused significant reduction in FPS.  
    These results indicate that injections of muscimol and semicarbazide into the DMH and PMD fail to change the FPS, whereas the enhancement of the GABA transmission in the AHN and VMHDM produces a reduction of the conditioned fear responses. On the other hand, the inhibition of this transmission led to an increase of this conditioned response in the AHN.  
    Thus, whereas DMH and PMD are known to be part of the caudal-most region of the medial hypothalamic defensive system, which integrates unconditioned fear, systems mediating conditioned fear select the AHN and VMHDM nuclei that belong to the rostral-most portion of the hypothalamic defense area. Thus, distinct subsets of neurons in the hypothalamus could mediate different aspects of the defensive responses.
     See:  Fear  for Related citations.   
The motor programs which are directly referred to:   unconditioned fear 



2008     (from a different search)  
Initiation of locomotion in lampreys  
http://www.ncbi.nlm.nih.gov/pubmed/17916380     
    "GABA inputs tonically maintain the MLR inhibited and removal of this inhibition initiates locomotion."

    Abstract
    "The spinal circuitry underlying the generation of basic locomotor synergies has been described in substantial detail in lampreys and the cellular mechanisms have been identified. The initiation of locomotion, on the other hand, relies on supraspinal networks and the cellular mechanisms involved are only beginning to be understood. 
    This review examines some of the findings relative to the neural mechanisms involved in the initiation of locomotion of lampreys. Locomotion can be elicited by sensory stimulation or by internal cues associated with fundamental needs of the animal such as food seeking, exploration, and mating. 
    We have described mechanisms by which escape swimming is elicited in lampreys in response to mechanical skin stimulation. A rather simple neural connectivity is involved, including sensory and relay neurons, as well as the brainstem rhombencephalic reticulospinal cells, which act as command neurons.  
    We have shown that reticulospinal cells have intrinsic membrane properties that allow them to transform a short duration sensory input into a long-lasting excitatory command that activates the spinal locomotor networks. These mechanisms constitute an important feature for the activation of escape swimming.  
    Other sensory inputs can also elicit locomotion in lampreys. For instance, we have recently shown that olfactory signals evoke sustained depolarizations in reticulospinal neurons and chemical activation of the olfactory bulbs with local injections of glutamate induces fictive locomotion.  
    The mechanisms by which internal cues initiate locomotion are less understood. Our research has focused on one particular locomotor center in the brainstem, the mesencephalic locomotor region (MLR). The MLR is believed to channel inputs from many brain regions to generate goal-directed locomotion. It activates reticulospinal cells to elicit locomotor output in a graded fashion contrary to escape locomotor bouts, which are all-or-none.  
    MLR inputs to reticulospinal cells use both glutamatergic and cholinergic transmission; nicotinic receptors on reticulospinal cells are involved. MLR excitatory inputs to reticulospinal cells in the middle (MRRN) are larger than those in the posterior rhombencephalic reticular nucleus (PRRN). Moreover at low stimulation strength, reticulospinal cells in the MRRN are activated first, whereas those in the PRRN require stronger stimulation strengths.  
    The output from the MLR on one side activates reticulospinal neurons on both sides in a highly symmetrical fashion. This could account for the symmetrical bilateral locomotor output evoked during unilateral stimulation of the MLR in all animal species tested to date. Interestingly, muscarinic receptor activation reduces sensory inputs to reticulospinal neurons and, under natural conditions, the activation of MLR cholinergic neurons will likely reduce sensory inflow. Moreover, exposing the brainstem to muscarinic agonists generates sustained recurring depolarizations in reticulospinal neurons through pre-reticular effects. 
    Cells in the caudal half of the rhombencephalon appear to be involved and we propose that the activation of these muscarinoceptive cells could provide additional excitation to reticulospinal cells when the MLR is activated under natural conditions.  
    One important question relates to sources of inputs to the MLR. We found that substance P excites the MLR, whereas GABA inputs tonically maintain the MLR inhibited and removal of this inhibition initiates locomotion.  
    Other locomotor centers exist such as a region in the ventral thalamus projecting directly to reticulospinal cells. This region, referred to as the diencephalic locomotor region, receives inputs from several areas in the forebrain and is likely important for goal-directed locomotion.  
    In summary, this review focuses on the most recent findings relative to initiation of lamprey locomotion in response to sensory and internal cues in lampreys.
    
See:  Initiation of Locomotion in Lampreys   for Related citations and Cited by's  .   
    The motor programs which are directly referred to:     Initiation of locomotion 


2008     (from a different search)  
Origin of excitatory drive to a spinal locomotor network.       
    "A long-standing hypotheses is that locomotion is turned on by descending excitatory synaptic drive. "
    Abstract
    "A long-standing hypotheses is that locomotion is turned on by descending excitatory synaptic drive. In young frog tadpoles, we show that prolonged swimming in response to a brief stimulus can be generated by a small region of caudal hindbrain and rostral spinal cord. Whole-cell patch recordings in this region identify hindbrain neurons that excite spinal neurons to drive swimming. Some of these hindbrain reticulospinal neurons excite each other. We consider how feedback excitation within the hindbrain may provide a mechanism to drive spinal locomotor networks.
   
The motor programs which are directly referred to:    spinal locomotor network

My comment:
    The strong bias toward locomotion reflects my biased interest in locomotion. 
 



SubC:  Behavioral Disinhibition 
180818 - 1229   



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