Different roles of intrahypothalamic and nigrostriatal dopaminergic systems in thermoregulatory responses of the rat

González, Marı́a José; Arevalo, R.; Castro, Rafael; Díaz-Palarea, M.D.; Rodrı́guez, Manuel

doi:10.1016/0024-3205(86)90018-4

Cited by 20 publications

(6 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Amphetamine, which provokes release and blocks reuptake of dopamine, also lowers body temperature (Lee, et al, 1985). In view of these and other findings, it has been proposed that dopaminergic projections connecting the anterior hypo-thalamus with the basal ganglia and substantia nigra are important in the detection of body temperature and the motor outputs that promote heat loss (Lee, et al, 1985;Gonzalez, et al, 1986). The importance of dopamine in the pathophysiology of Tourette syndrome is well established given the effectiveness of dopamine-blocking agents in the treatment of tics and the accumulating evidence that Tourette syndrome may be due to dysregulation of cortico-striatial-thalamic-cortical circuits.…”

Section: R S C U S S~o~mentioning

confidence: 99%

Thermal Sensitivity in Tourette Syndrome: Preliminary Report

et al. 2001

View full text Add to dashboard Cite

The effects of heat on tic symptoms were studied in a sample of 78 adults with Tourette syndrome. 62 men and 16 women completed a survey concerning the type, onset, and course of their tics. 10 adult male subjects also participated in a thermal challenge during which ambient temperature was raised from 22 degrees C to 35 degrees C following a control period. Of the 78, 24% or 19 reported increased tics upon exposure to heat. Compared to the remaining 59 subjects, there were no differences in sex distribution, current age, or overall course of illness. In the thermal challenge, there was general increase in tics that was correlated with sweat rate (r = .55, p = .001). This effect was prominent in 5 of 10 subjects (rs = .29 to .63). There were no mean differences in current age, age of onset, or current severity of symptoms between the five subjects of each group. Tic symptoms in a subgroup of patients with Tourette syndrome may be sensitive to heat. Abnormal heat regulation is not a likely explanation for the observed increase in tics. The increase may be due to normal heat-loss mechanisms through dopaminergic pathways.

show abstract

Section: R S C U S S~o~mentioning

confidence: 99%

Thermal Sensitivity in Tourette Syndrome: Preliminary Report

et al. 2001

View full text Add to dashboard Cite

show abstract

“…Among various dopaminergic systems in the brain the rostral incertohypothalamic dopaminergic neurons of the medial preoptic region as well as hypothalamic dopamine-sensitive structures are regarded to be involved in heat loss mechanisms (Lee et al, 1985;Gonzalez et al, 1986). Systemic injection of DA agonists as well as microinjection of apomorphine into the hypothalamus or the substantia nigra (SN) have been 130 M. Haj6s et al found to elicit hypothermia (Brown et al, 1982;Lin et al, 1982;Faunt and Crocker, 1987).…”

Section: Introductionmentioning

confidence: 98%

Capsaicin-sensitive vasodilatatory mechanisms in the rat substantia nigra and striatum

Hajós

Engberg

Nissbrandt

et al. 1988

J. Neural Transmission

View full text Add to dashboard Cite

Thermoregulatory and neurochemical effects of capsaicin microinjection into the substantia nigra (SN) or caudatus putamen (CPu) were studied in rats. Administration of capsaicin into these brain structures induced a peripheral vasodilatation which was associated with a decrease in body temperature. Pretreatment of the rats with capsaicin either as adults or neonates abolished the thermolytic response to the drug, indicating that the effect is executed specifically upon capsaicin sensitive structures. Analyses of the levels of monoamines and their metabolites in the striatum following injection of capsaicin into the SN or CPu revealed that dopaminergic neurons are not primarily involved in this effect. This view is also supported by our findings that neurochemical lesion of unilateral nigrostriatal dopaminergic neurons did not influence the vasodilatatory response. Since the pharmacological effect of intranigral capsaicin was not abolished by unilateral axotomy (hemisection) we presume a capsaicin-sensitive, non-dopaminergic descending vasodilatatory pathway from the SN.

show abstract

“…The striatum has an intricate relationship with thermoregulation through direct and indirect connections with the hypothalamus, the primary thermoregulatory center in the brain ( Feldman, 1966 ; Bolam and Ellender, 2016 ; Kullmann and Veit, 2021 ). Moreover, the striatum’s involvement in neurotransmitter release, especially dopamine, plays a pivotal role in thermoregulatory processes ( Gonzalez et al, 1986 ; Björklund and Dunnett, 2007 ; Shin et al, 2011 ; Jenkins et al, 2018 ). Given its functions in motor response generation and sensory integration, the striatum might influence behaviors aimed at temperature regulation ( Gonzalez et al, 1986 ).…”

Section: Discussionmentioning

confidence: 99%

“…This degeneration results in reduced dopamine (DA) levels in the dorsal striatum and other structures, such as the brain cortex, leading to the presence of motor and nonmotor symptoms ( McGregor and Nelson, 2019 ). A previous study proposed that the reduction in striatal DA synthesis and release could be linked to muscle thermogenesis ( Gonzalez et al, 1986 ).…”

Section: Introductionmentioning

confidence: 99%

Traumatic brain injury extending to the striatum alters autonomic thermoregulation and hypothalamic monoamines in recovering rats

Verduzco-Mendoza,

Mota-Rojas,

Olmos Hernández

et al. 2023

Front. Neurosci.

View full text Add to dashboard Cite

The brain cortex is the structure that is typically injured in traumatic brain injury (TBI) and is anatomically connected with other brain regions, including the striatum and hypothalamus, which are associated in part with motor function and the regulation of body temperature, respectively. We investigated whether a TBI extending to the striatum could affect peripheral and core temperatures as an indicator of autonomic thermoregulatory function. Moreover, it is unknown whether thermal modulation is accompanied by hypothalamic and cortical monoamine changes in rats with motor function recovery. The animals were allocated into three groups: the sham group (sham), a TBI group with a cortical contusion alone (TBI alone), and a TBI group with an injury extending to the dorsal striatum (TBI + striatal injury). Body temperature and motor deficits were evaluated for 20 days post-injury. On the 3rd and 20th days, rats were euthanized to measure the serotonin (5-HT), noradrenaline (NA), and dopamine (DA) levels using high-performance liquid chromatography (HPLC). We observed that TBI with an injury extending to the dorsal striatum increased core and peripheral temperatures. These changes were accompanied by a sustained motor deficit lasting for 14 days. Furthermore, there were notable increases in NA and 5-HT levels in the brain cortex and hypothalamus both 3 and 20 days after injury. In contrast, rats with TBI alone showed no changes in peripheral temperatures and achieved motor function recovery by the 7th day post-injury. In conclusion, our results suggest that TBI with an injury extending to the dorsal striatum elevates both core and peripheral temperatures, causing a delay in functional recovery and increasing hypothalamic monoamine levels. The aftereffects can be attributed to the injury site and changes to the autonomic thermoregulatory functions.

show abstract

Different roles of intrahypothalamic and nigrostriatal dopaminergic systems in thermoregulatory responses of the rat

Cited by 20 publications

References 35 publications

Thermal Sensitivity in Tourette Syndrome: Preliminary Report

Thermal Sensitivity in Tourette Syndrome: Preliminary Report

Capsaicin-sensitive vasodilatatory mechanisms in the rat substantia nigra and striatum

Traumatic brain injury extending to the striatum alters autonomic thermoregulation and hypothalamic monoamines in recovering rats

Contact Info

Product

Resources

About